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在大鼠中诱导热休克反应可调节随后进行高温治疗后的心率、肌酸激酶和蛋白质合成。

Induction of the heat shock response in rats modulates heart rate, creatine kinase and protein synthesis after a subsequent hyperthermic treatment.

作者信息

Currie R W, Ross B M, Davis T A

机构信息

Department of Anatomy, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

Cardiovasc Res. 1990 Feb;24(2):87-93. doi: 10.1093/cvr/24.2.87.

Abstract

STUDY OBJECTIVE - The aim of the study was to examine the effect of prior induction of the heat shock response on heat shock protein synthesis and physiological variables relevant to the shock response. DESIGN - Synthesis of heat shock protein (SP71, molecular mass 71,000) was induced in rats by 15 min hyperthermia (42 degrees C). Protein synthesis, heart rate, blood pressure and creatine kinase activity were determined in comparison with controls (no heat shock) and a group receiving two heat shock treatments 24 h apart (prior induction group). SUBJECTS - 24 male Sprague-Dawley rats (125-150 g) were used, divided into three groups: controls (n = 4), heat shock X 1 (HS, n = 11), heat shock X 2 (2 X HS, n = 9). Heat shock was induced under anaesthesia on a heating pad. MEASUREMENTS and RESULTS - Blood pressure and heart rate were measured at the beginning of the hyperthermia period, when body temperature first reached 42 degrees C (t = 0 min) and at the end of the hyperthermia treatment (t = 15 min). At t = 0 min systolic blood pressure and heart rate were increased compared to the control values in both HS and 2 X HS groups. At t = 15 min heart rate in the HS group was increased to 554 (SEM21) beats.min-1 v control 465(19) (p less than 0.05). In the 2 X HS group, heart rate of 494(14) beats.min-1 at t = 15 min was not significantly different from control. At t = 15 min, creatine kinase values in the hyperthermia treatment groups were not different from control. However at 2.5 h after hyperthermic treatment plasma creatine kinase was increased in the HS group to 481(83) mU.ml-1 (n = 6) v 223(20) in controls, but was not increased in the 2 X HS group [178(64), n = 4]. Rats were radiolabelled for 2 h with 1.0 mCi of [35S]-methionine 30 min after hyperthermic treatment in HS group and 30 min after the second hyperthermic treatment in 2 X HS group. Following the 2 X HS treatment, synthesis of SP71, though increased above control values, was lower than in the HS group. CONCLUSIONS - The reduction in heart rate, plasma creatine kinase and synthesis of SP71 following a second hyperthermic exposure could be caused by a protective influence of the first exposure.

摘要

研究目的——本研究旨在探讨预先诱导热休克反应对热休克蛋白合成以及与休克反应相关的生理变量的影响。

设计——通过15分钟的高温(42摄氏度)诱导大鼠体内热休克蛋白(SP71,分子量71,000)的合成。将蛋白质合成、心率、血压和肌酸激酶活性与对照组(未进行热休克)以及接受两次间隔24小时热休克处理的组(预先诱导组)进行比较。

研究对象——使用24只雄性Sprague-Dawley大鼠(125 - 150克),分为三组:对照组(n = 4)、热休克X1组(HS,n = 11)、热休克X2组(2XHS,n = 9)。在麻醉状态下于加热垫上诱导热休克。

测量与结果——在高温期开始时、体温首次达到42摄氏度时(t = 0分钟)以及高温处理结束时(t = 15分钟)测量血压和心率。在t = 0分钟时,HS组和2XHS组的收缩压和心率相较于对照组值均升高。在t = 15分钟时,HS组心率升高至554(标准误21)次/分钟,而对照组为465(19)次/分钟(p < 0.05)。在2XHS组,t = 15分钟时心率为494(14)次/分钟,与对照组无显著差异。在t = 15分钟时,高温处理组的肌酸激酶值与对照组无差异。然而,在高温处理后2.5小时,HS组血浆肌酸激酶升高至481(83)mU/ml(n = 6),而对照组为223(20),但2XHS组未升高[178(64),n = 4]。在HS组高温处理后30分钟以及2XHS组第二次高温处理后30分钟,用1.0毫居里的[35S]-甲硫氨酸对大鼠进行2小时的放射性标记。经过2XHS处理后,SP71的合成虽高于对照组值,但低于HS组。

结论——第二次高温暴露后心率、血浆肌酸激酶和SP71合成的降低可能是由首次暴露的保护作用引起的。

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