Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project.

Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project.
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动静脉畸形切除术后的脑充血与“突破性”并发症有关,但与供血动脉压无关。

DOI:
10.1097/00006123-199606000-00005
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发表时间:
1996
期刊:
影响因子:
4.8
通讯作者:
Stein,BM
Stein,BM
中科院分区:
医学1区
文献类型:
--
作者:
Young,WL;Kader,A;Ornstein,E;Baker,KZ;Ostapkovich,N;Pile-Spellman,J;Fogarty-Mack,P;Stein,BM

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为了研究动静脉畸形切除术后特发性术后脑肿胀或出血的病理生理学,称为正常灌注压突破(NPPB),我们在143例患者的152次手术中使用氙-133静脉注射法进行了脑血流量(CBF)研究。在研究的第一部分中,对95名患者在手术前后相对低碳酸血症期间的CBF进行了术中测量(异氟醚/N2 0麻醉)。NPPB组有更大的增加,平均值±标准差总体CBF(P< 0.0001)(28±6至47±16 ml/100 g/min,n= 5)(25±7至29±10 ml/100 g/min,n= 90);两个动静脉畸形组均表现出更大的增加,(P< 0.05)高于开颅手术组(23±6 ~ 23±6 ml/100 g/min,n= 22)。同侧和对侧CBF变化相似。在第二组动静脉畸形患者中,CBF在相对正常碳酸血症下测量,从术前到术后增加(P< 0.002)(40±13至49±15 ml/100 g/min,n= 57)。后一队列中无NPPB患者。术中切除前或术前末次栓塞时测量供血平均动脉压(n= 64)。平均供血动脉压(44±16 mm Hg)为体循环动脉压(78±12 mm Hg,P< 0.0001)的56%,与手术前后CBF的变化无关。从术前到术后的总体CBF增加与NPPB型并发症之间存在相关性,但这些CBF变化与术前局部动脉低血压无关。这些数据不支持一个独特的血流动力学机制,解释脑充血的结果,再加压膨胀血管床。
TO STUDY THE pathophysiology of idiopathic postoperative brain swelling or hemorrhage after arteriovenous malformation resection, termed normal perfusion pressure breakthrough (NPPB), we performed cerebral blood flow (CBF) studies during 152 operations in 143 patients, using the xenon-133 intravenous injection method. In the first part of the study, CBF was intraoperatively measured (isoflurane/N 2 0 anesthesia) during relative hypocapnia in 95 patients before and after resection. The NPPB group had a greater increase (P< 0.0001) in mean±standard deviation global CBF (28±6 to 47±16 ml/100 g/min, n= 5) than did the non-NPPB group (25±7 to 29±10 ml/100 g/min, n= 90); both arteriovenous malformation groups showed greater increase (P< 0.05) than did controls undergoing craniotomy for tumor (23±6 to 23±6 ml/100 g/min, n= 22). Ipsilateral and contralateral CBF changes were similar. In a second cohort of patients with arteriovenous malformations, CBF was measured at relative normocapnia and it increased (P< 0.002) from pre-to postresection (40±13 to 49±15 ml/100 g/min, n= 57). There were no NPPB patients in this latter cohort. The feeding mean arterial pressure was measured intraoperatively before resection or at the last embolization before surgery (n= 64). The feeding mean arterial pressure (44±16 mm Hg) was 56% of the systemic arterial pressure (78±12 mm Hg, P< 0.0001) and was not related to changes in CBF from pre-to postresection. There was an association between increases in global CBF from pre-to postresection and NPPB-type complications, but there was no relationship of these CBF changes to preoperative regional arterial hypotension. These data do not support a uniquely hemodynamic mechanism that explains cerebral hyperemia as a consequence of repressurization in hypotensive vascular beds.
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