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Effects of a novel Mac-1 inhibitor, NPC 15669, on hemostatic parameters during preconditioned myocardial infarction

机译：新型Mac-1抑制剂NPC 15669对预适应性心肌梗死期间止血参数的影响

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摘要

NPC 15669, a member of the leumedins family, inhibits leukocyte adhesion to the endothelium by blockage of upregulation of a member of #beta#2 integrin family Mac-1 (CD11b/CD18). Inhibition of neutrophil-endothelial interactions may alter the course of myocardial reperfusion injury. However, the effects of NPC 15669 supplementation on the hemostatic profile during ischemia-reperfusion are unknown. The aim of the present study was to define changes in the certain hemostatic factors in the natural course of preconditioned myocardial infarction. Twelve consecutive Yorkshire swine underwent myocardial stunning (8 min. left anterior descending artery occlusion followed by 90 min. of reperfusion) and then preconditioned myocardial infarction (50 min. occlusion followed by 3 hours of reperfusion) experiments. NPC 15669 (10 mg/kg loading dose followed by constant infusion at 6 mg kg~(-1) h~(-1)) was administered in 6 animals; another 6 swine received saline and served as controls. Blood samples were obtained at baseline, twice during occlusion; and three times during reperfusion. The levels of antithrombin-III, Protein C, total Protein S, fibronectin, endothelin-1, as well as the stable metabolites of thromboxane (TxB_2) and prostacyclin (6-keto-PGF_(1a)), were determined. NPC 15669 treatment was associated with diminished endothelin-1, TxB_2 levels and increased fibronectin, 6-keto-PGF_(1a), Protein C and total Protein S concentrations in the setting of preconditioned myocardial infarction. There were no changes in the plasma concentrations of antithrombin-III in NPC 15669 group when compared with controls. The increase in Protein C, total Protein S, and 6-keto-PGF_(1a) (favoring vasodilatation), and decrease in endothelin-1 and TxB_2 levels (favoring vasodilatation), following NPC 15669 may explain the reduction in in farct size previously reported with this agent.
机译：NPC 15669是leumedins家族的成员，它通过阻止＃beta＃2整合素家族Mac-1（CD11b / CD18）成员的上调来抑制白细胞与内皮细胞的粘附。中性粒细胞-内皮相互作用的抑制可能会改变心肌再灌注损伤的过程。但是，尚不清楚在缺血再灌注期间补充NPC 15669对止血曲线的影响。本研究的目的是确定预处理心肌梗塞自然过程中某些止血因子的变化。连续对十二只约克郡猪进行心肌电击试验（左前降支动脉阻塞8分钟，然后进行90分钟再灌注），然后进行预处理的心肌梗死（阻塞50分钟，再进行3小时再灌注）实验。在6只动物中施用NPC 15669（10mg / kg负荷剂量，然后以6mg kg·（-1）h〜（-1）恒定输注）;另外6只猪接受了生理盐水作为对照。在基线时，在阻塞期间两次采集血样。再灌注过程中的三倍。测定了抗凝血酶III，蛋白C，总蛋白S，纤连蛋白，内皮素-1的水平，以及血栓烷（TxB_2）和前列环素的稳定代谢产物（6-keto-PGF_（1a））。 NPC 15669治疗与预处理心肌梗死时内皮素-1，TxB_2水平降低，纤连蛋白，6-酮-PGF_（1a），蛋白C和总蛋白S浓度升高有关。与对照组相比，NPC 15669组的抗凝血酶-III血浆浓度没有变化。 NPC 15669之后，蛋白C，总蛋白S和6-酮-PGF_（1a）的增加（有利于血管舒张），内皮素1和TxB_2的水平降低（有利于血管舒张）可能解释了先前的ct缩尺寸减小向该代理商报告。

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