Takahata O, Ichihara K, Ogawa H
Department of Anesthesiology, Asahikawa Medical College, Japan.
Acta Anaesthesiol Scand. 1995 May;39(4):449-56. doi: 10.1111/j.1399-6576.1995.tb04098.x.
We studied the effect of sevoflurane on ischaemic myocardium in terms of myocardial energy and carbohydrate metabolism. Mongrel dogs were anaesthetized initially with sodium pentobarbitone, and then inhaled sevoflurane at 0% (0 MAC), 2.4% (1.0 MAC) or 4.7% (2.0 MAC) of inspired concentration for 60 min. Ischaemia was then induced for 3 min by ligating the left anterior descending coronary artery. The tissue levels of energy and carbohydrate metabolites were determined before and after sevoflurane inhalation, and after 3 min of ischaemia. Sevoflurane significantly decreased systolic and diastolic blood pressures, heart rate, and rate-pressure product in a dose dependent manner. When the animals did not inhale sevoflurane (0 MAC), ischaemia significantly decreased adenosine triphosphate and creatine phosphate levels, and produced alterations of carbohydrate metabolism. These metabolic changes induced by ischaemia were lessened by inhalation of sevoflurane. To exclude the influence of haemodynamic changes, blood pressure and heart rate were maintained during 1.0 MAC sevoflurane inhalation. Significant attenuation of ischaemia-induced metabolic changes caused by sevoflurane was still observed in some metabolites. These results indicate that the ischaemic influences on the myocardium may be reduced by sevoflurane, and this protective effect can be explained not only by its haemodynamic effect.
我们从心肌能量和碳水化合物代谢方面研究了七氟醚对缺血心肌的影响。杂种犬最初用戊巴比妥钠麻醉，然后分别以吸入浓度的0%（0MAC）、2.4%（1.0MAC）或4.7%（2.0MAC）吸入七氟醚60分钟。随后通过结扎左冠状动脉前降支诱导缺血3分钟。在吸入七氟醚前、吸入后以及缺血3分钟后测定能量和碳水化合物代谢产物的组织水平。七氟醚以剂量依赖的方式显著降低收缩压和舒张压、心率以及心率-血压乘积。当动物不吸入七氟醚（0MAC）时，缺血显著降低三磷酸腺苷和磷酸肌酸水平，并引起碳水化合物代谢改变。吸入七氟醚可减轻缺血诱导的这些代谢变化。为排除血流动力学变化的影响，在吸入1.0MAC七氟醚期间维持血压和心率。在一些代谢产物中仍观察到七氟醚对缺血诱导的代谢变化有显著减轻作用。这些结果表明，七氟醚可减轻缺血对心肌的影响，且这种保护作用不仅可由其血流动力学效应来解释。
