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去氨加压素是从兔和大鼠分离出的主动脉和肺动脉的强效血管舒张剂。

Desmopressin is a potent vasorelaxant of aorta and pulmonary artery isolated from rabbit and rat.

作者信息

Johns R A

机构信息

Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908.

出版信息

Anesthesiology. 1990 May;72(5):858-64. doi: 10.1097/00000542-199005000-00016.

Abstract

Hypotension related to the intraoperative use of desmopressin acetate to improve platelet function following cardiopulmonary bypass has recently been reported. To investigate the direct vascular actions of this drug as a potential mechanism of its induced hypotension, cumulative, dose-dependent (3.7 X 10(-10) to 1.2 X 10(-7) M) effects of desmopressin were studied in isolated phenylephrine precontracted rings of rat and rabbit thoracic aorta and rabbit pulmonary artery. Desmopressin was a potent vasodilator of all vessel types studied with significant (P less than 0.05) vasodilation beginning at 7.5 X 10(-9) M. Vascular relaxation of all vessels was greater when the vascular endothelium was intact (P less than 0.05). Indomethacin potentiated (P less than 0.05) vascular relaxation in rat and rabbit aortic rings and partially inhibited (P less than 0.05) relaxation in rabbit pulmonary artery rings. Selective antagonists of vasopressin V1 (d(CH2)5-Tyr(Me)AVP, 1 X 10(-6) M) and V2 (d(CH2)5[D-Ile2,Ala-NH2(9)] AVP, 1 X 10(-6) M) receptors and of histamine H1 (diphenhydramine, 1 X 10(-5) M) and H2 (cimetidine 1 X 10(-5) M) receptors had no effect on desmopressin-induced relaxation of rat aortic rings. Chlorobutanol, the diluent in which desmopressin is supplied, was devoid of vascular effects. To study the effects of desmopressin on vascular cyclic GMP and cyclic AMP concentrations, a cultured bovine aortic smooth muscle--rat vascular smooth muscle coculture model was employed. Desmopressin (1 X 10(-7) and 1 X 10(-8) M) did not significantly alter control values of either cyclic nucleotide.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

最近有报道称,术中使用醋酸去氨加压素改善体外循环后的血小板功能会导致低血压。为了研究这种药物直接的血管作用,将其作为诱导低血压的潜在机制,我们在大鼠和兔胸主动脉以及兔肺动脉的苯肾上腺素预收缩离体血管环中,研究了去氨加压素累积的、剂量依赖性(3.7×10⁻¹⁰至1.2×10⁻⁷M)效应。去氨加压素对所有研究的血管类型都是一种有效的血管扩张剂,从7.5×10⁻⁹M开始出现显著(P<0.05)的血管扩张。当血管内皮完整时,所有血管的血管舒张作用更强(P<0.05)。吲哚美辛增强了(P<0.05)大鼠和兔主动脉环的血管舒张,并部分抑制了(P<0.05)兔肺动脉环的舒张。血管加压素V1(d(CH₂)₅-Tyr(Me)AVP,1×10⁻⁶M)和V2(d(CH₂)₅[D-Ile₂,Ala-NH₂(9)] AVP,1×10⁻⁶M)受体以及组胺H1(苯海拉明,1×10⁻⁵M)和H2(西咪替丁1×10⁻⁵M)受体的选择性拮抗剂对去氨加压素诱导的大鼠主动脉环舒张没有影响。去氨加压素的稀释剂氯丁醇没有血管效应。为了研究去氨加压素对血管环磷酸鸟苷和环磷酸腺苷浓度的影响,采用了培养的牛主动脉平滑肌 - 大鼠血管平滑肌共培养模型。去氨加压素(1×10⁻⁷和1×10⁻⁸M)没有显著改变两种环核苷酸的对照值。(摘要截断于250字)

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