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[不同遗传品系大鼠热休克时的内皮细胞过度激活]

[Endothelial hyperactivation in heat shock in rats of different genetic strains].

作者信息

Manukhina E B, Azamatov Z Z, Malysheva E V, Malyshev I Iu

出版信息

Fiziol Zh Im I M Sechenova. 1996 May-Jun;82(5-6):59-65.

PMID:9053073
Abstract

Heat shock was found to induce a drop in the AP due to the endothelium-dependent relaxation of the vessels and potentiation of the endothelium suppression of the vasoconstrictor responses. The responses were more obvious in the August rats as compared with the Wistar line. No lines or rats revealed any changes in the sensitivity of adrenoceptors to the agonist which suggests a leading role of the nitrogen oxide hyperproduction in these effects of the heat shock. The data obtained show that inherent endothelial-dependent vascular responses to heat shock may play a role in resistance against the shock in rats of different genetic lines.

摘要

研究发现,热休克可导致动脉压下降,这是由于血管的内皮依赖性舒张以及内皮对血管收缩反应的抑制作用增强所致。与Wistar品系相比,这些反应在八月龄大鼠中更为明显。没有品系或大鼠显示出肾上腺素能受体对激动剂的敏感性有任何变化,这表明一氧化氮过度产生在热休克的这些效应中起主导作用。所获得的数据表明,热休克固有的内皮依赖性血管反应可能在不同遗传品系大鼠对休克的抵抗中发挥作用。

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