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Physiological significance of the defense response to intense auditory stimulation: a pharmacological blockade study
INTERNATIONAL JOURNALOF PSYCHOPHYSIOLOGY International Journal of Psychophysiology 17 (1994) 181-187
Short communication
Physiological significance of the defense response to intense auditory stimulation: a pharmacological blockade study Gustav0
A. Reyes de1 Paso a,*, Jaime Vila b and Ana Garcia
a
aDepartamento de Psicologia, Facultad de Humanidades, Unicersidad de Ja&, 23071 Jab, Spain, b Departamento de Personalidad, Ecaluacidn y Tratamiento Psicoldgico, Facultad de PsicologLa, Unicersidad de Granada, 18011 Granada, Spain Received 7 June 1993; revised 29 March 1994; accepted 29 March 1994
Abstract This paper examines through pharmacological blockade some questions related to the physiological significance of the defense response to intense auditory stimulation. Nine subjects received intravenous metoprolol (lo-15 mg i.v.>, intravenous atropine (0.03 mg/kg i.v.1, or a saline solution as placebo condition before undertaking a test of the defense response to a distorted sound of 400 Hz frequency, 109 dB intensity, 0.5 set duration and virtually instantaneous risetime. Dependent variables were continuous (beat-to-beat) heart rate, stroke volume and blood pressure. The results suggest: (1) a vagal origen of the first acceleration and first deceleration and a sympatheticparasympathetic interaction during the second acceleration and second deceleration of the heart rate response; (2) a
blood pressure response pattern characterized by an increase during the first heart rate deceleration (4-11 set), a posterior decrease coinciding with the second heart rate acceleration (from 12 to 37 set), and a lighter increase during the second heart rate deceleration (from 38 to 63 set); and (3) an implication of the baroreceptor reflex, including a baroreceptor mediated inhibition of the parasympathetic cardiac activity during the second accelerative component of the cardiac response. Key words:
Defense
response;
Pharmacological
blockade;
1. Introduction The Cardiac Defense Response (CDR) constitues a specific pattern of heart rate changes which is elicited by intense auditory or electrocutaneous stimuli [1,2]. The response consists of four components, two accelerative and two decel-
* Corresponding author. 0167~8760/94/$07.00 0 1994 Elsevier SSDI 0167-8760(94)00033-B
Science
Heart
rate; Stroke volume; Blood presure; Baroreflex
erative in alternating order occuring within the X0 set post-stimulus. Two outstanding characteristics of this response, which concern specially the second acceleration, are the existence of important individual differences and the display of unusually rapid short-term habituation after the first presentation of the stimulus. Research into the physiological significance of this response pattern using indirect measures of both sympathetic [3,4] and parasympathetic activation [5] suggests a parasympathetic mediation of the first accelera-
B.V. All rights reserved
182
G.A. Reyes del Paso et al. /International
tion and first deceleration and a sympatheticparasympathetic interaction during the second acceleration and second deceleration. As suggested by other authors [6,1] a better understanding of this interaction - in particular, the role that the baroreflex plays during the second acceleration - might be crucial to explain both the individual differences and the rapid habituation phenomenon. The aim of the present preliminary study was to advance our understanding of the physiological significance of the cardiac components of the defense response to intense auditory stimulation by using a pharmacological blockade procedure. This general aim was subdivided into two specific objetives: (a> to examine the effect of atropine administration versus a beta-adrenergic blocker on the accelerative and decelerative heart rate components of the response; and (b) to evaluate the stroke volume and the blood pressure components of the response together with the participation of the baroreceptor reflex in the elicitation of the CDR.
2. Method In the context of a collaborative research with the University of Bonn, 9 medical students from that university (aged between 23 and 25 years) participated as subjects. Six subjects constituted the experimental group and were investigated twice: three received atropine (0.03 mg/kg body weight i.v.1 on day 1 and metoprolol, a pl-selective beta-blocking agent, so as not to influence vasomotor activity, (up to 3 x 5 mg i.v.>, on day 2 (one week later) and the remaining 3 received the reverse order of drugs. Other three subjects constituted the control group and were investigated only once, receiving 3 x 5 ml of saline as a placebo condition. The psychophysiological reaction test consisted of 10 min rest period and one trial of intense auditory stimulation, a distorted sound of 400 Hz frequency, 109 dB intensity, 0.5 set duration and a virtually instantaneous rise time, followed by 3 min post-stimulus period. Once this first phase was over, drugs were injected during a period of 5 min (atropine) or during a maximum
Journal of Psychophysiology
I7 (1994) 1X1-187
of 3 X 5 min (metoprolol and saline). The dose of the beta-blocking agent was calculated according to the HR response: if HR was reduced by > 25%, the injection was stopped. This goal was achieved in all subjects with doses between 10 and 15 mg of metoprolol i.v. Two min after the end of the injection period the same psychophysiological reaction test was repeated. Accordingly, the interval between the two noise presentations was about 20 min for atropine subjects and 30 min for metoprolol and control subjects. Although this within-subject design is not the most appropriate one to study the CDR, due to the short-term habituation phenomenon, we expected that both the minimum interval between trials within the same session (over 20 min) and the week interval between the two sessions would reduce the possible contaminating effect of habituation. On the positive side, the within-subject design has the advantage of requiring a lower number of subjects to examine the same effect, an important advantage in pharmacological blockade studies. Dependent variables were continuous (beatto-beat) heart rate (ECG), stroke volume (through impedance cardiography 1711, and blood pressure (with the non-invasive FIN.A.PRES device [8]). For all these physiological variables the secondby-second values during the 80 set after stimulus onset expressed in terms of differential scores with respect to the average values during the 15 set prior to stimulus onset (baseline) were obtained. In order to analyze the form of the responses to the auditory stimulus the same methodology used in previous studies based on the medians of ten succesively longer intervals was applied [51. Analysis of the results was undertaken by means of both visual and statistic scrutin of the response patterns. In the present brief report only the visual analysis is commented upon.
3. Results and discussion Heart rate pattern Fig. 1 graphically illustrates the response pattern shown by the medians of the heart rate before and after drug administration as a func-
G.A. Reyes de1 Paso et al. /International
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Fig. 1. Heart rate 101 (top), atropine tion. (Numbers on of the 10 selected
FROM STIMULUS
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response pattern before and after metopro(medium) and placebo (bottom) administrathe horizontal axis represent the midpoints intervals.)
Journal of Psychophysiology 17 (1994) 181-187
183
tion of the groups. As can be appreciated, the heart rate components of the defense response have been poorly evoked in this study. Although the first acceleration and the two decelerations are present before the drug, there is only a tendency to show the second acceleration. This may be partly due to the small number of subjects used, since individual differences in the evocation of the CDR have been systematically reported [6,2]. On the other hand, the specific testing conditions using an invasive pharmacological procedure might have affected the frequency of subjects showing the CDR. Therefore, conclusions concerning the effect of the pharmacological blockade on the heart rate pattern can only be tentative. If the response pattern after atropine (see Fig. 1, middle) is interpreted as showing only the second acceleration and second deceleration, although temporarily advanced, and after the beta-adrenergic block (see Fig. 1, top) as showing the four components, although reduced in amplitude, then both the vagal block and the betaadrenergic block seem to coincide in the vagal origen of the first two components of the CDR (they tend to disappear after atropine and to persist after metoprolol) while with respect to the last two components the vagal block suggests a sympathetic mediation (they persist after atropine) and the beta-adrenergic block suggests a parasympathetic mediation (they persist after metoprolol), which leads us again to conclude a sympathetic-parasympathetic interaction during the second aceleration and second deceleration of the CDR. Stroke volume pattern Fig. 2 graphically illustrates the response pattern shown by the medians of the stroke volume for each group, before and after drug administration. As can be appreciated, the response pattern is fundamentally characterized by a short latency decrease that can spread until the 3rd median and an increase that, beginning in the 4th median, can maintain itself until the 9th or 10th median, as happened in the control group. This response pattern disappeared after metoprolol administration, although some short latency changes remained, and persists, with less ampli-
184
G.A. Reyes de1 Paso et al. /International
tude, after atropine administration. These results are consistent with those found previously using other indices of sympathetic activity which show a (ml)
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clear beta-adrenergic activation in association with the second acceleration of the CDR [3,4]. On the other hand, a comparison of stroke volume and heart rate response patterns in the atropine group where heart rate is predominantly under sympathetic control, show that the patterns of both activities, far from coinciding, manifest opposite directions. This suggests that the inotropic and chronotropic sympathetic influences on the heart are not neccesarily parallel, showing the independence and specificity of such parameters. Blood pressure pattern Figs. 3 and 4 graphically illustrate the response pattern shown by the medians of the systolic and diastolic blood pressure in terms of the groups, before and after drug administration. As can be appreciated, the response pattern is characterized before drug administration by an increase in the second and third medians (set 4-ll), a posterior decrease in the fourth and fifth medians that could spread to the seventh (set 12-37) and a lighter increase from the 8th median to the 9th (set 38-63). After the drug administration the response pattern is substantially similar, the greater differences being found in the group that received atropine. In this group the first increase component becomes larger and delayed with respect to the response pattern previous to the drug administration. Comparing these results with previous studies [3,9] with respect to the vascular components of the defense reaction, it can be deduced that the first increase component in blood pressure, when the stroke volume has still not increased, could be due to the short latency peripheral vasconstriction that accompanies the intense auditory stimulation, while the reduction component of the blood pressure, in association with the great increase produced in stroke volume, could be due to the vasodilatation component in the skeletal muscles that also accompany the defense reaction. The fact that in the present study the heart rate component of the defense reaction to intense auditory stimulation has been evoked with less intensity than the other cardiovascular components reproduces the results of previous studies [9] that found that subjects who
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Journal of Psychophysiology I7 (1994) 181-187
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Fig. 2. Stroke volume response pattern before and after metoprolol (top), atropine (medium) and placebo (bottom) administration. (Numbers on the horizontal axis represent the midpoints of the 10 selected intervals.)
G.A. Reyes de1 Paso et al. /International
6
Journal of Psychophysiology
185
I7 (I 994) 181-187
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Fig. after tom) sent
3. Systolic blood pressure response pattern before and metoprolol (top), atropine (medium) and placebo (botadministration. (Numbers on the horizontal axis reprethe midpoints of the 10 selected intervals.)
Fig. after tom) sent
4. Diastolic blood pressure response pattern before and metoprolol (top), atropine (medium) and placebo (botadministration. (Numbers on the horizontal axis reprethe midpoints of the 10 selected intervals.)
did not present the second cardiac aceleration associated with the CDR did present, on the other hand, the vascular components, muscular
186
vasodilation traditionally
G.A. Reyes de1 Paso et al. /International
and peripheral vasoconstriction, that have defined the defense reaction.
Comparison between heart rate and blood pressure before drug administration As can be observed in the figures in which the blood pressure and the heart rate parameters appear, with the exception of that after atropine administration in which the cardiac branch (mainly vagal) of the baroreflex is blocked and only the more slow vasomotor branch (sympathetic) is operating, both activities seem to show opposite directions. The first increase component in the blood pressure (mainly in the 2nd and 3rd medians) corresponds with the period of the first cardiac deceleration, the posterior reduction in the blood pressure (which begins in the 4th median and can extend until the 7th) corresponds with the period of the second cardiac acceleration and the increase component in the blood pressure in the last medians corresponds with the period of the second decelerative component of the CDR. This suggests an implication of the baroreceptor reflex in the CDR, including a baroreceptor mediated inhibition of the parasympathetic cardiac activity during the second accelerative component of the CDR in association with the decrease in blood pressure.
4. Conclusions The results of this preliminary study shows, first, that while the reliability of the CDR profiles has been low, probably due to individual differences and the small number of subjets used, the reliability of the stroke volume and blood pressure profiles has been high. Second, a significant response pattern in blood pressure concomitant with the CDR has been observed, including a decrease in association with the second cardiac accelerative component, which is more clearly observed when considering diastolic than systolic blood pressure. Third, in relation to this decrease component in blood pressure, the results obtained also suggests a baroreceptor mediated inhibition of parasympathetic cardiac activity dur-
Journal of Psychophysiology I7 (1994) 181-187
ing the second accelerative component of the CDR. Some authors [6,1] have suggested that individual differences in the second accelerative component of the CDR might be explained by differences in baroreceptor control. Similarly, the rapid short-term habituation of the second acceleration has been attributed to a response supression mechanism due to the baroreflex action. This explanation may also account for the apparent fractionation between the heart rate and the other cardiovascular components of the response less affected by baroreceptor activity. However, this idea was based on the prediction that blood pressure should be increased during the second acceleration. In such a case, it is indeed neccessary to postulate an inhibition of the baroreceptor regulation of heart rate, since under normal conditions the increase in blood pressure should produce a baroreceptor mediated decrease in heart rate. Contrary to this prediction, we found that blood pressure, as average, is decreased during the period of the second cardiac acceleration. Therefore a general inhibition of the baroreflex regulation during the second acceleration can not be postulated as such. However, given the large natural variability in blood pressure, also present during the CDR, and the sensitivity of the baroreflex to transitory changes in blood pressure, the presence of the second accelerative component could require inhibition of the baroreceptor regulation of heart rate during the increase phases in blood pressure, while during the decrease phases the inhibition of vagal activity by baroreflex could be facilited. In our study, the subjects which received atropine showed with more regularity, as compared with subjects under control conditions, the observed accelerative component (set 3-12). It should be noted that under control conditions, without pharmacological blockade, this accelerative component might not be observed, as it occurs in the first stimulus presentation before drug, since such an acceleration could be supressed by the baroreceptor vagal activation triggered by the simultaneous increase in blood pressure. Consequently, comparison of the heart rate response patterns before and after atropine administration shows some evidence that
G.A. Ryes del Paso et al. /International
vagal activation is able to mask sympathetic activity, showing that sympathetic effects are present during the response but are not manifested due to the dominance of vagal restraint.
Acknowledgements This research was supported by a grant of the Commission of the European Communities Medical and Health Research Programe. Concerted Action: Quantification of Parameters for the Study of Breakdown in Human Adaptation. We would also like to thank W. Langewitz from the University of Bonn and L.J.M. Mulder and his colleagues from the University of Groningen for their support and collaboration to carry out this research.
Journal of Psychophysiology 17 (1994) 181-187
187
References [ll Turpin, G. (1986) Psychophysiology 23, i-14. [2] Vila, J., Fernindez, M.C., and Godoy, J. (1992) J. Psychophysiol. 6, 140-154. G., and Siddle, D.A. (1978) Biol. Psychol. 6, [31 T&n, 267-282. M.C., and Vila, J. (1989) Biol. Psychol. 28, [41 Fernindez, 123-133. [51 Reyes del Paso, G.A., Godoy, J., and Vila, J. (1993) Biol. Psychol. 35, 17-35. [hl Eves, F.F., and Gruzelier, J.H. (1984) Psychophysiology 21, 342-352. f71 Shetwood, A., Allen, M.T., Kelsey, R.M., Lovallo, W.R., and van Doornen, L.J.P. (1990) Psychophysiology 27, l-33. [81 Settles, J.J., and Wesseling, K.H. (1985) in Psychophysiology of Cardiovascular Control (J. Orlebeke, G. Mulder and L. Doornen, eds.), pp. 267-283. New York: Plenum Press. [91 Eves, F.F., and Gruzelier, J.H. (1987) J. Psychophysiol. 1, 161-172.
Short communication
Physiological significance of the defense response to intense auditory stimulation: a pharmacological blockade study Gustav0
A. Reyes de1 Paso a,*, Jaime Vila b and Ana Garcia
a
aDepartamento de Psicologia, Facultad de Humanidades, Unicersidad de Ja&, 23071 Jab, Spain, b Departamento de Personalidad, Ecaluacidn y Tratamiento Psicoldgico, Facultad de PsicologLa, Unicersidad de Granada, 18011 Granada, Spain Received 7 June 1993; revised 29 March 1994; accepted 29 March 1994
Abstract This paper examines through pharmacological blockade some questions related to the physiological significance of the defense response to intense auditory stimulation. Nine subjects received intravenous metoprolol (lo-15 mg i.v.>, intravenous atropine (0.03 mg/kg i.v.1, or a saline solution as placebo condition before undertaking a test of the defense response to a distorted sound of 400 Hz frequency, 109 dB intensity, 0.5 set duration and virtually instantaneous risetime. Dependent variables were continuous (beat-to-beat) heart rate, stroke volume and blood pressure. The results suggest: (1) a vagal origen of the first acceleration and first deceleration and a sympatheticparasympathetic interaction during the second acceleration and second deceleration of the heart rate response; (2) a
blood pressure response pattern characterized by an increase during the first heart rate deceleration (4-11 set), a posterior decrease coinciding with the second heart rate acceleration (from 12 to 37 set), and a lighter increase during the second heart rate deceleration (from 38 to 63 set); and (3) an implication of the baroreceptor reflex, including a baroreceptor mediated inhibition of the parasympathetic cardiac activity during the second accelerative component of the cardiac response. Key words:
Defense
response;
Pharmacological
blockade;
1. Introduction The Cardiac Defense Response (CDR) constitues a specific pattern of heart rate changes which is elicited by intense auditory or electrocutaneous stimuli [1,2]. The response consists of four components, two accelerative and two decel-
* Corresponding author. 0167~8760/94/$07.00 0 1994 Elsevier SSDI 0167-8760(94)00033-B
Science
Heart
rate; Stroke volume; Blood presure; Baroreflex
erative in alternating order occuring within the X0 set post-stimulus. Two outstanding characteristics of this response, which concern specially the second acceleration, are the existence of important individual differences and the display of unusually rapid short-term habituation after the first presentation of the stimulus. Research into the physiological significance of this response pattern using indirect measures of both sympathetic [3,4] and parasympathetic activation [5] suggests a parasympathetic mediation of the first accelera-
B.V. All rights reserved
182
G.A. Reyes del Paso et al. /International
tion and first deceleration and a sympatheticparasympathetic interaction during the second acceleration and second deceleration. As suggested by other authors [6,1] a better understanding of this interaction - in particular, the role that the baroreflex plays during the second acceleration - might be crucial to explain both the individual differences and the rapid habituation phenomenon. The aim of the present preliminary study was to advance our understanding of the physiological significance of the cardiac components of the defense response to intense auditory stimulation by using a pharmacological blockade procedure. This general aim was subdivided into two specific objetives: (a> to examine the effect of atropine administration versus a beta-adrenergic blocker on the accelerative and decelerative heart rate components of the response; and (b) to evaluate the stroke volume and the blood pressure components of the response together with the participation of the baroreceptor reflex in the elicitation of the CDR.
2. Method In the context of a collaborative research with the University of Bonn, 9 medical students from that university (aged between 23 and 25 years) participated as subjects. Six subjects constituted the experimental group and were investigated twice: three received atropine (0.03 mg/kg body weight i.v.1 on day 1 and metoprolol, a pl-selective beta-blocking agent, so as not to influence vasomotor activity, (up to 3 x 5 mg i.v.>, on day 2 (one week later) and the remaining 3 received the reverse order of drugs. Other three subjects constituted the control group and were investigated only once, receiving 3 x 5 ml of saline as a placebo condition. The psychophysiological reaction test consisted of 10 min rest period and one trial of intense auditory stimulation, a distorted sound of 400 Hz frequency, 109 dB intensity, 0.5 set duration and a virtually instantaneous rise time, followed by 3 min post-stimulus period. Once this first phase was over, drugs were injected during a period of 5 min (atropine) or during a maximum
Journal of Psychophysiology
I7 (1994) 1X1-187
of 3 X 5 min (metoprolol and saline). The dose of the beta-blocking agent was calculated according to the HR response: if HR was reduced by > 25%, the injection was stopped. This goal was achieved in all subjects with doses between 10 and 15 mg of metoprolol i.v. Two min after the end of the injection period the same psychophysiological reaction test was repeated. Accordingly, the interval between the two noise presentations was about 20 min for atropine subjects and 30 min for metoprolol and control subjects. Although this within-subject design is not the most appropriate one to study the CDR, due to the short-term habituation phenomenon, we expected that both the minimum interval between trials within the same session (over 20 min) and the week interval between the two sessions would reduce the possible contaminating effect of habituation. On the positive side, the within-subject design has the advantage of requiring a lower number of subjects to examine the same effect, an important advantage in pharmacological blockade studies. Dependent variables were continuous (beatto-beat) heart rate (ECG), stroke volume (through impedance cardiography 1711, and blood pressure (with the non-invasive FIN.A.PRES device [8]). For all these physiological variables the secondby-second values during the 80 set after stimulus onset expressed in terms of differential scores with respect to the average values during the 15 set prior to stimulus onset (baseline) were obtained. In order to analyze the form of the responses to the auditory stimulus the same methodology used in previous studies based on the medians of ten succesively longer intervals was applied [51. Analysis of the results was undertaken by means of both visual and statistic scrutin of the response patterns. In the present brief report only the visual analysis is commented upon.
3. Results and discussion Heart rate pattern Fig. 1 graphically illustrates the response pattern shown by the medians of the heart rate before and after drug administration as a func-
G.A. Reyes de1 Paso et al. /International
6 -HR S-
(b.p’m.)
0
4-
-Q-
HO DRUG
Y
YCTOPMLOL
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’
-,
-
-2
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Fig. 1. Heart rate 101 (top), atropine tion. (Numbers on of the 10 selected
FROM STIMULUS
-Q-
“0 DWC
*
PUCFlm
ONSET
response pattern before and after metopro(medium) and placebo (bottom) administrathe horizontal axis represent the midpoints intervals.)
Journal of Psychophysiology 17 (1994) 181-187
183
tion of the groups. As can be appreciated, the heart rate components of the defense response have been poorly evoked in this study. Although the first acceleration and the two decelerations are present before the drug, there is only a tendency to show the second acceleration. This may be partly due to the small number of subjects used, since individual differences in the evocation of the CDR have been systematically reported [6,2]. On the other hand, the specific testing conditions using an invasive pharmacological procedure might have affected the frequency of subjects showing the CDR. Therefore, conclusions concerning the effect of the pharmacological blockade on the heart rate pattern can only be tentative. If the response pattern after atropine (see Fig. 1, middle) is interpreted as showing only the second acceleration and second deceleration, although temporarily advanced, and after the beta-adrenergic block (see Fig. 1, top) as showing the four components, although reduced in amplitude, then both the vagal block and the betaadrenergic block seem to coincide in the vagal origen of the first two components of the CDR (they tend to disappear after atropine and to persist after metoprolol) while with respect to the last two components the vagal block suggests a sympathetic mediation (they persist after atropine) and the beta-adrenergic block suggests a parasympathetic mediation (they persist after metoprolol), which leads us again to conclude a sympathetic-parasympathetic interaction during the second aceleration and second deceleration of the CDR. Stroke volume pattern Fig. 2 graphically illustrates the response pattern shown by the medians of the stroke volume for each group, before and after drug administration. As can be appreciated, the response pattern is fundamentally characterized by a short latency decrease that can spread until the 3rd median and an increase that, beginning in the 4th median, can maintain itself until the 9th or 10th median, as happened in the control group. This response pattern disappeared after metoprolol administration, although some short latency changes remained, and persists, with less ampli-
184
G.A. Reyes de1 Paso et al. /International
tude, after atropine administration. These results are consistent with those found previously using other indices of sympathetic activity which show a (ml)
SV
2
5
1
9
v
I
14
20
I
27
34
SECONS
2.
44
FROM STIMULUS
57
70
ONSET
SV b-4
1
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5
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,
9
14
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,
20
27 SECONS
50 40
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1
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44
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,
,
,
,
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clear beta-adrenergic activation in association with the second acceleration of the CDR [3,4]. On the other hand, a comparison of stroke volume and heart rate response patterns in the atropine group where heart rate is predominantly under sympathetic control, show that the patterns of both activities, far from coinciding, manifest opposite directions. This suggests that the inotropic and chronotropic sympathetic influences on the heart are not neccesarily parallel, showing the independence and specificity of such parameters. Blood pressure pattern Figs. 3 and 4 graphically illustrate the response pattern shown by the medians of the systolic and diastolic blood pressure in terms of the groups, before and after drug administration. As can be appreciated, the response pattern is characterized before drug administration by an increase in the second and third medians (set 4-ll), a posterior decrease in the fourth and fifth medians that could spread to the seventh (set 12-37) and a lighter increase from the 8th median to the 9th (set 38-63). After the drug administration the response pattern is substantially similar, the greater differences being found in the group that received atropine. In this group the first increase component becomes larger and delayed with respect to the response pattern previous to the drug administration. Comparing these results with previous studies [3,9] with respect to the vascular components of the defense reaction, it can be deduced that the first increase component in blood pressure, when the stroke volume has still not increased, could be due to the short latency peripheral vasconstriction that accompanies the intense auditory stimulation, while the reduction component of the blood pressure, in association with the great increase produced in stroke volume, could be due to the vasodilatation component in the skeletal muscles that also accompany the defense reaction. The fact that in the present study the heart rate component of the defense reaction to intense auditory stimulation has been evoked with less intensity than the other cardiovascular components reproduces the results of previous studies [9] that found that subjects who
-0.NO D”“G iyCUCLBO
A
9
70
Journal of Psychophysiology I7 (1994) 181-187
I
34
I
44
FROM STIY”L”S
57
70
ONSET
Fig. 2. Stroke volume response pattern before and after metoprolol (top), atropine (medium) and placebo (bottom) administration. (Numbers on the horizontal axis represent the midpoints of the 10 selected intervals.)
G.A. Reyes de1 Paso et al. /International
6
Journal of Psychophysiology
185
I7 (I 994) 181-187
SBP (mmHg)
: I
x
SECONS FROM SIIUULUS ONYX1 I
2 5
9
20
14
34
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Fig. after tom) sent
3. Systolic blood pressure response pattern before and metoprolol (top), atropine (medium) and placebo (botadministration. (Numbers on the horizontal axis reprethe midpoints of the 10 selected intervals.)
Fig. after tom) sent
4. Diastolic blood pressure response pattern before and metoprolol (top), atropine (medium) and placebo (botadministration. (Numbers on the horizontal axis reprethe midpoints of the 10 selected intervals.)
did not present the second cardiac aceleration associated with the CDR did present, on the other hand, the vascular components, muscular
186
vasodilation traditionally
G.A. Reyes de1 Paso et al. /International
and peripheral vasoconstriction, that have defined the defense reaction.
Comparison between heart rate and blood pressure before drug administration As can be observed in the figures in which the blood pressure and the heart rate parameters appear, with the exception of that after atropine administration in which the cardiac branch (mainly vagal) of the baroreflex is blocked and only the more slow vasomotor branch (sympathetic) is operating, both activities seem to show opposite directions. The first increase component in the blood pressure (mainly in the 2nd and 3rd medians) corresponds with the period of the first cardiac deceleration, the posterior reduction in the blood pressure (which begins in the 4th median and can extend until the 7th) corresponds with the period of the second cardiac acceleration and the increase component in the blood pressure in the last medians corresponds with the period of the second decelerative component of the CDR. This suggests an implication of the baroreceptor reflex in the CDR, including a baroreceptor mediated inhibition of the parasympathetic cardiac activity during the second accelerative component of the CDR in association with the decrease in blood pressure.
4. Conclusions The results of this preliminary study shows, first, that while the reliability of the CDR profiles has been low, probably due to individual differences and the small number of subjets used, the reliability of the stroke volume and blood pressure profiles has been high. Second, a significant response pattern in blood pressure concomitant with the CDR has been observed, including a decrease in association with the second cardiac accelerative component, which is more clearly observed when considering diastolic than systolic blood pressure. Third, in relation to this decrease component in blood pressure, the results obtained also suggests a baroreceptor mediated inhibition of parasympathetic cardiac activity dur-
Journal of Psychophysiology I7 (1994) 181-187
ing the second accelerative component of the CDR. Some authors [6,1] have suggested that individual differences in the second accelerative component of the CDR might be explained by differences in baroreceptor control. Similarly, the rapid short-term habituation of the second acceleration has been attributed to a response supression mechanism due to the baroreflex action. This explanation may also account for the apparent fractionation between the heart rate and the other cardiovascular components of the response less affected by baroreceptor activity. However, this idea was based on the prediction that blood pressure should be increased during the second acceleration. In such a case, it is indeed neccessary to postulate an inhibition of the baroreceptor regulation of heart rate, since under normal conditions the increase in blood pressure should produce a baroreceptor mediated decrease in heart rate. Contrary to this prediction, we found that blood pressure, as average, is decreased during the period of the second cardiac acceleration. Therefore a general inhibition of the baroreflex regulation during the second acceleration can not be postulated as such. However, given the large natural variability in blood pressure, also present during the CDR, and the sensitivity of the baroreflex to transitory changes in blood pressure, the presence of the second accelerative component could require inhibition of the baroreceptor regulation of heart rate during the increase phases in blood pressure, while during the decrease phases the inhibition of vagal activity by baroreflex could be facilited. In our study, the subjects which received atropine showed with more regularity, as compared with subjects under control conditions, the observed accelerative component (set 3-12). It should be noted that under control conditions, without pharmacological blockade, this accelerative component might not be observed, as it occurs in the first stimulus presentation before drug, since such an acceleration could be supressed by the baroreceptor vagal activation triggered by the simultaneous increase in blood pressure. Consequently, comparison of the heart rate response patterns before and after atropine administration shows some evidence that
G.A. Ryes del Paso et al. /International
vagal activation is able to mask sympathetic activity, showing that sympathetic effects are present during the response but are not manifested due to the dominance of vagal restraint.
Acknowledgements This research was supported by a grant of the Commission of the European Communities Medical and Health Research Programe. Concerted Action: Quantification of Parameters for the Study of Breakdown in Human Adaptation. We would also like to thank W. Langewitz from the University of Bonn and L.J.M. Mulder and his colleagues from the University of Groningen for their support and collaboration to carry out this research.
Journal of Psychophysiology 17 (1994) 181-187
187
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