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磷酸己糖旁路在实验性诱导心肌肥大中的意义。

Significance of the hexose monophosphate shunt in experimentally induced cardiac hypertrophy.

作者信息

Zimmer H G, Ibel H, Gerlach E

出版信息

Basic Res Cardiol. 1980 Jan-Feb;75(1):207-13. doi: 10.1007/BF02001415.

Abstract
  1. In three models of cardiac hypertrophy in rats (aortic constriction, application of a single dose of isoproterenol and daily injections of triiodothyronine) the biosynthesis of myocardial adenine nucleotides was enhanced. 2. In hypertrophying hearts due to aortic constriction and isoproterenol application, the activity of glucose-6-phosphate dehydrogenase and the available pool of 5-phosphoribosyl-1-pyrophosphate were increased indicating a stimulation of the hexose monophosphate shunt. In triiodothyronine-treated animals only the cardiac pool of 5-phosphoribosyl-1-pyrophosphate turned out to be elevated. 3. In all three models of cardiac hypertrophy, the enhancement of myocardial adenine nucleotide biosynthesis was exaggerated by ribose. It thus appears that the 5-phosphoribosyl-1-pyrophosphate pool is the limiting factor for the increase of adenine nucleotide biosynthesis under these conditions. 4. Long-term i.v. infusion of ribose (200 mg/kg/h) in isoproterenol-treated rats prevented the decrease of the cardiac ATP concentration induced by isoproterenol. However, the isoproterenol-induced stimulation of total cardiac protein synthesis was not altered, suggesting that the ATP decline may not be the trigger for stimulating protein synthesis in this model of myocardial hypertrophy.
摘要
  1. 在大鼠心脏肥大的三种模型(主动脉缩窄、单次注射异丙肾上腺素和每日注射三碘甲状腺原氨酸)中,心肌腺嘌呤核苷酸的生物合成增强。2. 在因主动脉缩窄和应用异丙肾上腺素导致的心脏肥大中,葡萄糖-6-磷酸脱氢酶的活性和5-磷酸核糖-1-焦磷酸的可利用池增加,表明磷酸戊糖途径受到刺激。在三碘甲状腺原氨酸处理的动物中,仅5-磷酸核糖-1-焦磷酸的心脏池升高。3. 在所有三种心脏肥大模型中,核糖可加剧心肌腺嘌呤核苷酸生物合成的增强。因此,在这些条件下,5-磷酸核糖-1-焦磷酸池似乎是腺嘌呤核苷酸生物合成增加的限制因素。4. 对异丙肾上腺素处理的大鼠长期静脉输注核糖(200mg/kg/h)可防止异丙肾上腺素诱导的心脏ATP浓度降低。然而,异丙肾上腺素诱导的心脏总蛋白合成刺激并未改变,这表明在这种心肌肥大模型中,ATP下降可能不是刺激蛋白合成的触发因素。

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