Naumov O G, Klebanov G I, Zaĭtsev K T, Banin V V, Borisova L V, Ribarov S, Peneva V, Vladimirov Iu A
Department of Physics, Sofia, Bulgaria.
Biull Eksp Biol Med. 1991 Oct;112(10):371-4.
It is well known that isoprenaline (1-3-4-dihydroxy-phenyl-isopropyl-aminoethanol) (IP) induce necrosis in myocardium of laboratory animals, which is similar to pathomorphological development of clinical myocardial infarction. This process is accompanied by peripheral blood leukocytes. The IP-inductor effects on arachidonate-dependent aggregation and endothelial adhesion of peripheral blood neutrophils (PN) were studied in this paper. The enhancement of PN aggregational properties within 2-4 hours after intravenous IP-injection to rats was demonstrated. Using the method of vital microscopy it was shown that intravenous IP-injection to rats or IP-application on rat mesentery lead to an increase of leukocyte's marginal pool on the endothelium of mesenteric venules. However, it was noted that the change of cell functional properties is not due to the direct influence of IP on PN. The pathogenetic mechanisms of IP-induced cardiomyopathy in rats were discussed.
众所周知,异丙肾上腺素(1-3-4-二羟基苯异丙氨基乙醇)(IP)可诱导实验动物心肌坏死,这与临床心肌梗死的病理形态学发展相似。这一过程伴有外周血白细胞。本文研究了IP诱导剂对花生四烯酸依赖性外周血中性粒细胞(PN)聚集和内皮黏附的影响。静脉注射IP给大鼠后2-4小时内,PN聚集特性增强得到证实。采用活体显微镜检查法表明,静脉注射IP给大鼠或在大鼠肠系膜上应用IP会导致肠系膜小静脉内皮上白细胞边缘池增加。然而,值得注意的是,细胞功能特性的改变并非由于IP对PN的直接影响。文中讨论了IP诱导大鼠心肌病的发病机制。