Bombig Maria Teresa Nogueira, Ferreira Celso, Mora Osvaldo, Soares Joaquim Domingos, Póvoa Rui, Luna Filho Braulio, Simões Manoel De Jesus, Ferreira Filho Celso, Murad Neif, Costa Andrea
Setor de Cardiologia Experimental, Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil.
Jpn Heart J. 2003 Mar;44(2):243-55. doi: 10.1536/jhj.44.243.
The aim of this research was to evaluate the possible protective effect of pravastatin on ultrastructural alterations induced by cold stress in the myocardium of rats. Sixteen EPM-Wistar rats (Rattus norvegicus albinus) were used and distributed into four groups: 1) control; 2) pravastatin; 3) cold stress, and 4) pravastatin + cold stress. A daily oral dose of 10 mg/kg of weight of pravastatin was administered to each rat in groups 2 and 4 for 15 days. The stress induced by cold was obtained by keeping the group 3 and 4 rats in a freezer at -8 degrees C for 4 hours. The animals were killed and the heart and fragments of the left ventricles (LV) were removed and processed prior to conducting electron microscopic analysis. The ultrastructural alterations in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristalysis). The group subjected only to cold stress showed a significant increase in cristalysis (391.9) when compared with control group (42.0). In the cold stress and pravastatin pretreatment group, a statistically significant (96.9)*, P<0.05 cristalysis reduction was observed when compared with cold stress group. The mitochondrial cristalysis profiles of the control and pravastatin groups were 42.0 and 65.7, respectively. Cold stress induced a significant increase in the rate of mitochondrial cristalysis. In the group that received pravastatin and was exposed to cold stress, the drug protected the LV cardiomyocytes. This fact was confirmed by a reduction mitochondrial cristalysis pattern.
本研究的目的是评估普伐他汀对冷应激诱导的大鼠心肌超微结构改变可能具有的保护作用。选用16只EPM-Wistar大鼠（白化挪威大鼠），分为四组：1）对照组；2）普伐他汀组；3）冷应激组；4）普伐他汀+冷应激组。第2组和第4组的每只大鼠每天口服10 mg/kg体重的普伐他汀，持续15天。通过将第3组和第4组大鼠置于-8℃的冷冻箱中4小时来诱导冷应激。处死动物后，取出心脏和左心室（LV）片段，在进行电子显微镜分析之前进行处理。通过线粒体嵴模式（嵴溶解）的数量对心肌细胞的超微结构改变进行量化。仅接受冷应激的组与对照组（42.0）相比，嵴溶解显著增加（391.9）。在冷应激和普伐他汀预处理组中，与冷应激组相比，观察到嵴溶解有统计学意义的降低（96.9）*，P<0.05。对照组和普伐他汀组的线粒体嵴溶解情况分别为42.0和65.7。冷应激导致线粒体嵴溶解率显著增加。在接受普伐他汀并暴露于冷应激的组中，该药物对左心室心肌细胞起到了保护作用。线粒体嵴溶解模式的降低证实了这一事实。
