The Bezold-Jarisch reflex (BJR), produced by the administration of 5-hydroxytryptamine (5-HT, 4-16 micrograms/kg, iv), was evaluated in awake rats bearing short- (1 day) or long-term (30 days) myocardial infarction. Heart chronotropic response produced by acetylcholine was further assessed by Langendorff's isolated heart perfusion technique. Compared to the sham-operated group, infarcted rats showed either hypotension and tachycardia or bradycardia following short- or long-term myocardial infarction, respectively. Whereas the long-term myocardial infarction attenuated 5-HT-induced hypotension and bradycardia by about -25 and -80%, respectively, no significant response changes were observed in short-term infarcted rats. Impairment of BJR correlated significantly (P < 0.01) with the extent of myocardial necrosis in the 30-days infarcted group. Chronotropic responsiveness of the heart to acetylcholine in infarcted rats did not differ from the sham-operated group. Transmural antero-medio-lateral infarcted areas spanned over nearly 37% (1-day group) and 35% (30-days group) of the left ventricular circumference. These results indicate that cardioinhibitory and vasodepressor reflex responses to 5-HT are significantly impaired in chronic myocardial infarction associated with (1) marked hypertrophy of left atrium and/or of non-infarcted left ventricle, which are the main origin of vagal chemosensitive C-fibers, (2) morphological damage of this innervation due to the necrotic injury of the left ventricle, (3), possible attenuation in the vagal afferents located in the lungs and/or (4) enhancement of the chemical sensitivity of cardiac sympathetic afferents.