Zink B J, Sheinberg M A, Wang X, Mertz M, Stern S A, Betz A L
Department of Surgery, University of Michigan, Ann Arbor, USA.
J Neurosurg. 1998 Dec;89(6):983-90. doi: 10.3171/jns.1998.89.6.0983.
Traumatic brain injury (TBI) is exacerbated by hypotension and hypoventilation. Because previous studies have shown a potentiating effect of ethanol (EtOH) on TBI and hemorrhagic shock (HS), the authors investigated the effects of EtOH on the early physiological response to TBI with and without HS.
Anesthetized swine, weighing approximately 20 kg each, underwent fluid-percussion TBI of 3 atm with or without 30 ml/kg hemorrhage for a period of 30 minutes. The mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure (CPP), cardiac output, cerebral venous oxygen saturation, and metabolic parameters were monitored for 3 hours postinjury. Ventilation and the response to hypercapnia were also measured. Regional cerebral blood flow and renal blood flow were measured using dye-labeled microspheres. Five groups were studied: control, TBI, TBI/EtOH, TBI/HS, and TBI/HS/EtOH. The EtOH (3.5 g) was given intragastrically 100 minutes preinjury. The TBI/HS/EtOH group demonstrated a 3-hour mortality rate of 56% and postinjury apnea requiring ventilation in 44% of animals compared with 0% in all other groups. Minute ventilation and the hypercapnic ventilatory response were significantly reduced in the postinjury period in the TBI/HS/EtOH group. The animals in this group had significantly lower CPP and cardiac output in the first 60 minutes postinjury, as well as lower renal and cerebral blood flow. Postinjury cerebral venous lactate levels were higher, and cerebral venous pH was lower in the TBI/HS/EtOH group.
In this model of TBI, acute EtOH intoxication in the presence of HS potentiates the physiological and metabolic alterations that may contribute to secondary brain injury.
创伤性脑损伤（TBI）会因低血压和通气不足而加重。由于先前的研究表明乙醇（EtOH）对TBI和失血性休克（HS）有增强作用，作者研究了EtOH对伴有或不伴有HS的TBI早期生理反应的影响。
对体重约20千克的麻醉猪进行3个大气压的液体冲击性TBI，伴有或不伴有30毫升/千克出血，持续30分钟。在受伤后3小时监测平均动脉血压、颅内压、脑灌注压（CPP）、心输出量、脑静脉血氧饱和度和代谢参数。还测量了通气和对高碳酸血症的反应。使用染料标记的微球测量局部脑血流量和肾血流量。研究了五组：对照组、TBI组、TBI/EtOH组、TBI/HS组和TBI/HS/EtOH组。在受伤前100分钟经胃给予EtOH（3.5克）。与所有其他组的0%相比，TBI/HS/EtOH组显示3小时死亡率为56%，44%的动物受伤后出现需要通气的呼吸暂停。TBI/HS/EtOH组在受伤后阶段的分钟通气量和高碳酸血症通气反应显著降低。该组动物在受伤后最初60分钟内CPP和心输出量显著降低，肾血流量和脑血流量也较低。TBI/HS/EtOH组受伤后脑静脉乳酸水平较高，脑静脉pH值较低。
在这个TBI模型中，存在HS时的急性EtOH中毒会增强可能导致继发性脑损伤的生理和代谢改变。
