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Circulatory effects of renin-angiotensin system antagonists during halothane anaesthesia in hypertensive rats.

作者信息

Kaukinen S, Kataja J, Ylitalo P

出版信息

Acta Anaesthesiol Scand. 1983 Feb;27(1):81-6. doi: 10.1111/j.1399-6576.1983.tb01910.x.

Abstract

The circulatory effects of captopril, an angiotensin I-converting enzyme inhibitor, and saralasin, a competitive angiotensin II antagonist, were studied during halothane anaesthesia in spontaneously hypertensive (SH) rats. Captopril decreased blood pressure significantly in unanaesthetized rats. Pretreatment with indomethacin, a prostaglandin synthesis inhibitor, did not modify the antihypertensive action of captopril. During 1 MAC halothane anaesthesia, the mean arterial pressure (MAP) in unmedicated SH control rats was maintained at a relatively high level (16.2 +/- 0.7 kPa, mean +/- s.e. mean), while in captopril-treated rats MAP decreased to 8.8 +/- 1.1 kPa. Indomethacin somewhat inhibited MAP decrease in the captopril-medicated group. Saralasin infusion in halothane-anaesthetized rats decreased MAP in the same way as captopril alone. The tolerance to haemorrhagic shock was markedly impaired in rats receiving captopril or saralasin, compared to untreated controls. During halothane anaesthesia, the plasma renin activities in the captopril, captopril + indomethacin, and saralasin groups were significantly higher than in untreated animals. Plasma kininogen was unaffected by any of the medications. The results suggest that the renin-angiotensin system is important in maintaining blood pressure in halothane anaesthesia, and that the tolerance to haemorrhagic shock is particularly impaired by drugs inhibiting the renin-angiotensin system.

摘要

相似文献

1
Circulatory effects of renin-angiotensin system antagonists during halothane anaesthesia in hypertensive rats.
Acta Anaesthesiol Scand. 1983 Feb;27(1):81-6. doi: 10.1111/j.1399-6576.1983.tb01910.x.
7
Hypotensive action of captopril and saralasin in intact and anephric spontaneously hypertensive rats.
Hypertension. 1980 Mar-Apr;2(2):119-24. doi: 10.1161/01.hyp.2.2.119.

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