Sympathetic-parasympathetic mediation of the cardiac defense response in humans

Biological Psychology

28 (1989)

123-133

123

North-Holland

SYMPATHETIC-PARASYMPATHETIC MEDIATION OF THE CARDIAC DEFENSE RESPONSE IN HUMANS Maria

Carmen

Accepted

FERNANDEZ

of Psychology,

Department

for publication

This paper reports mediation

of

response

(CDR)

Thirteen 400-Hz

the

decelerative first

an investigation

replicated

in alternating

in the second a description

components

rate

underwent

two components

support

1988

which examined

response cardiac

period (CP)

a physiological

sequence.

the changes

and pulse transit

reaction

and/or

stimulation

-

pattern

CP

in CP and PTT

and interpretation

of the CDR

with both vagal and sympathetic

and

decelerative moved

PTT

of a distorted

The results

regarding

two accelerative

changes

components in opposite

defense

simultaneously.

test with a single presentation

with four components:

As regards and second

parasympathetic

the cardiac

time (PTT)

rise time and 0.5 s duration.

the typical

accelerative

the sympathetic

to intense’auditory

of 109 dB, instantaneous

form of the CDR occurred

1 December

heart

VILA

Unruersity of Granada, 1801 I Granada, Spam

- by recording

subjects sound

and Jaime

*

the only

coincidences

of the response. directions.

in terms of both accelerative

the

and two

These

In the results

and decelerative

mediation.

1. Introduction Research into the physiological significance of the defence response - also called defense reaction or defense reflex ~ has been greatly influenced by Cannon’s relevance

classical studies on the fight-flight response and by the special attributed by him to the role of the sympathetic branch of the

autonomic nervous system in all emotional and motivational states (Cannon, 1929). The description and physiological interpretation of the defense response put forward by Cannon investigated

have received support

it by means

of the electrical

defense area in animals (Abrahams, Lisander, 1970). From a descriptive

mainly from studies which have

stimulation

of the hypothalamic

Hilton, & Zbrozyna, 1960; Bard, 1960; point of view, the cardiovascular compo-

nents of the defense response include an increase in cardiac activity (positive chronotropic and inotropic effects) and an increase in the volume of blood * This research **

was supported

Scientific

and Technological

Requests

for reprints

Personalidad, B), Universidad

0301-0511/89/$3.50

be addressed 18011

Elsevier

from the Spanish

Consulting

Committee

for

Departamento

de

(CAICYT).

y Tratamiento

de Granada.

0 1989,

PR82-1933

Research

should

Evaluaci6n

by grant

to: Maria

Psicolhgico,

Granada,

Science

Carmen Facultad

Fernlndez, de Filosofia

Spain.

Publishers

B.V. (North-Holland)

y Letras

(Edificio

124

M.C. Ferndnder

and J. Vda / Cardux

defense

response

in humans

supply to the skeletal muscles, accompanied by a decrease in blood supply to the skin and viscera. It is assumed that such reactions are mediated by an increment in sympathetic activation through both neural pathways (stimulation of the sympathetic nerve fibres to the heart and blood vessels) and humoral pathways (increment in circulating catecholamines secreted by the adrenal medulla). This interpretation rules out vagal influences and, in particular, the baroreceptor reflex in the mediation of the defense response (Lisander, 1970). From this point of view, it would seem contradictory to consider the cardiac defense response (CDR) as a pattern of heart rate (HR) changes with both

accelerative

and

decelerative

pathetic

mediation.

However,

auditory

and electrocutaneous

components

descriptive stimulation

those

and duration

of other

intense auditory 1984; Pegalajar,

(Fernandez,

investigators

who have

both

unequivocally

plex response pattern with four components decelerative - in alternating order and perfectly tude, latency

and

vagal

and

data on the HR response demonstrate

- two accelerative defined parameters

1986). These data confirm studied

the CDR

sym-

to intense a comand two of ampliand extend

in humans

using

stimulation (Eves & Gruzelier, 1984, 1985; Knott & Bulmer, 1986; Turpin & Siddle, 1978, 1980, 1981, 1983) and they are

very similar to those obtained by Bond (1943) who investigated emotional responses in unanaesthetized dogs and cats using the same paradigm (short unexpected intense noise). Research into the physiological significance of this response pattern has been carried out using different methodological strategies. Bond (1943) examined it in animals by differential extirpation of the sympathetic-vagal nerves and the adrenal glands and discovered an important sympathetic-vagal interaction

in the elicitation

been focused

on the second

of the response accelerative

1986; Turpin & Siddle, 1978, activation the T-wave amplitude differential

of the carotid

pattern.

component

In humans,

research

of the response

has

(Turpin,

1981). Using as a measure of sympathetic of the ECG, forearm blood flow and the first

pulse (dP/dt),

Turpin

and Siddle have offered

data

which point towards a P-adrenergic interpretation of the second acceleration. Interpretation of the other accelerative and decelerative components has not been attempted directly, although Turpin’s data (Turpin, 1986) would appear to indicate a non-sympathetic mediation of the first acceleration. However, in agreement with Cannon’s proposal on the non-participation of the parasympathetic nervous system in emotions and with the results of studies on electrical stimulation of the hypothalamic defence area, Turpin (1986) identifies the cardiac defense response exclusively with the second accelerative component. Nevertheless, both the assumption of the non-participation of the parasympathetic nervous system in emotions and the definition of the defense response as described in studies on electrical stimulation of the hypothalamic defense

area are questionable

from several points

of view.

125

M.C. Fernrindez and .I. Vila / Cardiac defense response in humans

The

involvement

of the parasympathetic

nervous

system

in stress

and

emotions has been clearly demonstrated 1985, for a review). Vagal predominance

by numerous authors (see Vingerhoets, may form part of a complex response

pattern to some stressors characterized nied by fainting, bradycardia and/or

by enhanced vagal activity, accompaarrythmias (Vingerhoets, 1984, 1985).

Grossman and Svebak (1987) have also reported parasympathetic effects and sympathetic-parasympathetic interactions in stressor tasks, finding exaggerated HR responses associated with extreme parasympathetic withdrawal. On the other hand, the definition of the defense response with reference to the response components elicited by the electrical stimulation of a cerebral “area”

or “centre”

a localizationist vascular

has two important

limitations.

vision of the functioning

reactions

are known

organized

longitudinally

Provoots,

& Shapiro,

to form

throughout 1977;

part

system, when cardio-

of integrated

the central

Gellman,

In the first place, it assumes

of the nervous

nervous

Schneiderman,

response system

Wallach,

patterns (De

Jong,

& Le Blanc,

1981; Hilton, 1975; Larsen, Schneiderman, & De Carlo Pasin, 1986). Secondly, it directs the criterion for the definition of the defense response towards the efferent

components

of the response

itself, neglecting

the situational

context

in

which it is elicited. Cannon stressed the link between the fight-flight reaction and the demands of the situation to which the organism responds in an attempt to adapt itself. Moreover, researchers strongly influenced by Cannon have

preferred to study the defense response in the context of natural situations rather than use electrical stimulation of specific brain centres (Adams, Baccelli, Mancia, & Zanchetti, 1971; Bond, 1943). Under such conditions and in clear contrast to the studies on electrical stimulation (Lisander, 1970), the above-mentioned investigators did encounter accelerative and decelerative changes in HR with both sympathetic and vagal influences. The aim of the present investigation was to examine the sympathetic and/or parasympathetic mediation of the accelerative and decelerative components of the CDR described in previous studies (Fernandez, 1986) by adequately evoking the four-component CDR pattern and by recording cardiac period (CP) and pulse transit time (PTT) simultaneously. As mentioned above, previous work on the autonomic mediation of the HR response to intense stimulation in humans has been limited to the examination of the first and second accelerative components, no mention being made of the two decelerative ones. Progress in the understanding of the physiological significance of the CDR requires, firstly, a precise description of the response pattern itself on which to base further research and, secondly, an accurate analysis of the parametric characteristics of the eliciting stimulus, namely, sensory modality and intensity. The present study takes into consideration the results of a recent descriptive and parametric investigation (Fernandez, 1986) in order to evoke and describe the CDR pattern adequately. AS regards the dependent variable, PTT has been considered as an indirect

126

M. C. Ferminder

and J. Vda / Cardiac

defense

response

m humans

measure of ventricular contractility and, therefore, as a psychophysiological index of P-adrenergic influences on myocardiac performance (Obrist, Light, McCubbin, Hutcheson, & Hoffer, 1979). Consequently, we would expect the recording of PTT during the elicitation of the CDR to permit us to determine whether its specific HR components correspond exclusively to sympathetic mediation, as has been traditionally postulated. Although the problem of preference among different indirect indices of sympathetic activation - namely T-wave and P’IT - is still a controversial issue (Furedy, Heslegrave, & Scher, 1984; Larsen et al., 1986; Schwartz & Weiss, 1983) our choice of PTT has been based not on superiority but on the fact that PTT is one of the few relevant indices which has not been investigated so far in relation to the CDR. The choice

of this index would provide

allow us to compare using T-wave Siddle,

PTT

amplitude,

carotid

d P/dt

1978, 1981). Such a comparison

contractility-based

new evidence

and, at the same time,

results with those obtained

sympathetic

indices,

by earlier investigators

and forearm

blood

is indeed relevant for example

flow (Turpin

&

since PTT, like other

carotid

dP/dt,

may not

be a perfect index of sympathetic activation (Heslegrave & Furedy, 1980; Obrist & Light, 1980). Therefore final interpretation of PTT results should take into consideration the presence or absence of convergent data from previous

studies.

2. Method 2. I. Subjects The subjects were 13 male volunteers; students from the University of Granada subjects receiving

had no cardiovascular psychiatric

disorders

or pharmacological

all were final-year psychology aged between 23 and 26. The

or auditory

deficiencies

and were not

treatment.

2.2. Apparatus A lafayett polygraph was used to monitor HR and pulse amplitude through the LA-76403 cardiotachometer and the LA-76405 pulse amplifier. Both amplifiers received the same input signal provided by a Letica TRU-030 photoelectric plethysmograph, placed on the distal phalanx of the left index finger. The recording of pulse amplitude in this case was done exclusively to control possible artifacts in the cardiotachometer resulting from the use of the photoplethysmograph to activate the cardiotachometer. By simultaneously recording HR and pulse amplitude we were able to control the cardiotachometer trigger level, as well as detect or correct possible artifacts due to double trigger or loss of trigger. The cardiotachometer

amplifier

monitored

HR within

M. C. Fernlinda

and J. Vila / Cardiac defense response m humans

127

a range of 40-120 beats/mm, the cardiotachometer being calibrated before and after each subject. The recording was carried out at a paper speed of 2.5 mm/s. A Leti-Graph 2000 polygraph was used to measure PTI by monitoring the ECG and the pulse amplitude through HSC-400 and CAR-300 amplifiers. The HSC-400 monitored ECG in the lead II configuration using silver-plated electrodes. The CAR-300 amplifier monitored pulse amplitude through a Letica TRU-030 photoelectric plethysmograph, placed on the distal phalanx of the right index finger. The ECG and pulse amplitude recordings were carried out by means of thermic pens on thermosensitive paper at a speed of 100 mm/s. A Letica LE-150 auditory stimulator was used to produce a distorted 400-Hz sound of 109 dB, virtually instantaneous rise time and a duration of 0.5 s. The sounds were presented through SUNSE-20 headphones. The sound pressure level of the stimulus was measured by a Briiel and Kjaer SPL meter using scale A. A Letica LE-100 stimulus programmer, comprising ten independent timers, was used to monitor the sequence and duration of the stimulus and to mark its beginning and end on the polygraph. 2.3. Procedure All subjects underwent a physiological reaction test designed to evoke the CDR following the methodological recommendations derived from previous descriptive and parametric studies (Fernandez, 1986). This consisted of a single presentation of a high-intensity auditory stimulus of 109 dB and 0.5 s duration in the following sequence: (a) lo-min adaptation period; (b) the auditory stimulus presentation; (c) 80-s post-stimulus period. During the test the physiological measures described in section 2.2 were recorded. The tests for all subjects were carried out in the afternoon in the laboratory, which consisted of two sound-attenuated rooms: the subject’s room and the experimenter’s room. The first was a 3 x 3 X 3m room with controlled temperature between 20 o C and 23’ C. On arrival at the laboratory, the subject sat at a desk and was given general information about the session and completed a personal questionnaire with information relevant to the selection criteria. The subject then sat down in an armchair and the instructions for the physiological reaction test were read to him. These described the test as a routine procedure to examine the effect of sound on relaxation. The instructions requested the subject to remain still throughout the test and try to breathe as normally and evenly as possible. Then the experimenter placed the items of apparatus on the subject in the following order: the headphones, the ECG electrodes, the Leti-Graph plethysmograph and the Lafayett plethysmograph. During the test, the experimenter left the subject’s room and turned down the lighting to a

128

M. C. Ferncinder and J. Vda / Curdmc defense response m humans

pre-established

subdued

level.

Once

the

test

returned to the subject’s room, removed the plethysmographs and concluded the session.

was

over,

the

headphones,

experimenter

electrodes

and

2.4. Data analysis 2.4. I. Cardiac defence response Descriptive and

followed

analysis the

of the CDR

was done in terms of CP instead

methodological

recommendations

derived

from

of HR previous

studies (Fernandez, 1986). Accordingly, the response was defined as the second-by-second CP during the 60 s after stimulus onset expressed in terms of differential

scores with respect

the 15 s prior

to stimulus

onset

to the average second-by-second (baseline).

The

second-by-second

CP during CP was

calculated from the recordings provided by the cardiotachometer at the very end of each second withoug weighting for partial inter-beat intervals. Then the 60 CP values were reduced progressively longer intervals: 446) the next interval of of 7 s (seconds 12-18, Finally, the 10 medians reduction of the 60 CP allowed us to apply the variance

without distorting

to 10 corresponding the first two intervals

to the medians of 10 of 3 s (seconds l-3 and

5 s (seconds 7-11) and the following seven intervals 19-25, 26632, 33339, 40-46, 47753 and 54-60). for each subject were converted into Z-scores. The values to 10 using progressively longer intervals trend analysis of the CP changes using analysis of the shape of the CDR

pattern.

On the other hand,

the use of medians instead of means permitted us to exclude extreme values which might not truly represent the temporal

the influence of sequence of the

cardiac

direct

changes.

Finally,

the Z-score

transformation

allowed

compari-

son of the CP and the PTT values. 2.4.2. Pulse Transit Time This was defined as the interval in milliseconds between the peak (first point of maximum amplitude) of the R-wave of the ECG and the peak of the finger pulse wave associated with the same cardiac contraction. Analysis of the PTT was carried out following the same method applied to the CDR. PTT was measured during the 15 s prior to and the 60 s following stimulus onset. These data were converted into second-by-second PTT, by selecting the PTT of the nearest R-wave to each second. The response was then defined as the secondby-second PTT during the 60 s after stimulus onset expressed in terms of differential scores with respect to the average second-by-second PTT during the 15 s prior to stimulus onset (baseline). The 60 PTT values were reduced to 10 corresponding to the medians of the same 10 intervals as selected in the case of CP. Finally, these 10 values for each subject were converted into Z-scores.

129

M. C. Ferncinder and .I. Vila / Cardiac defense response in humans

3. Results Fig. 1 shows the cardiac response to the auditory stimulus expressed in raw CP values. The negative scores indicate HR acceleration while the positive scores indicate HR deceleration, The form of the response replicates the typical CDR pattern described in previous studies (FernLndez, 1986) with its four components, quence.

two accelerative

Fig. 2 shows the PTT values.

The negative

increment

in PIT.

coincides

and

response

scores

to the auditory

indicate

a decrement

As may be observed

temporarily

two decelerative,

in alternating

stimulus

an intial increase

with the first accelerative

expressed

and the positive

in raw

scores

is produced

component

se-

of the CDR.

an

which This

9 ;;;il

li SECONDS

Fig.

1. Cardiac

(Numbers

2

period

4 1; SECONDS

Fig.

2’9

2. Pulse

transit

3’6

STIMULUS

response

on the horizontal

iii

(Numbers

2; FROM

5b ONSET

to

the

axis represent

i2 FROM

2’9 ;6 STIMULUS

time

response

on the horizontal

L’3

;3

5’7

intense

5b ONSET

stimulus

expressed

of the 10 selected

in

raw

values.

intervals.)

5?,

to the intense

axis represent

auditory

the midpoints

auditory

the midpoints

stimulus

expressed

of the 10 selected

in raw values.

intervals.)

M. C. Ferminder and J. Vila / Cardrac defense response in humans

130

-I 00

bi

<

i

1’5

SECONDS

Fig. 3. Cardiac expressed

A? FROM

i6

i9

L13

STIMULUS

io

period (CP) and Pulse transit

in Z-scores.

(Numbers

517

ONSET

time (P’IT)

on the horizontal

response

axis represent

to the intense

auditory

the midpoints

of the 10 selected

stimulus

intervals.)

increase in PTT is immediately reaches its maximum decremental

followed by a progressive decrease point coinciding with the maximum

tude of the second accelerative HR component. towards the baseline is observed, coinciding component of the cardiac response.

which ampli-

Finally, a progressive recovery with the second decelerative

A (2 x 10 X s) ANOVA, the first factor being the type of physiological variable (CP versus PTT) and the second being the form of the response (10 medians),

both

factors

of repeated

measures,

was carried

out on the trans-

formed CP and PTT values. The results showed a significant main effect of the form factor, F(9,lOS) = 9.14, p < .OOl, and a significant effect of the type X form interaction, easily interpreted of their

response.

F(9,108)

= 8.82,

p < .OOl. The

by fig. 3. The two physiological Statistical

analysis

of the form

significant variables

interaction

is

differ in the form

of the response

for each

variable shows that, while CP has significant effects of the linear, F(1,12) = 12.20, p < .Ol, and cubic, F(1,12) = 13.06, p < .Ol, trends, PTT has significant effects of the quadratic F(1,12) = 51.82, p < .OOl, and cubic, F(1,12) = 12.48, p < .Ol, trends. On the other hand, the significant differences between the two variables are seen only in medians 1, F(1,12) = 65.98, p < .OOl, 3, F(1,12) = 10.32, p < .Ol, and 4, F(1,12) = 11.39, p -C .Ol, corresponding to the first accelerative and first decelerative component of the CDR. No significant differences are observed in the rest of the medians, the F values being especially

low from medians

5 to 10.

4. Discussion The results regarding CP confirm previous studies. As far as the PTT

the typical CDR pattern described in results are concerned, the data clearly

131

M. C. Fermindez and J. Vila / Cardiac defense response in humans

indicate

that the only coincidences

between

the CP and the PTT changes

occur

in the second accelerative and second decelerative components of the cardiac response. In the two first components, the changes in CP and PTT move in opposite directions. Consequently, assuming ergic influences on the heart, our results acceleration

and second deceleration

tion, the first acceleration

that PTT does reflect P-adrensuggest that while the second

may be explained

and the first deceleration

by sympathetic

cannot

media-

be explained

in the

same way. Moreover, taking into account the temporal sequence of the PTT changes, the sympathetic influences begin temporarily a few seconds before the initiation the presence

of the second cardiac acceleration, from which we may deduce of a vagally mediated inhibitory effect on the HR which dis-

sipates

a few seconds

after

acceleration. Our results

regarding

to allow

the full onset

the autonomic

mediation

of the second of the first

cardiac

and

second

acceleration bear out those obtained by Turpin and Siddle, who used as a measure of sympathetic activation the T-wave amplitude of the ECG (Turpin & Siddle, 1978), forearm blood flow (Turpin & Siddle, 1981) and the carotid d P/dt (Turpin & Siddle, 1981). Interestingly, Turpin and Siddle’s results regarding these sympathetic indices are remarkably similar to those observed in PTT, suggesting that there is a phasic decrease in sympathetic activation at the beginning of the CDR (first acceleration) and an increase in sympathetic activation

during the second acceleration.

the results of a discriminant applied to the differentiation the second accelerative tive component. higher

number

analysis between

component)

In the typical of non-specific

Our data are equally consistent (Fernandez, the typical

and a pattern

CDR

pattern,

skin resistance

with

Robles, & Vila, in press) CDR pattern (presence of without the second accelera-

greater

vasoconstriction

responses

were observed

and a pre-

cisely during the second acceleration. Consequently, convergent data from different autonomic indices seem to support the interpretation of the cardiac measures employed in the present study. Our data do not provide information as to the possible

mechanism

of the

sympathetic control of the second cardiac acceleration. Sympathetic control may be produced both at a neural level (direct influence on the heart) and at a humoral level (indirect influence through catecholamine production). Bond’s research with animals (Bond, 1943) suggests sympathetic adrenal medullary mediation of the second acceleration and clear vagal mediation of the first deceleration. The vagal mediation of the first deceleration is consistent with the results of the present investigation, which also point towards parasympathetic inhibition as a possible cause of the first acceleration.Thus, our results suggest the presence of important vagal and sympathetic influences in the cardiac defense response. The first two components seem to be controlled vagally whereas the final two components appear to be controlled sympathetically. Furthermore, the alternating pattern of the accelerative and the decelera-

132

M. C. Fermindez

and J. Vila / Cardmc

defense

response

in humans

tive components and the almost perfect coincidence of the amplitudes of the accelerative components, on the one hand, and the decelerative components, on the other, suggest the presence of compensatory homeostatic mechanisms within the cardiovascular system as a whole, although this hypothesis needs further empirical support. The description and interpretation of the CDR supported by our data are contrary

to the traditional

exclusively electrical

view of the defense

on the results stimulation

of studies

which

of the hypothalamic

the unidirectionality

response,

defense

of the HR changes

which is based almost

investigated

it by means

of the

area in animals and assumes

(acceleration)

and its exclusive

sym-

pathetic mediation. However, the results of more behavioral and naturalistic studies on the defense response in animals (Adams et al., 1971; Bond, 1943) as well as on the stress response in general William, & Shapiro, 1982; Vingerhoets,

(Grossman & Svebak, 1987; Surwitt, 1985) are not at all contrary to but

coherent with a description and interpretation of the cardiac as the one proposed here, in terms of both accelerative components

and both vagal and sympathetic

defense response, and decelerative

mediation.

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