Welles E G, Boudreaux M K, Tyler J W
Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849-5519.
Am J Vet Res. 1993 Aug;54(8):1235-43.
Cats with cardiomyopathy, especially dilated cardiomyopathy associated with taurine deficiency, often develop systemic thrombi. To investigate the relation of taurine deficiency to formation and persistence of thrombi, cats were made taurine-deficient by consumption of a casein-based taurine-deficient diet, then were evaluated for anticoagulant and profibrinolytic activities and platelet function. The cats served as their own controls in the taurine-replete state; then, values were compared for the taurine-deficient state. Plasma (P < 0.01), blood (P < 0.05), and platelet (P < 0.05) taurine concentrations were decreased markedly after cats consumed the taurine-deficient diet for 6 weeks, compared with baseline concentrations before diet. Compared with the taurine-replete state, taurine deficiency induced significantly (P < 0.05) increased mean antithrombin III activity, no significant change in plasminogen and fibrinolytic activities, and similar clot retraction/lysis test results. Decreased (P < 0.01) adenosine diphosphate (ADP)-induced platelet aggregation and [14C]serotonin release, and slightly increased (P < 0.05) collagen-induced platelet [14C]serotonin release, but unchanged collagen-induced platelet aggregation were observed in taurine-deficient cats, compared with taurine-replete cats. Changes in antithrombin III activity most likely reflected hepatocellular acute-phase reaction, which indicates that taurine deficiency may induce a stress-responsive state. Results of platelet function testing indicate that taurine may modulate platelet responsiveness to physiologic agonists, but not in consistent manner. That platelets from the taurine-deficient cats had decreased responsiveness to ADP, but increased responsiveness to collagen is surprising, because irreversible aggregation is mediated by release of granule-associated ADP after sufficient initial stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
患有心肌病的猫，尤其是与牛磺酸缺乏相关的扩张型心肌病猫，常常会形成全身性血栓。为了研究牛磺酸缺乏与血栓形成和持续存在之间的关系，通过给猫喂食基于酪蛋白的牛磺酸缺乏饮食使其缺乏牛磺酸，然后评估其抗凝和纤溶活性以及血小板功能。这些猫在牛磺酸充足状态下作为自身对照；然后，比较牛磺酸缺乏状态下的各项数值。与喂食前的基线浓度相比，猫食用牛磺酸缺乏饮食6周后，血浆（P < 0.01）、血液（P < 0.05）和血小板（P < 0.05）中的牛磺酸浓度显著降低。与牛磺酸充足状态相比，牛磺酸缺乏显著（P < 0.05）增加了抗凝血酶III活性的平均值，纤溶酶原和纤溶活性无显著变化，凝血块回缩/溶解试验结果相似。与牛磺酸充足的猫相比，牛磺酸缺乏的猫中观察到二磷酸腺苷（ADP）诱导的血小板聚集和[14C]5-羟色胺释放减少（P < 0.01），胶原诱导的血小板[14C]5-羟色胺释放略有增加（P < 0.05），但胶原诱导的血小板聚集未改变。抗凝血酶III活性的变化很可能反映了肝细胞的急性期反应，这表明牛磺酸缺乏可能诱导一种应激反应状态。血小板功能测试结果表明，牛磺酸可能调节血小板对生理激动剂的反应性，但方式并不一致。牛磺酸缺乏的猫的血小板对ADP的反应性降低，但对胶原的反应性增加，这很令人惊讶，因为不可逆聚集是由足够的初始刺激后颗粒相关ADP的释放介导的。（摘要截短于250字）
