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血栓素A2引起的脑动脉平滑肌收缩。

Cerebral arterial smooth muscle contraction by thromboxane A2.

作者信息

Ellis E F, Nies A S, Oates J A

出版信息

Stroke. 1977 Jul-Aug;8(4):480-3. doi: 10.1161/01.str.8.4.480.

Abstract

The contractile effects of thromboxane A2 (TxA2), a labile arachidonic acid metabolite, were studied in arterial smooth muscle strips. TxA2 was generated upon the addition of 255 nM prostaglandin cyclic endoperoxide H2 to human platelet particles in the muscle bath. Using the isometric contaction produced by 40 mM K+ in isotonic saline as the reference contraction, bovine middle cerebral artery strips contracted to 153 +/- 14% of the reference response while bovine coronary and porcine coronary, renal and common carotid strips contracted to 47 +/- 3, 26 +/- 5, 43 +/- 2 and 2 +/- 1% of reference, respectively. The cerebral artery response to the TxA2 generating system was as great as the maximum response to prostaglandin F2alpha and two times the maximum response to 5-hydroxytryptamine. Because TxA2 is formed by brain tissue and released from aggregating platelets, it may be important in the pathogenesis of spasm associated with injured brain tissue or pathologic changes leading to platelet aggregation.

摘要

不稳定的花生四烯酸代谢产物血栓素A2(TxA2)对动脉平滑肌条的收缩作用进行了研究。在肌槽中,向人血小板颗粒添加255 nM前列腺素环内过氧化物H2后可生成TxA2。以等渗盐水中40 mM K+产生的等长收缩作为对照收缩,牛大脑中动脉条收缩至对照反应的153±14%,而牛冠状动脉、猪冠状动脉、肾动脉和颈总动脉条分别收缩至对照的47±3%、26±5%、43±2%和2±1%。大脑动脉对TxA2生成系统的反应与对前列腺素F2α的最大反应一样大,是对5-羟色胺最大反应的两倍。由于TxA2由脑组织形成并从聚集的血小板中释放,它在与受伤脑组织相关的痉挛或导致血小板聚集的病理变化的发病机制中可能起重要作用。

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