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大鼠体内一氧化氮合酶抑制:褪黑素可降低血压并减小缺血/再灌注诱导的梗死面积。

Nitric oxide synthase inhibition in rats: melatonin reduces blood pressure and ischemia/reperfusion-induced infarct size.

作者信息

Deniz Esra, Sahna Engin, Aksulu Hakki Engin

机构信息

Department of Pharmacology, Faculty of Medicine, Firat University, Elazig, Turkey.

出版信息

Scand Cardiovasc J. 2006 Aug;40(4):248-52. doi: 10.1080/14017430600833116.

Abstract

Reduction in the synthesis or bioavailability of nitric oxide plays a significant role in the development of myocardial infarction and hypertension. Numerous studies suggest that melatonin reduces blood pressure (BP) and ischemia/reperfusion (I/R) injury in rats. The effects of melatonin on the BP and I/R-induced cardiac infarct size in L-NAME-induced hypertensive rats remains unknown. This study was designed to investigate the effects of melatonin on BP and the I/R-induced infarct size in chronic nitric oxide synthase inhibited rats by L-NAME. Rats received L-NAME for 15 days to produce hypertension and melatonin the last 5 days before I/R studies. To produce cardiac damage, the left coronary artery was occluded for 30 min, followed by 120 min reperfusion. L-NAME led to a significant increase in BP. Melatonin administration (10 mg/kg) to L-NAME treated rats significantly reduced BP and infarct size. Also, melatonin attenuated the mortality resulting from I/R, but this was not statistically significant. Melatonin administration would seem important to reduce BP and infarct size resulting from I/R in L-NAME-induced hypertensive rats.

摘要

一氧化氮合成或生物利用度的降低在心肌梗死和高血压的发生发展中起重要作用。大量研究表明,褪黑素可降低大鼠血压(BP)和减轻缺血/再灌注(I/R)损伤。褪黑素对L-NAME诱导的高血压大鼠的血压及I/R诱导的心肌梗死面积的影响尚不清楚。本研究旨在探讨褪黑素对L-NAME抑制慢性一氧化氮合酶的大鼠的血压及I/R诱导的梗死面积的影响。大鼠接受L-NAME处理15天以产生高血压,并在I/R研究前最后5天给予褪黑素。为造成心脏损伤,将左冠状动脉闭塞30分钟,然后再灌注120分钟。L-NAME导致血压显著升高。给L-NAME处理的大鼠给予褪黑素(10mg/kg)可显著降低血压和梗死面积。此外,褪黑素减轻了I/R导致的死亡率,但这在统计学上不显著。给予褪黑素对于降低L-NAME诱导的高血压大鼠因I/R导致的血压和梗死面积似乎很重要。

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