Haelewyn B, Yvon A, Hanouz J L, MacKenzie E T, Ducouret P, Gérard J L, Roussel S
Laboratory of Experimental Anaesthesiology and Cellular Physiology, University of Caen, UPRES EA 3212, Département d'Anesthésie Réanimation, Centre Hospitalier Universitaire (CHU), Côte de Nacre, Caen, France.
Br J Anaesth. 2003 Sep;91(3):390-6. doi: 10.1093/bja/aeg186.
We studied the potential neuroprotective effects of halothane and desflurane, compared with the awake state, on infarct size following 2 h of intraluminal middle cerebral artery occlusion (MCAo) and 22 h of reperfusion.
Male Sprague-Dawley rats were anaesthetized with desflurane or halothane, intubated, and mechanically ventilated. Mean arterial pressure (MAP), blood gases, and pH were controlled. Body temperature was maintained at 37.5-38 degrees C. Animals were assigned to one of four groups according to the anaesthetic type (halothane or desflurane) and the duration of anaesthesia: "short-duration", during the preparation only; "long-duration", during both preparation and ischaemia. Twenty-four hours after MCAo, infarcts were visualized by staining with 2,3,5-triphenyltetrazolium chloride. Two additional groups of rats were subjected to the same protocol as that of long-duration halothane and long-duration desflurane with additional pericranial temperature measurements made.
Physiological parameters were comparable between the groups but MAP was higher (P<0.0001) in the short-duration groups. In the short-duration groups, cerebral infarct volumes were not significantly different between anaesthetics (short-duration halothane: 288 (61) mm(3), mean (SD); short-duration desflurane: 269 (71) mm(3), P>0.56). Compared with the awake state (short-duration groups), halothane and desflurane significantly reduced infarct volumes (long-duration halothane: 199 (54) mm(3), P<0.0047 vs short-duration halothane; long-duration desflurane: 121 (55) mm(3), P<0.0001 vs short-duration desflurane). The mean infarct volume in the long-duration desflurane group was significantly lower than that in the long-duration halothane group (P<0.0053). Pericranial temperatures were similar in the desflurane and halothane long-duration groups (P>0.17).
In rats, desflurane-induced neuroprotection against focal cerebral ischaemia was greater than that conferred by halothane.
我们研究了与清醒状态相比,在大脑中动脉腔内闭塞(MCAo)2小时及再灌注22小时后,氟烷和地氟烷的潜在神经保护作用对梗死体积的影响。
雄性Sprague-Dawley大鼠用氟烷或地氟烷麻醉,插管并进行机械通气。控制平均动脉压(MAP)、血气和pH值。体温维持在37.5-38摄氏度。根据麻醉类型(氟烷或地氟烷)和麻醉持续时间,将动物分为四组之一:“短时间组”,仅在准备过程中;“长时间组”,在准备和缺血过程中。MCAo后24小时,用2,3,5-三苯基氯化四氮唑染色观察梗死灶。另外两组大鼠采用与长时间氟烷和长时间地氟烷相同的方案,并额外测量颅周温度。
各组间生理参数具有可比性,但短时间组的MAP较高(P<0.0001)。在短时间组中,不同麻醉剂之间的脑梗死体积无显著差异(短时间氟烷组:288(61)mm³,均值(标准差);短时间地氟烷组:269(71)mm³,P>0.56)。与清醒状态(短时间组)相比,氟烷和地氟烷显著降低了梗死体积(长时间氟烷组:199(54)mm³,与短时间氟烷组相比P<0.004;长时间地氟烷组:121(55)mm³,与短时间地氟烷组相比P<0.0001)。长时间地氟烷组的平均梗死体积显著低于长时间氟烷组(P<0.0053)。地氟烷和氟烷长时间组的颅周温度相似(P>0.17)。
在大鼠中,地氟烷诱导的对局灶性脑缺血的神经保护作用大于氟烷。