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组胺引起的胎儿肺血管舒张:对H1和H2刺激的反应。

Fetal pulmonary vasodilation by histamine: response to H1 and H2 stimulation.

作者信息

Truog R D, Accurso F J, Wilkening R B

机构信息

Department of Pediatrics, University of Colorado School of Medicine, Denver.

出版信息

Dev Pharmacol Ther. 1990;14(3):180-6.

PMID:1973090
Abstract

We measured pulmonary vasodilation induced by histamine, H1 and H2 antagonists, and H1 and H2 agonists in chronically prepared, normally oxygenated fetal sheep in order to study the response of H1 and H2 stimulation in late gestation. Blood flow was measured in the left pulmonary artery; pressures were measured in the main pulmonary artery and abdominal aorta. Histamine administered into the left pulmonary artery caused dose-dependent increases in left pulmonary blood flow without changes in either pulmonary arterial or aortic pressures. Cimetidine (H2 antagonist) and/or diphenhydramine (H1 antagonist) shifted the histamine dose-response curve to the right. 2-Pyridylethylamine (H1 agonist) and dimeprit (H2 agonist) caused vasodilation which was selectively blocked by its respective antagonist. We conclude that both H1 and H2 stimulation cause pulmonary vasodilation in the ovine fetus.

摘要

为了研究妊娠晚期H1和H2刺激的反应,我们在长期制备的、正常氧合的胎羊中测量了组胺、H1和H2拮抗剂以及H1和H2激动剂诱导的肺血管舒张。测量左肺动脉的血流量;测量主肺动脉和腹主动脉的压力。向左肺动脉注射组胺导致左肺血流量呈剂量依赖性增加,而肺动脉压和主动脉压均无变化。西咪替丁(H2拮抗剂)和/或苯海拉明(H1拮抗剂)使组胺剂量反应曲线右移。2-吡啶乙胺(H1激动剂)和二甲双胍(H2激动剂)引起血管舒张,其各自的拮抗剂可选择性阻断这种舒张。我们得出结论,H1和H2刺激均可导致绵羊胎儿肺血管舒张。

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