Shibata M, Einhaus S, Schweitzer J B, Zuckerman S, Leffler C W
Department of Physiology and Biophysics, University of Tennessee, Memphis.
J Neurosurg. 1993 Nov;79(5):696-704. doi: 10.3171/jns.1993.79.5.0696.
Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in alpha-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 +/- 0.06 atm applied for 23.7 +/- 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the animals. The brains showed changes consistent with traumatic brain injury such as subarachnoid hemorrhage, contusions, or reactive axonal swelling; none showed histological evidence of a global alternative pathogenetic mechanism such as hypoxic ischemic damage. While CBF of uninjured control animals did not change over a 3-hour observation period, after brain injury blood flow decreased 30% +/- 1% below the baseline level within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial arteriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diameter. The present results support the hypothesis that increased sympathetic outflow to the cephalic vasculature following the fluid-percussion brain injury causes cerebral vasoconstriction decreasing pial arteriolar diameter and regional CBF.
在α-氯醛糖麻醉的仔猪中，于流体冲击脑损伤前后及损伤后3小时，检测脑血流量（CBF）、软脑膜小动脉直径、动脉血压、气体及pH值的变化。通过对右侧顶叶皮层施加2.28±0.06大气压，持续23.7±0.5毫秒的冲击来诱导脑损伤。用放射性微球测量局部脑血流量，并使用封闭的颅骨窗口监测左侧顶叶皮层软脑膜小动脉直径的变化。脑损伤后立即出现，平均血压短暂（约10分钟）升高或降低，然后在所有动物中均出现持续下降。大脑呈现出与创伤性脑损伤一致的变化，如蛛网膜下腔出血、挫伤或反应性轴突肿胀；未发现有诸如缺氧缺血性损伤等全身性替代致病机制的组织学证据。在3小时的观察期内，未受伤对照动物的脑血流量没有变化，但脑损伤后，血流量在10分钟内降至基线水平以下30%±1%，并在创伤后持续2至3小时。肾上腺素能阻断后，在未受伤对照动物或受伤动物的3小时期间内，脑血流量在任何时候均未下降。伴随脑损伤后血流量的减少，软脑膜小动脉直径比损伤前水平降低了14%。然而，在用肾上腺素能受体拮抗剂治疗的仔猪中，未受伤对照动物和脑损伤动物的软脑膜小动脉直径均未出现下降。目前的结果支持这样的假设，即流体冲击脑损伤后，向头部血管系统的交感神经输出增加会导致脑血管收缩，从而减小软脑膜小动脉直径和局部脑血流量。
