首页> 外文期刊>Neurosurgery >The temporal profile of cerebral blood flow and tissue metabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.
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The temporal profile of cerebral blood flow and tissue metabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.

机译:脑血流和组织代谢产物的时间变化表明大鼠实验性蛛网膜下腔出血后持续代谢抑制。

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BACKGROUND: Derangement of cerebral metabolism occurs after various insults such as ischemia, traumatic brain injury, and subarachnoid hemorrhage (SAH). OBJECTIVE: To investigate the course of cerebral blood flow and metabolic parameters in the first hours after experimental SAH. METHODS: Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (8 rats in each group). Local cerebral blood flow and intracranial pressure were measured continuously. Microdialysis samples were acquired in 30-minute intervals for 6 hours after SAH. Concentrations of glucose, lactate, pyruvate, and glutamate were determined. RESULTS: After induction of SAH, cerebral perfusion pressure and local cerebral blood flow sharply decreased. The decrease in local cerebral blood flow exceeded the decrease in cerebral perfusion pressure throughout the observation period. Glutamate concentrations in microdialysis samples increased sixfold and recovered to baseline levels. Lactate concentrations immediately increased after SAH, recovered incompletely, and remained above the levels of control animals until the end of the sampling period. Pyruvate concentrations showed a delayed increase starting 2 hours after SAH. CONCLUSION: The course of cerebral blood flow after SAH resembles global ischemia followed by a continuous low-flow state caused by a sudden decrease in cerebral perfusion pressure and acute vasoconstriction. The courses of lactate and pyruvate concentrations indicate a persistently deranged aerobic metabolism.
机译:背景:脑代谢紊乱发生在各种损伤后,例如缺血,脑外伤和蛛网膜下腔出血(SAH)。目的:研究实验性SAH后头几个小时的脑血流量和代谢参数。方法:使用血管内细丝模型对16只Sprague-Dawley大鼠进行SAH或作为对照组(每组8只大鼠)。连续测量局部脑血流量和颅内压。 SAH后以30分钟的间隔采集微透析样品,持续6小时。测定葡萄糖,乳酸盐,丙酮酸盐和谷氨酸盐的浓度。结果:SAH诱导后,脑灌注压和局部脑血流量急剧下降。在整个观察期间,局部脑血流量的减少超过了脑灌注压力的减少。微透析样品中的谷氨酸盐浓度增加了六倍,并恢复到基线水平。 SAH后,乳酸浓度立即增加,不完全恢复,并一直保持高于对照动物的水平,直到采样期结束。丙酮酸浓度显示在SAH后2小时开始延迟增加。结论:SAH后的脑血流过程类似于整体缺血,随后由于脑灌注压的突然降低和急性血管收缩而导致持续的低血流状态。乳酸和丙酮酸浓度的变化过程表明有氧代谢持续紊乱。

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