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培养动脉平滑肌细胞中的实验性血管痉挛。第1部分:氧合血红蛋白引起的收缩和超微结构变化。

Experimental vasospasm in cultured arterial smooth-muscle cells. Part 1: Contractile and ultrastructural changes caused by oxyhemoglobin.

作者信息

Fujii S, Fujitsu K

机构信息

Department of Neurosurgery, Yokohama City University School of Medicine, Japan.

出版信息

J Neurosurg. 1988 Jul;69(1):92-7. doi: 10.3171/jns.1988.69.1.0092.

Abstract

Smooth-muscle cells were cultured from rat aortic media, then oxyhemoglobin and other agents including serotonin, norepinephrine, and angiotensin II were added separately to the medium. Contractile and ultrastructural changes of the cells were examined with electron microscopy during the first 2 weeks of incubation. Oxyhemoglobin not only produced progressive contraction of the arterial smooth-muscle cells, but it also caused ultrastructural changes that resembled myonecrosis. In contrast, there was no evidence of progressive contraction or ultrastructural changes either in control cultures or in cultures with the other vasoactive agents. Although washout of oxyhemoglobin 3 hours after administration prevented continued contraction of the cells, washout 24 hours or longer after administration had no preventive effect. Judging from these results and from the fact that the culture medium was changed every 2 days, it is unlikely that accumulation of exogenous vasoactive agents caused these changes. The contraction and suggestive myonecrosis of the arterial smooth-muscle cells are probably caused by some intrinsic process initiated by oxyhemoglobin. The culture of cerebral arterial smooth-muscle cells requires further technical improvement; nevertheless, these results obtained with the smooth-muscle cells of rat aortic media indicate that arterial smooth-muscle cells in culture provide a promising new experimental model for chronic in vitro study of cerebral arterial spasm. It is suggested from these results that cerebral arteries are particularly prone to vasospasm because of structural differences as compared to noncerebral arteries.

摘要

从大鼠主动脉中膜培养平滑肌细胞,然后分别向培养基中加入氧合血红蛋白以及其他物质,包括5-羟色胺、去甲肾上腺素和血管紧张素II。在培养的前两周内,用电子显微镜检查细胞的收缩和超微结构变化。氧合血红蛋白不仅使动脉平滑肌细胞逐渐收缩,还引起了类似于肌坏死的超微结构变化。相比之下,在对照培养物或添加其他血管活性物质的培养物中,均未观察到逐渐收缩或超微结构变化的证据。尽管给药3小时后洗去氧合血红蛋白可阻止细胞持续收缩,但给药24小时或更长时间后洗去则没有预防作用。根据这些结果以及每两天更换一次培养基这一事实判断,外源性血管活性物质的积累不太可能导致这些变化。动脉平滑肌细胞的收缩和提示性肌坏死可能是由氧合血红蛋白引发的一些内在过程所致。脑动脉平滑肌细胞的培养需要进一步的技术改进;然而,用大鼠主动脉中膜平滑肌细胞获得的这些结果表明,培养的动脉平滑肌细胞为脑动脉痉挛的慢性体外研究提供了一个有前景的新实验模型。从这些结果推测,与非脑动脉相比,脑动脉由于结构差异而特别容易发生血管痉挛。

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