Effects of prostaglandins on baroreflex during reperfusion of the ischaemic myocardium

1. The present study was planned to: (i) determine whether the baroreflex c ontrol of heart rate (HR) and renal sympathetic nerve activity (RSNA) was a ttenuated during reperfusion of short-term ischaemic myocardium; and (ii) s tudy whether blockade of prostaglandin synthesis with indomethacin reversed the inhibitory baroreflex. 2. Arterial pressure was lowered with intravenous sodium nitroprusside befo re coronary occlusion and 3 min after release of a 5 min occlusion of the l eft circumflex coronary artery in anaesthetized rabbits. The protocol was r epeated 20 min after indomethacin (5 mg/kg, i.v.) or indomethacin vehicle ( 50 mmol/L tris(hydroxymethyl)aminomethane buffer, pH 8.4) treatment. In add ition, this study was performed in a group of vagotomized rabbits. 3. Before indomethacin treatment, the slope of the mean arterial pressure ( MAP)-RSNA relationship decreased from -3.3 +/- 0.77 to -2.01 +/- 0.69% chan ge in RSNA/mmHg (P < 0.05) during reperfusion of ischaemic myocardium in in tact rabbits. The decrease in the slope was reversed by administration of i ndomethacin, However, the decrease in the slope was not reversed by indomet hacin vehicle. Furthermore, the reduction in the slope of the MAP-RSNA rela tionship during reperfusion of ischaemic myocardium was abolished in vagoto mized rabbits. However, there was no inhibition of the slope of the MAP-HR relationship during reperfusion of ischaemic myocardium in either intact or vagotomized rabbits. 4. In conclusion, our data suggest that prostaglandins released by ischaemi c myocardium can attenuate the baroreflex-mediated response of RSNA to lowe red arterial pressure via vagal afferents during reperfusion of short-term ischaemic myocardium.