Kecskeméti V, Balogh I
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.
Exp Toxicol Pathol. 1995 Dec;47(6):463-70. doi: 10.1016/S0940-2993(11)80329-5.
Platelet-activating factor-induced ultrastructural changes of myocardium were examined in isolated perfused guinea pig heart. The platelet-activating factor (10(-9)-10(7) M) caused the following electron microscopic changes: a) dilated capillaries filled with platelets and aggregated platelets. The endothelial cells adjoining the platelets remained uninjured but pericapillary oedema was observed. b) in the myocardium intracellular oedema, myofibrillar alterations, decrease of matrix density and rupture of crest in mitochondria can be seen. c) Ca2+ deposits in the cytoplasm increased and appeared in mitochondria, too. d) the intramitochondrially localised cytochromoxydase and succinic dehydrogenase activities were decreased. e) using lanthanum tracer permeability alterations were observed. Pretreatment with BN 52021 (10(6) M) completely prevented the morphological effects of the platelet-activating factor. From these results we conclude that the platelet-activating factor-induced vascular and ischemic like cellular damage appear to play an important role in the pathophysiology of myocardial ischemia.
在离体灌注豚鼠心脏中研究了血小板活化因子诱导的心肌超微结构变化。血小板活化因子（10⁻⁹ - 10⁻⁷ M）引起了以下电子显微镜下的变化：a）毛细血管扩张，充满血小板和聚集的血小板。与血小板相邻的内皮细胞未受损伤，但观察到毛细血管周围水肿。b）在心肌中可见细胞内水肿、肌原纤维改变、基质密度降低和线粒体嵴断裂。c）细胞质中的钙沉积增加，线粒体中也出现钙沉积。d）线粒体中定位的细胞色素氧化酶和琥珀酸脱氢酶活性降低。e）使用镧示踪剂观察到通透性改变。用BN 52021（10⁻⁶ M）预处理可完全预防血小板活化因子的形态学效应。从这些结果我们得出结论，血小板活化因子诱导的血管和缺血样细胞损伤似乎在心肌缺血的病理生理学中起重要作用。
