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大鼠肾上腺素诱导肺水肿的研究。II. 血流动力学变化。

Studies on epinephrine-induced lung edema in the rat. II. Hemodynamic changes.

作者信息

Guarini S, Baggio G, Ferrari W

出版信息

Arch Int Pharmacodyn Ther. 1986 May;281(1):100-9.

PMID:3753094
Abstract

In order to elucidate the pathogenesis of epinephrine (E)-induced lung edema (LE) as well as the mechanism of protection afforded by alpha-adrenoceptor blockade in urethane-anesthetized and bivagotomized rats, we investigated the influence of phentolamine (Phe) and prazosin (Praz) on arterial hypertension and LE provoked by continuous intravenous infusion of E and on blood pressure changes in left (LHV) and right (RHV) heart ventricles caused by a bolus injection of E at a LE-producing dose (1800 nmol/kg). Our results show that neither LE nor death are related to E-induced hypertension and also that LE-induction is accompanied by significant increases in LHV (telediastolic and systolic) as well as in RHV (systolic) pressures, of which the LHV telediastolic and the RHV systolic pressure increases are prevented by Phe and Praz at a dose capable of counteracting E-induced LE. The significance of this finding is briefly discussed.

摘要

为了阐明肾上腺素(E)诱发肺水肿(LE)的发病机制以及α-肾上腺素受体阻断在氨基甲酸乙酯麻醉和双侧迷走神经切断大鼠中所提供的保护机制,我们研究了酚妥拉明(Phe)和哌唑嗪(Praz)对持续静脉输注E所诱发的动脉高血压和LE的影响,以及在产生LE的剂量(1800 nmol/kg)下静脉推注E引起的左心室(LHV)和右心室(RHV)血压变化的影响。我们的结果表明,LE和死亡均与E诱发的高血压无关,并且LE的诱导伴随着LHV(舒张末期和收缩期)以及RHV(收缩期)压力的显著升高,其中LHV舒张末期和RHV收缩期压力的升高可被能够抵消E诱发LE的剂量的Phe和Praz所阻止。本文简要讨论了这一发现的意义。

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