Einfluss von Xenon und Isofluran auf die Hämodynamik und den myokardialen Reperfusionsschaden

BACKGROUND: Impairment of left ventricular function (LV function) during acute ischemia and reperfusion can be modified by anesthetics. Volatiles have been frequently investigated and seem to have positive effects on the myocardial reperfusion injury while having negative inotropic effects on LV function. There are also positive effects on myocardial reperfusion injury described for xenon while showing no impairment of ventricular contractility. But no data are available on its direct myocardial effects in vivo during acute ischemia and reperfusion. Therefore we examined the myocardial function during administration of xenon and isoflurane in a pig model of myocardial reperfusion injury and tested the hypothesis that xenon anesthesia would be superior to isoflurane. METHODS: Ischemia was induced in an open-chest pig model (n=27) by 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. Hemodynamic parameters were recorded during thiopental narcosis and during inhalation of 0,55 MAC isoflurane (0,9 Vol.%) or xenon (70 Vol.%) with concomitant reduction of thiopental. The influence of the narcotics was described before ischemia and after 120 minutes of reperfusion. In addition to measurement of global hemodynamics (heart rate, blood pressure, cardiac output) LV function was assessed by conductance-catheter. Load-independent parameters of LV diastolic function (end-diastolic pressure-volume relation: EDPVR, time constant of relaxation: tau) and systolic function (end-systolic pressure-volume relation: ESPVR, preload-recruitable stroke work: PRSW) were used to describe myocardial properties in detail.RESULTS: Before ischemia global hemodynamics were stable in the control group, while there was an increase in preload and a decline in afterload. Contractility and diastolic function did not appear to be affected. In comparison isoflurane and xenon showed a decreased cardiac output. Contractility seemed to be unaffected while xenon induced a diastolic dysfunction by increasing tau. Reperfusion impaired global hemodynamics and worsened diastolic function in the control group. Global contractility was unchanged, as a consequence of compensatory hypercontractility of the non-ischemic myocardium. Pretreatment with isoflurane or xenon did not result in an overall improvement of global hemodynamics, systolic or diastolic function.CONCLUSION: In concentrations below 1 MAC, xenon was not superior to isoflurane in prevention of hemodynamic compromise induced by myocardial reperfusion injury. Whereas xenon impaired active relaxation, isoflurane demonstrated its vasodilatory properties. Both drugs showed comparable effects on myocardial contractility