Abstract
We evaluated the effect of acute increase in parasympathetic function, elicited by pyridostigmine (PYR), shortly after myocardial infarction (MI) in anesthetized rats. Acute MI was elicited in urethane anesthetized rats by left coronary artery ligation under continuous recording of electrocardiogram (ECG) and arterial pressure (AP). Ten min after MI the rats were treated with PYR (0.25 mg/kg, iv, N=10) or saline (control, N=8) and ECG/AP recordings lasted 4 hours. At the end of experiments, the hearts were removed and perfused with Evans’ blue to evaluate the infarcted area. MI size was similar between PYR treated (52±4%) and control rats (46±4%). A fall in mean AP (115±3 to 83±5 mmHg) and a trend to bradycardia (450±6 to 436±8 bpm, p=0,051) were observed immediately after MI. AP remained 46 to 54 mmHg lower than basal values during the 4 hours after MI and PYR did not affect this parameter. A tachycardia was observed 3 and 4 hours after MI (38±17 and 45±15 bpm, respectively) in control rats. PYR elicited a prompt bradycardia (−94±19 bpm) and prevented the tachycardia 3 and 4 hours after MI. Premature ventricular beats (PVB) were more frequent in control as compared to PYR treated rats. Segments of 2,000 beats were examined every hour after MI to identify PVB. Four out of 8 control rats showed 1 to 15 PVB while only 2 out of 10 PYR treated rats showed 1 to 4 PVB within the 4 h after MI.
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