1. The present study was planned to: (i) determine whether the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) was attenuated during reperfusion of short-term ischaemic myocardium; and (ii) study whether blockade of prostaglandin synthesis with indomethacin reversed the inhibitory baroreflex. 2. Arterial pressure was lowered with intravenous sodium nitroprusside before coronary occlusion and 3 min after release of a 5 min occlusion of the left circumflex coronary artery in anaesthetized rabbits. The protocol was repeated 20 min after indomethacin (5 mg/kg, i.v.) or indomethacin vehicle (50 mmol/L tris(hydroxymethyl)aminomethane buffer, pH 8.4) treatment. In addition, 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% change in RSNA/mmHg (P < 0.05) during reperfusion of ischaemic myocardium in intact rabbits. The decrease in the slope was reversed by administration of indomethacin. However, the decrease in the slope was not reversed by indomethacin vehicle. Furthermore, the reduction in the slope of the MAP-RSNA relationship during reperfusion of ischaemic myocardium was abolished in vagotomized 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 ischaemic myocardium can attenuate the baroreflex-mediated response of RSNA to lowered arterial pressure via vagal afferents during reperfusion of short-term ischaemic myocardium.

Adrenergic Fibers↗

PubMedDate not supplied

Dynamic systemic vascular resistance in a sheep supported with a Nimbus AxiPump.

Changes in systemic vascular resistance (SVR) in response to diminished pulse perfusion were analyzed over a dynamic range of flow conditions. An axial flow LVAD (Nimbus AxiPump, Rancho Cordova, CA) was implanted in a sheep for 28 days, during which time SVR was determined over several conditions of posture and excitability. Total arterial resistance (TR) was calculated dynamically as an index of SVR by analysis of pump flow in diastole, and systemic pressure estimated from the characteristic pressure-flow-speed relation of the AxiPump. TR was evaluated over a range of flow rates, including maximum flow--for which the pressures and flows were essentially nonpulsatile. Throughout the course of support, and independent of pulsatility, TR dropped when the sheep stood and was significantly lower than that in the sitting position (P < 0.01). Response to excitement followed the same trend: TR was significantly higher during agitation than during normal temper (P < 0.01). In spite of changes in pulse pressure and flow rate, SVR changes occurred according to expected physiologic responses for pulsatile perfusion. Because pump flow and pressure are sensitive to afterload, the results of these studies suggest that pump speed control must compensate for changes in SVR to maintain acceptable perfusion.

Animals↗

PubMedDate not supplied

Optimal timing for application of ventricular assist devices in patients who cannot be weaned from cardiopulmonary bypass. An experimental study.

Missing the moment for application of ventricular assist devices (VAD) may be one of the major causes of multiple organ failure in patients who are to be weaned from cardiopulmonary bypass (CPB) with the aid of VAD. To determine the optimal timing for application of VAD in such patients, we examined the effect of a CPB assist on cardiac functional recovery from severe global ischemia using an experimental canine system. In the present study we created myocardial ischemia by clamping the aorta for 20 minutes (Group I; N = 7) or 45 minutes (Group II; N = 11) under normothermic CPB. The reliability of the method in creating severe cardiac failure was confirmed by testing the levels of adenosine triphosphate (ATP), creatine phosphate (CP), and lactate. After reperfusion of the myocardium, the heart was assisted by a totally vented CPB. The left ventricular end-systolic pressure-volume relationship (Emax), which is a load-independent index of contractility, was obtained every 15 minutes for up to 120 minutes of reperfusion. The Emax revealed that the function of the damaged heart recovers exponentially with time after reperfusion. From curves of the functional recovery of the heart, CPB support appeared to be beneficial for the first 60 minutes after reperfusion, and aided in the recovery of cardiac function in hearts damaged by global myocardial ischemia. However, CPB assist thereafter may not be effective in further improving cardiac function. We therefore concluded that the decision to use VAD should be determined by cardiac function by 60 minutes of reperfusion to avoid prolonging CPB time.

Adenosine Triphosphate↗