Feola M, Rovetto M, Soriano R, Cho S Y, Wiener L
J Thorac Cardiovasc Surg. 1976 Oct;72(4):631-43.
A possible protective effect of glucocorticoids on the ischemic myocardium was investigated in in situ dog hearts subjected to regional ischemia and in isolated rat hearts subjected to global ischemia. In the whole-animal preparation, the left anterior descending coronary artery (LAD) was occluded for 3 hours, or for 2 1/2 hours followed by 30 minutes of reperfusion. Dexamethasone phosphate was randomly administered (20 mg. per kilogram intravenously) after 15 minutes of ischemia. Its effects were studied on the following: (1) myocardial cell membrane integrity, using electron microscopic examination of tissue biopsies treated with colloidal lanthanum; (2) myocardial water content, measuring the wet/dry weight of myocardial tissue; (3) ischemic injury, by a count of fuchsinophilic cells at light microscopy. In isolated rat hearts, ischemia was produced by a 60 per cent reduction of coronary flow. Randomized hearts were perfused for 2 hours with dexamethasone, 15 mg. per milliliter in buffered salt solution. Study included determination of tissue water content and coronary vascular resistance. Lanthanum was confined to the extracellular spaces in normal dog myocardium, but it was found all intracellularly after 3 hours of ischemia or after reperfusion. This was associated with morphologic changes characteristic of irreversible cell injury. In the hearts treated with dexamethasone, lanthanum remained excluded from the cells, water content was less (p less than 0.005), and fuchsinophilia less severe (p less than 0.005). Likewise, water content was less (p less than 0.005) and the increase in coronary vascular resistance resulting from ischemia less severe (p less than 0.005) in the dexamethasone-treated isolated rat hearts. Thus dexamethasone administered in pharmacologic doses, early, appeared to stabilize the cell membrane, limit myocardial edema, and reduce the severity of injury, both during ischemia and upon reperfusion.
在遭受局部缺血的原位犬心脏以及遭受全心缺血的离体大鼠心脏中，研究了糖皮质激素对缺血心肌可能的保护作用。在整体动物实验中，左冠状动脉前降支（LAD）闭塞3小时，或闭塞2个半小时后再灌注30分钟。缺血15分钟后随机给予磷酸地塞米松（静脉注射，20毫克/千克）。研究其对以下方面的影响：（1）心肌细胞膜完整性，通过用胶体镧处理的组织活检进行电子显微镜检查；（2）心肌含水量，测量心肌组织的湿/干重；（3）缺血损伤，通过光学显微镜下对嗜品红细胞计数。在离体大鼠心脏中，通过将冠状动脉流量减少60%产生缺血。随机选取的心脏用含地塞米松15毫克/毫升的缓冲盐溶液灌注2小时。研究包括测定组织含水量和冠状血管阻力。在正常犬心肌中，镧局限于细胞外间隙，但在缺血3小时后或再灌注后发现其存在于所有细胞内。这与不可逆细胞损伤的形态学变化相关。在用糖皮质激素处理的心脏中，镧仍被排除在细胞外，含水量较低（p<0.005），嗜品红现象较轻（p<0.005）。同样，在用糖皮质激素处理的离体大鼠心脏中，含水量较低（p<0.005），缺血导致的冠状血管阻力增加较轻（p<0.005）。因此，早期给予药理剂量的地塞米松似乎能稳定细胞膜、限制心肌水肿并减轻缺血期间和再灌注时的损伤严重程度。
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