Cardiac baroreflex properties in myocardial infarcted rats

Recent studies demonstrated that chronic but not acute myocardial infarction impairs the cardiopulmonary reflex. The aim of the present study was to evaluate the baroreflex in awake rats bearing short-term (1 day) or long-term (30 days) myocardial infarction. Left ventricular infarction was produced by ligation of the anterior descending branch of the left coronary artery. In order to examine the baroreceptor reflex function by means of sigmoidal curvefitting analysis in conscious rats, reflex heart rate responses were elicited by alternate intravenous injections of phenylephrine (change, +5 to +40 mmHg) and sodium nitroprusside (change, -5 to -40 mmHg). Infarcted rats showed either hypotension plus tachycardia (1 day) or bradycardia (30 days) in resting conditions. The baroreceptor reflex gain (sensitivity) was significantly increased in 30 days (5.20 +/- 0.33 bpm/mmHg, p < 0.01) but not in 1 day (3.78 +/- 0.20 bpm/mmHg) infarcted rats when compared to sham rats (3.83 +/- 0.16 bpm/mmHg). Transmural antero-medio-lateral infarcted areas spanned over nearly 37% (1 day group) and 35% (30 days group) of the left ventricular circumference. Myocardial hypertrophy was showed in right ventricle (39%, p < 0.01) as well as in right (35%, P < 0.05) and left atria (127%, p < 0.001) in the 30 days but not in the 1 day infarcted group. The enhancement of baroreflex correlated significantly with the extent of myocardial necrosis in the 30 days infarcted group. We conclude that baroreflex control of heart rate is well preserved in short- but exaggerated in long-term myocardial infarction. The enhancement of the baroreflex gain could reflect a compensatory mechanism to the impairment of the cardiopulmonary reflex following chronic myocardial infarction and thus contributing to sustain the arterial pressure and heart rate in low levels.