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猴子的血管痉挛因蛛网膜下腔血凝块的溶解和包裹而缓解。

Vasospasm in monkeys resolves because of loss of and encasement of subarachnoid blood clot.

作者信息

Zhang Z D, Yamini B, Komuro T, Ono S, Johns L, Marton L S, Weir B, Macdonald R L

机构信息

Section of Neurosurgery, Department of Surgery, Pritzker School of Medicine, University of Chicago Medical Center, Chicago, Illinois, USA.

出版信息

Stroke. 2001 Aug;32(8):1868-74. doi: 10.1161/01.str.32.8.1868.

Abstract

BACKGROUND AND PURPOSE

We studied in monkeys why vasospasm resolves after subarachnoid hemorrhage (SAH).

METHODS

Monkeys underwent angiography and right (n=17) or bilateral (n=8) SAH. Animals with bilateral SAH underwent angiography 1, 3, 5, and 7 days later. Animals with right SAH underwent angiography 7 days later. The clot was then not removed (n=5), removed and replaced with fresh clot (n=7), or removed and not replaced (n=5). At the same time on day 7, the removed clot (n=12) or fresh clot (n=5) was placed on the left side. Angiography was repeated every 2 days until day 14.

RESULTS

SAH caused significant vasospasm on day 7 that resolved by day 14. Removal of clot on day 7 resulted in more rapid resolution of vasospasm. Placement of fresh clot onto arteries that had already been exposed to clot for 7 days produced vasospasm that persisted without resolving for an additional 7 days. Placement of 7-day-old clot from the right onto previously unexposed left arteries or of clot from blood removed from an animal 7 days after SAH caused significantly more rapid onset of vasospasm compared with de novo vasospasm. Microscopic examination of the clots showed they were surrounded by macrophages 7 days after SAH. Arterial compliance and contractility were reduced in relation to duration of the exposure of arteries to clot.

CONCLUSIONS

Vasospasm resolves because of loss of subarachnoid blood clot. We hypothesize that reduced spasmogen release from the clot contributes to resolution of vasospasm. There was no response in the cerebral arteries that rendered them less responsive to the subarachnoid clot.

摘要

背景与目的

我们在猴子身上研究蛛网膜下腔出血(SAH)后血管痉挛缓解的原因。

方法

对猴子进行血管造影及右侧(n = 17)或双侧(n = 8)SAH。双侧SAH的动物在1、3、5和7天后进行血管造影。右侧SAH的动物在7天后进行血管造影。然后,血凝块不被清除(n = 5)、被清除并替换为新鲜血凝块(n = 7)或被清除但不替换(n = 5)。在第7天的同一时间,将清除的血凝块(n = 12)或新鲜血凝块(n = 5)放置在左侧。每2天重复进行血管造影直至第14天。

结果

SAH在第7天引起显著的血管痉挛,并在第14天缓解。第7天清除血凝块导致血管痉挛更快缓解。将新鲜血凝块放置在已经暴露于血凝块7天的动脉上会产生血管痉挛,且持续7天不缓解。将右侧7日龄的血凝块放置在先前未暴露的左侧动脉上,或放置SAH 7天后从动物体内取出的血液中的血凝块,与新生血管痉挛相比,会导致血管痉挛发作明显更快。血凝块的显微镜检查显示,SAH 7天后它们被巨噬细胞包围。动脉顺应性和收缩性与动脉暴露于血凝块的持续时间相关而降低。

结论

血管痉挛因蛛网膜下腔血凝块的消失而缓解。我们推测血凝块中痉挛原释放减少有助于血管痉挛的缓解。脑动脉没有出现使其对蛛网膜下腔血凝块反应性降低的反应。

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