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动静脉畸形切除术后压力自动调节功能完好。

Pressure autoregulation is intact after arteriovenous malformation resection.

作者信息

Young W L, Kader A, Prohovnik I, Ornstein E, Fleischer L H, Ostapkovich N, Jackson L D, Stein B M

机构信息

Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York.

出版信息

Neurosurgery. 1993 Apr;32(4):491-6; discussion 496-7. doi: 10.1227/00006123-199304000-00001.

Abstract

The loss of autoregulatory control of cerebral perfusion to changes in perfusion pressure in tissue remote from an arteriovenous malformation (AVM) has been proposed as the mechanism underlying "normal perfusion pressure breakthrough." This study is the first direct test of this mechanism. Studies were performed during the resection of moderate to large AVMs in 25 patients undergoing 28 procedures under isoflurane anesthesia. Cerebral blood flow (CBF) was measured (xenon-133 method) in the hemisphere adjacent to the nidus before resection after dural exposure (pre), after AVM removal before dural closure at spontaneous systemic blood pressure (post), and, finally, with the mean arterial pressure increased by 20 mm Hg, using phenylephrine (post-BP). AVM resection resulted in a significant enhancement of perfusion in the adjacent hemisphere (30 +/- 2 vs. 25 +/- 1 ml/100g/min, P < 0.01), but no further increase of CBF occurred during increased perfusion pressure (30 +/- 2 ml/100g/min). One patient suffered a postoperative hemorrhage and another developed intraoperative brain swelling during the course of the resection that necessitated staging the procedure. These two patients had the highest increases in CBF, but intact pressure autoregulation. Preserved autoregulation to increased mean arterial pressure after resection does not support a hemodynamic mechanism for the observed increase in CBF from before the resection to after the resection. Pathological events, however, do appear to be related to increases in hemispheric perfusion.

摘要

脑灌注自动调节功能丧失,无法应对动静脉畸形(AVM)周围组织灌注压的变化,这被认为是“正常灌注压突破”的潜在机制。本研究首次对该机制进行了直接验证。研究在25例患者接受28次异氟烷麻醉下的中大型AVM切除术中进行。在硬脑膜暴露后切除前(术前)、切除AVM后硬脑膜闭合前自然体循环血压状态下(术后)以及最后使用去氧肾上腺素使平均动脉压升高20 mmHg时(升压后),采用氙-133法测量病变侧相邻半球的脑血流量(CBF)。AVM切除导致相邻半球灌注显著增强(30±2 vs. 25±1 ml/100g/min,P<0.01),但在灌注压升高时CBF未进一步增加(30±2 ml/100g/min)。1例患者术后出血,另1例在切除过程中出现术中脑肿胀,需分期进行手术。这2例患者的CBF升高幅度最大,但压力自动调节功能完好。切除后对升高的平均动脉压保留自动调节功能,不支持从切除前到切除后观察到的CBF增加的血流动力学机制。然而,病理事件似乎确实与半球灌注增加有关。

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