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[奎纳克林通过稳定膜磷脂代谢和β-肾上腺素能受体对热损伤发展的预防作用]

[Preventive effect of quinacrine on the development of heat injury by stabilizing membrane phospholipids metabolism and beta-adrenoceptor].

作者信息

Xing C, Lu B Z, Wang L M, Shan J R, Liu Y X

机构信息

Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing.

出版信息

Sheng Li Xue Bao. 1995 Feb;47(1):11-8.

PMID:7784893
Abstract

Previous studies have demonstrated that the activation of phospholipase A2 (PLA2) during heat stress would caused disorder of membrane phospholipids metabolism, accompanied by a decrease in phosphatidylcholine and phosphatidyl-serine and an increase in arachidonic acid. In heat stressed rats, a down-regulation of beta-adrenergic receptor in lung tissue was observed due to activation of PLA2. In the present work, it was demonstrated that pretreatment of rats with PLA2 inhibitor, quinacrine (20 mg/kg, I.P.), 1 h before heat stress could block these membrane lipid alterations, and the tolerance of rats to heat exposure was enhanced. The effect of quinacrine on the thermotolerance of marching soldiers with 15 kg of load under hot environment was also investigated. The results indicated that in the soldiers taken orally 200 mg quinacrine 1 h before marching, their heart rate, body temperature, accumulation of blood lactic acid and the changes of index of heart function were significantly improved as compared to the control group at the end of 3 h marching. According to these data, it can be concluded that quinacrine is a useful drug to prevent derangement of beta-adrenoceptor and membrane phospholipids metabolism in the development of heat stress. So as to prevent heat injury, and to improve tolerance to heat stress.

摘要

先前的研究表明,热应激期间磷脂酶A2(PLA2)的激活会导致膜磷脂代谢紊乱,伴随着磷脂酰胆碱和磷脂酰丝氨酸减少以及花生四烯酸增加。在热应激大鼠中,由于PLA2的激活,观察到肺组织中β-肾上腺素能受体下调。在本研究中,结果表明,在热应激前1小时用PLA2抑制剂喹吖因(20mg/kg,腹腔注射)预处理大鼠,可以阻止这些膜脂质改变,并增强大鼠对热暴露的耐受性。还研究了喹吖因对负重15kg的行军士兵在炎热环境下热耐受性的影响。结果表明,在行军前1小时口服200mg喹吖因的士兵中,与对照组相比,在行军3小时结束时,他们的心率、体温、血乳酸积累以及心功能指标的变化均有显著改善。根据这些数据,可以得出结论,喹吖因是一种有用的药物,可防止热应激发生时β-肾上腺素能受体和膜磷脂代谢紊乱。从而预防热损伤,并提高对热应激的耐受性。

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