It is known that volatile anaesthetics protect myocardial tissue against ischaemic and reperfusion injury in vitro. In this investigation, we have determined the effects of the inhalation anaesthetics, enflurane, isoflurane, sevoflurane and desflurane, administered only during early reperfusion, on myocardial reperfusion injury in vivo. Fifty chloralose-anaesthetized rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. Left ventricular pressure (LVP, tip-manometer), cardiac output (CO, ultrasonic flow probe) and infarct size (triphenyltetrazolium staining) were determined. During the first 15 min of reperfusion, five groups of 10 rabbits each received 1 MAC of enflurane (enflurane group), isoflurane (isoflurane group), sevoflurane (sevoflurane group) or desflurane (desflurane group), and 10 rabbits served as untreated controls (control group). Haemodynamic baseline values were similar between groups (mean LVP 106 (SEM 2) mm Hg; CO 281(7) ml min-1). During coronary occlusion, LVP and CO were reduced to the same extent in all groups (LVP 89% of baseline; CO 89%). Administration of inhalation anaesthetics during early reperfusion further reduced both variables, but they recovered after discontinuation of the anaesthetics to values not different from control animals. Infarct size was reduced from 49 (5)% of the area at risk in the control group to 32 (3)% in the desflurane group (P = 0.021), and to 36 (2)% in the sevoflurane group (P = 0.097). In the enflurane group, infarct size was 39 (5)% (P = 0.272). Isoflurane had no effect on infarct size (48 (5)%, P = 1.000). The results show that desflurane and sevoflurane markedly reduced infarct size and therefore can protect myocardium against reperfusion injury in vivo. Enflurane had only a marginal effect and isoflurane offered no protection against reperfusion injury in vivo. These different effects suggest different protective mechanisms at the cellular level.

Isoflurane-induced preconditioning depends on the release of free radicals.

Volatile anaesthetics protect the heart against reperfusion injury. We investigated whether the cardioprotection induced by sevoflurane against myocardial reperfusion injury was concentration-dependent. Fifty-eight alpha-chloralose anaesthetized rats were subjected to 25 min of coronary artery occlusion followed by 90 min of reperfusion. Sevoflurane was administered for the first 15 min of reperfusion at concentrations corresponding to 0.75 (n=11), 1.0 (n=11), 1.5 (n=13), or 2.0 MAC (n=12). Eleven rats served as untreated controls. Left ventricular peak systolic pressure (LVPSP, tipmanometer) and cardiac output (CO, flowprobe) was measured. Infarct size (IS, triphenyltetrazolium staining) was determined as percentage of the area at risk. Baseline LVPSP was 131 (126-135) mm Hg (mean (95% confidence interval)) and CO 33 (31-36) ml min(-1), similar in all groups. During early reperfusion, sevoflurane reduced LVPSP in a concentration-dependent manner to 78 (67-89)% of baseline at 0.75 MAC (not significant vs controls 99 (86-112)%), 71 (62-80)% at 1 MAC (P<0.05), 66 (49-83)% at 1.5 MAC (P<0.05) and 56 (47-65)% at 2 MAC (P<0.05). CO remained constant. While 0.75 MAC of sevoflurane had no effect on IS (34 (27-41)% of the area at risk) compared with controls (38 (31-45)%, P=0.83), 1.0 MAC reduced IS markedly to 23 (17-30)% (P<0.05). Increasing the concentration to 1.5 MAC (23 (17-30)%) and 2 MAC (23 (13-32)%, both P<0.05 vs controls) had no additional protective effect. One MAC sevoflurane protected against myocardial reperfusion injury. Increasing the sevoflurane concentration above 1 MAC resulted in no further protection.

The noble gas xenon can be used as an anesthetic gas with many of the properties of the ideal anesthetic. Other volatile anesthetics protect myocardial tissue against reperfusion injury. We investigated the effects of xenon on reperfusion injury after regional myocardial ischemia in the rabbit. Chloralose-anesthetized rabbits were instrumented for measurement of aortic pressure, left ventricular pressure, and cardiac output. Twenty-eight rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. During the first 15 min of reperfusion, 14 rabbits inhaled 70% xenon/30% oxygen (Xenon), and 14 rabbits inhaled air containing 30% oxygen (Control). Infarct size was determined at the end of the reperfusion period by using triphenyltetrazolium chloride staining. Xenon reduced infarct size from 51%+/-3% of the area at risk in controls to 39%+/-5% (P<0.05). Infarct size in relation to the area at risk size was smaller in the xenon-treated animals, indicated by a reduced slope of the regression line relating infarct size to the area at risk size (Control: 0.70+/-0.08, r = 0.93; Xenon: 0.19+/-0.09, r = 0.49, P<0.001). In conclusion, inhaled xenon during early reperfusion reduced infarct size after regional ischemia in the rabbit heart in vivo.

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