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心肌缺血的早期病理过程与炎症有关,包括在缺血区释放激肽与前列腺素、白细胞浸润及血小板集聚,同时增加心肌溶酶体水解酶的释放。糖皮质激素可阻止急性梗塞的扩展,但非固醇类抗炎剂尚未证实有明显抗梗塞作用。消炎痛、抗炎酸与阿斯匹林能有效抑制心脏前列腺素的释放,但增加动脉压,故增加心肌需氧量,且不能在心肌缺血时明显稳定溶酶体膜。Ibuprofen是一非固醇类抗炎剂,可抑制前列腺素释放和稳定溶酶体膜,而无升压作用。本文旨在估价Ibuprofen对猫急性心肌缺血时缺血性损伤早期(初5小时)的作用,以及有关的生物学作用,包括溶酶体稳定、心肌的收缩能性及血管作用。
The early pathological process of myocardial ischemia is associated with inflammation, including the release of kinins and prostaglandins, leukocyte infiltration and platelet aggregation in the ischemic area, as well as increased release of cardiac lysosomal hydrolase. Glucocorticoids block the expansion of acute infarcts, but non-steroidal anti-inflammatory agents have not demonstrated significant anti-infarct effects. Indomethacin, anti-inflammatory acid and aspirin can effectively inhibit the release of prostaglandins in the heart, but increase arterial pressure, it increases myocardial oxygen demand, and can not be significantly stable lysosomal membrane in myocardial ischemia. Ibuprofen is a non-steroidal anti-inflammatory agent that inhibits prostaglandin release and stabilizes lysosomal membranes without boosting. This article aims to evaluate the role of Ibuprofen in the early (first 5 hours) ischemic injury of acute myocardial ischemia in cats, as well as related biological actions including lysosomal stabilization, myocardial contractility and vascular effects.