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异丙肾上腺素诱导心肌梗死合并糖尿病后,动脉粥样硬化大鼠与非动脉粥样硬化大鼠的代谢和组织病理学变化

Metabolic and histopathologic changes in arteriosclerotic versus nonarteriosclerotic rats following isoproterenol-induced myocardial infarction with superimposed diabetes.

作者信息

Wexler B C

出版信息

Metabolism. 1975 Dec;24(12):1321-37. doi: 10.1016/0026-0495(75)90049-9.

Abstract

Male and female, arteriosclerotic and nonarteriosclerotic rats were subjected to acute myocardial infarction by two, subcutaneous injections (spaced 24 hr apart) of isoproterenol. During the immediate postinfarct repair phase all of the experimental animals were made severely diabetic with alloxan. Two weeks later the animals were sacrificed and their blood and pertinent organs analyzed for biochemical and pathologic changes. Females survived the myocardial infarct with superimposed diabetes in significantly greater than males. In addition to marked loss in body weight all of the experimental animals developed marked adrenal hypertrophy and thymus gland involution, cardiac hypertrophy, and unusual increase in ovarian or testicular size and weight. The combined conditions of myocardial infarction + diabetes led to substantial increases in serum creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase (SGOT) whereas the enzymes glutamic pyruvic transaminase (SGPT) and lactic dehydrogenase (LDH) were reduced. Although serum triglyceride levels were greatly elevated, total cholesterol and free fatty acids were reduced. All of the animals were severely hyperglycemic and had greatly increased B.U.N. levels. Diabetes caused hypercalcemia but diabetes + myocardial infarction was associated with a definite reduction of this hypercalcemia. Despite marked adrenal hypertrophy, circulating Cmpd. B levels were subnormal. The diabetic condition and its attendant hyperlipidemia did not alter the morphologic nature of the arterial lesions in the breeder rats but the diabetes did cause definite impairment of the usual myocardial repair process observed in these rats with a particularly high incidence of left ventricular aneurysms in males.

摘要

对雄性和雌性、动脉粥样硬化和非动脉粥样硬化大鼠,通过皮下注射两次异丙肾上腺素(间隔24小时)使其发生急性心肌梗死。在梗死即刻修复期,所有实验动物均用四氧嘧啶诱导成严重糖尿病。两周后处死动物,分析其血液和相关器官的生化及病理变化。雌性在叠加糖尿病的情况下,心肌梗死后的存活率显著高于雄性。除体重明显减轻外,所有实验动物均出现明显的肾上腺肥大和胸腺萎缩、心脏肥大,以及卵巢或睾丸大小和重量异常增加。心肌梗死 + 糖尿病的联合情况导致血清肌酸磷酸激酶(CPK)和谷草转氨酶(SGOT)大幅升高,而谷丙转氨酶(SGPT)和乳酸脱氢酶(LDH)降低。尽管血清甘油三酯水平大幅升高,但总胆固醇和游离脂肪酸降低。所有动物均严重高血糖,血尿素氮(BUN)水平大幅升高。糖尿病导致高钙血症,但糖尿病 + 心肌梗死与这种高钙血症的明显降低有关。尽管肾上腺明显肥大,但循环中化合物B水平低于正常。糖尿病状态及其伴随的高脂血症并未改变繁殖大鼠动脉病变的形态学性质,但糖尿病确实导致这些大鼠中常见的心肌修复过程明显受损,雄性大鼠左心室动脉瘤的发生率特别高。

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