Circulation Research, Vol 66, 163-175, Copyright © 1990 by American Heart Association

ARTICLES

Prostaglandins in the pericardial fluid modulate neural regulation of cardiac electrophysiological properties

T Miyazaki, HP Pride and DP Zipes
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202.

In response to various stimuli, the pericardium produces prostaglandins that might play a role in neural regulation of cardiac electrophysiological properties by modulating epicardial nerve effects. We determined the effects of various epicardial superfusates on efferent cardiac responses, induced by bilateral efferent ansae subclaviae (SS) and cervical vagal (VS) stimulation, and afferent cardiac reflexes elicited by intracoronary injections of bradykinin (25 micrograms) and nicotine (50 micrograms). Pericardial instillation of arachidonic acid in normal Tyrode's solution (3 micrograms/ml) increased the concentration of pericardial prostacyclin (PGI2), measured by radioimmunoassay as the stable metabolite 6-keto-PGF1 alpha, and of prostaglandin E2 (PGE2). Arachidonic acid superfusion reduced SS-induced shortening of sinus cycle length (SCL), atrio-His interval (AH), and effective refractory period (ERP) of the right and left ventricular myocardium and prevented intra-aortic angiotensin II (30 ng/kg/min) from augmenting SS effects on these variables. Pericardial arachidonic acid plus indomethacin (1 microgram/ml) eliminated the prostaglandin increase and restored the responses of SCL, AH, and ERP to SS and to angiotensin II infusion. Pericardial PGE2 (30 or 50 ng/ml) or PGI2 (50 ng/ml) reversibly suppressed SS-induced shortening of SCL and ERP. Pericardial arachidonic acid or PGI2, however, did not blunt the shortening of ERP induced by intravenous infusion of norepinephrine. Pericardial arachidonic acid did not affect VS-induced lengthening of ERP or the duration of sinus arrest, or arterial blood pressure and heart rate responses to bradykinin or nicotine. We conclude that an increase in the concentration of prostaglandins in the pericardial fluid inhibits efferent sympathetic nerve effects on cardiac electrophysiological variables and antagonizes the facilitatory action of angiotensin II on efferent sympathetic stimulation by acting at presynaptic sites. Increased concentration of pericardial prostaglandins in response to various stimuli may constitute a physiological negative-feedback control mechanism that regulates efferent cardiac sympathetic stimulation.

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