No study has been performed on reflexes originating from receptors in the h
eart that might be involved in the pathological lesions of Chagas' heart di
sease. Our study was undertaken to analyze the role of cardiopulmonary refl
ex on cardiovascular control in Chagas' disease. We studied 14 patients wit
h Chagas' disease without heart failure and 12 healthy matched volunteers.
Central venous pressure, arterial blood pressure, heart rate, forearm blood
flow, and forearm vascular resistance were recorded during deactivation of
cardiopulmonary receptors. By reducing central venous pressure by applying
-10 and -15 mm Hg of negative pressure to the lower body, we observed (a)
a similar decrease of central venous pressure in both groups; (b) a marked
increase :in forearm vascular resistance in the control group but a blunted
increase in the Chagas' group; and (c) no significant changes in blood pre
ssure and heart rate. To analyze cardiopulmonary and arterial receptors, we
applied -40 mm Hg of lower-body negative pressure. As a consequence, (a) c
entral venous pressure decreased similarly in both groups; (b) blood pressu
re was maintained in the control group, whereas in patients with Chagas' di
sease, a decrease in systolic and mean arterial pressure occurred; (c) hear
t rate increased in both groups; and (d) forearm vascular resistance increa
sed significantly and similarly in both groups. Unloading of receptors with
low levels of lower-body negative pressure did not increase forearm vascul
ar resistance in patients with Chagas' disease, which suggests that the ref
lex mediated by cardiopulmonary receptors is impaired in patients with Chag
as' disease without heart failure. Overall control of circulation appears t
o be compromised because patients did not maintain blood pressure under hig
h levels of lower-body negative pressure.