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Heart rate changes in rats with acute Chagasic myocarditis
851
TRAASACI-IONS OP THE ROYAL SOCIETYOF TROPICALMBDICIXF AND HYGIENE(1988) 82, 851
1 Short Report 1 Heart rate changes in rats with acute Chagasic myocarditis Carlos F. Got&erg, Jose H. Donis, Argenis Tortes, Abdel J. Fuenmayor and Diego F. Davila Departamento de Biologia, Centro Cardiovascular, Universidad de Los Andes, Merida, 5101, Venezuela
Cardiac parasympathetic neurons are thought to be destroyed by myocarditis cmzi infection
influences
induced by Typanosoma
1970) and supression of vagal
(TAFURI,
on the sinus node should provoke
a
persistent sinus tachycardia (KAYE, 1977). We have examined the heart rate changes, over a period of 60 d, in 70 rats, inoculated intraperitoneally with 200 000 parasites (‘Y’ strain of T. cruzi), and in 70 age-matched controls. An electrocardiogram was recorded every third day, beginning on the day before inoculation, after the animals were anaesthetizedwith ether and secured prone on an animal board, using a Grass 7 polygraph; the electrodes were no. 25 hypodermic needles attached to a platinum wire. Standard limb leads were used, and the paper speed was 50 mm/set. The procedure lasted on the average 1-2 min.
/
+
2
.
.
,
1
I
/
/
+
1
.7-r+,
rT,~+,
30 40 IO 20 Days after inoculation
.
1,
1
7
50
Figure. Heart rate changesin acute ~+ypanosanacruzr-infected rats.
Values are meam f standard errors; -, infected rats; ----, uninfected control rats. Statistically significant differences are indicated by A(P
In the infected animals, the heart rate progressively increased and reached a plateau between days 14 and
21. Eight randomly selected animals were killed at this time, and their hearts showed diffuse myocarditis; parasites were present in 6 hearts. After day 22, the heart rate returned to control levels (Figure). The rectal temperature was similar in both groups of animals. The heart rate changes closely paralleled the histological course of experimentally induced acute
Addressfor correspondence: CarlosF. Gottberg,,Facultad de Ciencias, Universidad de Los Andes, Menda, 5101, Venezuela.
Chagasic myocarditis (SCORZA& SCORZA,1972), and correspond to a transient sinus tachycardia. Our findings may be influenced by the repeated exposure of the animals to anaesthetic.,and to the procedure for recording the electrocardogram. However, both groups of animals were subjected to the same experimental design, and only the infected animals showed sinus tachycardia. Furthermore, sinus tachycardia is one of the most common electrocardiographic abnormalities of naturally infected rats (BLANDON
et al.,
1974).
It is unlikely that this transient sinus tachycardia represents major irreversible cardiac vagal neuronal damage. There are several possible explanations for this unexpected finding. First, the destruction of the cardiac neurons may take place at a later stageof the disease. However, in most laboratory animals, the histological evidence of vagal neuronal damage is present in the first 2 weeksafter inoculation (TAFURY, 1970). Secondly the transient heart rate changesmay represent functional and reversible impairment of the cardiac parasympathetic system. The progressive return of the heart rate to normal values would indicate that the cardiac vagal mechanisms were operating normally (HIGGINS et al., 1973). Recent investigations have shown no evidence of cardiac vagal postganglionic denervation in the hearts of mice with myocarditis induced by T. cmzi (TANOWITZ et al., 1985) and the cardiac vagus response to high frequency electrical stimulation of rats with acute Chagasicmyocarditis is similar to that of non-infected controls (Davila et al., unpublished observations). Consequently, it seemsreasonableto suggestthat the transient sinus tachycardia observed in our infected animals representsa functional and reversible impairment of the cardiac vagal postganglionic neurons. This research was supported by grants from ConsejoCientifico, Hurnanistico y Tecnolbgico (CDCHTM-201,G163). References Blandon,E., Edgcomb,J. H., Guevara,J. F. &Johnson,C. M. (1974).Electrocardiographic changesin Panamanian Rattus rattus naturally infected by Typanosoma cruzi. American Heart Journal, 88, 758-764.
Hieeins. C. B.. Vatner. S. F. & Braunwald. E. 11973X IFara;ympa&etic co&o1 of hearr rate. 6har&col$y
Reviews, 25, 119-155. Kaye, M. P. (1977). Denervation and reinnervation of the heart. In: Neural Control of the Heart, Randall, W. C.
(editor). New York: Oxford University Press, pp. 345-378. Tafuri, W. L. 1970.Pathogenesisof lesionsof the autonomic nervous system of the mouse in experimental acute Chagas’ disease. American 3ourn41 of Tropical Medicine and Hygiene, 19, 405-417. Tanowitz,, H. B., Davies, P. & Winner,
M. 1985. Alrera-
tions m acetylcholine receptors in experimental Chagas’ disease. Jour& of InfectGus Diseases,147, 460-466. Scorza, C. & Scorza, J. V. 1972. Acute myocarditis in rats
inoculated with Ttypanosoma cm’: study of animals sacrificed between the fourth and twenty-ninth day after
infection. Revista do Institute de Medic&a Tropical de SCo Paulo, 14, 171-177.
Received 4 Januay 1988; revised 18 April accepted for publication 27 April 1988
1988;
TRAASACI-IONS OP THE ROYAL SOCIETYOF TROPICALMBDICIXF AND HYGIENE(1988) 82, 851
1 Short Report 1 Heart rate changes in rats with acute Chagasic myocarditis Carlos F. Got&erg, Jose H. Donis, Argenis Tortes, Abdel J. Fuenmayor and Diego F. Davila Departamento de Biologia, Centro Cardiovascular, Universidad de Los Andes, Merida, 5101, Venezuela
Cardiac parasympathetic neurons are thought to be destroyed by myocarditis cmzi infection
influences
induced by Typanosoma
1970) and supression of vagal
(TAFURI,
on the sinus node should provoke
a
persistent sinus tachycardia (KAYE, 1977). We have examined the heart rate changes, over a period of 60 d, in 70 rats, inoculated intraperitoneally with 200 000 parasites (‘Y’ strain of T. cruzi), and in 70 age-matched controls. An electrocardiogram was recorded every third day, beginning on the day before inoculation, after the animals were anaesthetizedwith ether and secured prone on an animal board, using a Grass 7 polygraph; the electrodes were no. 25 hypodermic needles attached to a platinum wire. Standard limb leads were used, and the paper speed was 50 mm/set. The procedure lasted on the average 1-2 min.
/
+
2
.
.
,
1
I
/
/
+
1
.7-r+,
rT,~+,
30 40 IO 20 Days after inoculation
.
1,
1
7
50
Figure. Heart rate changesin acute ~+ypanosanacruzr-infected rats.
Values are meam f standard errors; -, infected rats; ----, uninfected control rats. Statistically significant differences are indicated by A(P
In the infected animals, the heart rate progressively increased and reached a plateau between days 14 and
21. Eight randomly selected animals were killed at this time, and their hearts showed diffuse myocarditis; parasites were present in 6 hearts. After day 22, the heart rate returned to control levels (Figure). The rectal temperature was similar in both groups of animals. The heart rate changes closely paralleled the histological course of experimentally induced acute
Addressfor correspondence: CarlosF. Gottberg,,Facultad de Ciencias, Universidad de Los Andes, Menda, 5101, Venezuela.
Chagasic myocarditis (SCORZA& SCORZA,1972), and correspond to a transient sinus tachycardia. Our findings may be influenced by the repeated exposure of the animals to anaesthetic.,and to the procedure for recording the electrocardogram. However, both groups of animals were subjected to the same experimental design, and only the infected animals showed sinus tachycardia. Furthermore, sinus tachycardia is one of the most common electrocardiographic abnormalities of naturally infected rats (BLANDON
et al.,
1974).
It is unlikely that this transient sinus tachycardia represents major irreversible cardiac vagal neuronal damage. There are several possible explanations for this unexpected finding. First, the destruction of the cardiac neurons may take place at a later stageof the disease. However, in most laboratory animals, the histological evidence of vagal neuronal damage is present in the first 2 weeksafter inoculation (TAFURY, 1970). Secondly the transient heart rate changesmay represent functional and reversible impairment of the cardiac parasympathetic system. The progressive return of the heart rate to normal values would indicate that the cardiac vagal mechanisms were operating normally (HIGGINS et al., 1973). Recent investigations have shown no evidence of cardiac vagal postganglionic denervation in the hearts of mice with myocarditis induced by T. cmzi (TANOWITZ et al., 1985) and the cardiac vagus response to high frequency electrical stimulation of rats with acute Chagasicmyocarditis is similar to that of non-infected controls (Davila et al., unpublished observations). Consequently, it seemsreasonableto suggestthat the transient sinus tachycardia observed in our infected animals representsa functional and reversible impairment of the cardiac vagal postganglionic neurons. This research was supported by grants from ConsejoCientifico, Hurnanistico y Tecnolbgico (CDCHTM-201,G163). References Blandon,E., Edgcomb,J. H., Guevara,J. F. &Johnson,C. M. (1974).Electrocardiographic changesin Panamanian Rattus rattus naturally infected by Typanosoma cruzi. American Heart Journal, 88, 758-764.
Hieeins. C. B.. Vatner. S. F. & Braunwald. E. 11973X IFara;ympa&etic co&o1 of hearr rate. 6har&col$y
Reviews, 25, 119-155. Kaye, M. P. (1977). Denervation and reinnervation of the heart. In: Neural Control of the Heart, Randall, W. C.
(editor). New York: Oxford University Press, pp. 345-378. Tafuri, W. L. 1970.Pathogenesisof lesionsof the autonomic nervous system of the mouse in experimental acute Chagas’ disease. American 3ourn41 of Tropical Medicine and Hygiene, 19, 405-417. Tanowitz,, H. B., Davies, P. & Winner,
M. 1985. Alrera-
tions m acetylcholine receptors in experimental Chagas’ disease. Jour& of InfectGus Diseases,147, 460-466. Scorza, C. & Scorza, J. V. 1972. Acute myocarditis in rats
inoculated with Ttypanosoma cm’: study of animals sacrificed between the fourth and twenty-ninth day after
infection. Revista do Institute de Medic&a Tropical de SCo Paulo, 14, 171-177.
Received 4 Januay 1988; revised 18 April accepted for publication 27 April 1988
1988;