Manjarrez-Gutiérrez Gabriel, Hernández-Chávez Victor, Neri-Gómez Teresa, Boyzo-Montes de Oca Alfonso, Mondragón-Herrera José Antonio, Hernández-Rodríguez Jorge
Unidad de Investigación Biomolecular del Hospital de Cardiología, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico DF, Mexico.
Departamento de Patología, Hospital de Cardiología, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico DF, Mexico.
Cir Cir. 2014 Jan-Feb;82(1):11-9.
The diabetic cardiomyopathy occurs in both type 1 and type 2 diabetes mellitus. Hyperglycemia and associated metabolic changes participate in the pathogenesis of this disease.
To characterizes various pathological changes occurring during the development of diabetic cardiomyopathy in rats.
Diabetic rats were used for streptozotocin administration. At 7, 14, 21 and 30 days after toxic administration, the heart was obtained and placed in a Hartman solution and 4% p-formaldehyde. Five-micrometer thick sections were stained with hematoxylin-eosin, Masson trichrome and immunocytochemistry using anti-β-tubulin antibody.
At 14 days after application of streptozotocin, dilated sinusoids with endothelial lining in the myocardium and collagen deposits in the cardiac interstitium and between the Purkinje fibers were observed. At 21 days there was a slight decrease of the arteriolar lumen due to hyperplasia of the medial layer. It is important to note that cardiac sinusoids as well as collagen deposits became more evident at 30 day of the study, as well as a major derangement of the microtubular system of the cardiomyocytes.
Cardiac sinusoids representing fetal vascular pattern and interstitial fibrosis in the myocardium and the microtubular derangement of cardiomyocytes support the fact that the pathophysiological mechanism of diabetic cardiomyopathy begins in the coronary microcirculation due to changes in cardiac metabolism, contributing to the development of myocardial dysfunction in diabetes.
1型和2型糖尿病均会发生糖尿病性心肌病。高血糖及相关代谢变化参与了该疾病的发病机制。
明确大鼠糖尿病性心肌病发展过程中出现的各种病理变化。
使用链脲佐菌素处理大鼠。在给药后7、14、21和30天,取出心脏,置于哈特曼溶液和4%多聚甲醛中。制作5微米厚的切片,用苏木精-伊红染色、马松三色染色,并使用抗β-微管蛋白抗体进行免疫细胞化学染色。
应用链脲佐菌素后14天,观察到心肌内有内衬内皮的扩张血窦,以及心脏间质和浦肯野纤维之间有胶原沉积。21天时,由于中层增生,小动脉管腔略有减小。需要注意的是,在研究的第30天,心脏血窦以及胶原沉积变得更加明显,同时心肌细胞微管系统出现严重紊乱。
代表胎儿血管模式的心脏血窦、心肌间质纤维化以及心肌细胞微管紊乱支持了这样一个事实,即糖尿病性心肌病的病理生理机制始于心脏代谢变化导致的冠状动脉微循环,进而促使糖尿病患者心肌功能障碍的发展。