Cardiac Vagal Reflex Modulates Intestinal Vascular Capacitance and Ventricular Preload in Anesthetized Dogs With Acute Myocardial Infarction

BACKGROUND: The purpose of the present study was to examine the effects of the cardiac vagal reflex on intestinal vascular capacitance and cardiac filling pressure during experimental acute myocardial infarction (AMI). METHODS AND RESULTS: AMI was induced in anesthetized dogs through injection of microspheres into the left main coronary artery. Intestinal blood volume was measured with blood-pool scintigraphy. Portal venous pressure was varied through graded inflation of a portal venous constrictor to determine the intestinal vascular pressure-volume relation. Induction of AMI decreased intestinal blood volume to 88 +/- 3% of the control value (P < .01) and shifted the pressure-volume relation toward the pressure axis. This change was associated with increased left ventricular (LV) end-diastolic pressure (LVEDP) (from 6 +/- 1 to 17 +/- 2 mm Hg, P < .01) and LV segment length (to 112 +/- 4% of the control value, P < .01). During AMI, blockade of the cardiac vagal reflex by intrapericardial application of 2% lidocaine further decreased intestinal blood volume (to 83 +/- 3% of the control value, P < .05, versus AMI without lidocaine), increased LVEDP (to 22 +/- 2 mm Hg, P < .05, versus AMI without lidocaine), and tended to increase LV segment length (to 115 +/- 5%, P < .10). Lidocaine had no effect in dogs with AMI that had been vagotomized. CONCLUSIONS: These results suggest that the cardiac vagal reflex modulates the decrease in the intestinal vascular capacitance induced by AMI and modulates ventricular preload through pooling of blood in the intestinal circulation.