Carrick J B, Morris D D, Moore J N
Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens 30602.
Equine Vet J. 1993 Mar;25(2):152-7. doi: 10.1111/j.2042-3306.1993.tb02927.x.
Platelet-activating factor (PAF) is an important mediator of endotoxaemia and various PAF receptor antagonists prevent many of the adverse effects of experimental endotoxaemia in laboratory animals. In this study a specific PAF receptor antagonist was used to investigate the role of PAF in equine endotoxaemia. At an interval of not greater than 10 days, 6 horses were each challenged with endotoxin and endotoxin with concurrent administration of SRI 63-441, a PAF receptor antagonist. The order of the treatments was randomised. Clinical signs, serum biochemical and coagulation profiles, and platelet aggregation in vitro were monitored in all horses for 24 h after treatment. Challenge with endotoxin increased maximal platelet aggregation induced by PAF. This response was blocked by administration of SRI 63-441 concurrently with endotoxin. No changes in percentage maximal platelet aggregation to ADP or collagen were noted after administration of endotoxin. The PAF receptor antagonist delayed the onset of fever, tachycardia, leucopenia and lactic acidaemia. Lack of more profound beneficial alterations of the horses' responses to endotoxin may have been due to the low dose of endotoxin administered in this model or to only partial effectiveness of SRI 63-441 in blocking the effects of endotoxin-induced PAF.
血小板活化因子（PAF）是内毒素血症的重要介质，多种PAF受体拮抗剂可预防实验性内毒素血症在实验动物中产生的许多不良反应。在本研究中，使用一种特异性PAF受体拮抗剂来研究PAF在马内毒素血症中的作用。每隔不超过10天，对6匹马分别进行内毒素攻击，以及内毒素与PAF受体拮抗剂SRI 63 - 441联合给药。治疗顺序是随机的。在所有马匹治疗后24小时监测其临床症状、血清生化和凝血指标以及体外血小板聚集情况。内毒素攻击可增加PAF诱导的最大血小板聚集。同时给予SRI 63 - 441与内毒素可阻断这一反应。给予内毒素后，对ADP或胶原的最大血小板聚集百分比未出现变化。PAF受体拮抗剂延迟了发热、心动过速、白细胞减少和乳酸性酸中毒的发作。马匹对内毒素反应缺乏更显著的有益改变可能是由于该模型中给予的内毒素剂量较低，或者是由于SRI 63 - 441在阻断内毒素诱导的PAF作用方面仅部分有效。
