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眼镜蛇毒液的体外促凝血和抗凝血特性。

In vitro procoagulant and anticoagulant properties of Naja naja naja venom.

作者信息

Sundell I B, Rånby M, Zuzel M, Robinson K A, Theakston R D G

机构信息

Department of Haematology, University of Liverpool, Liverpool L69 3GA, UK.

出版信息

Toxicon. 2003 Sep;42(3):239-47. doi: 10.1016/s0041-0101(03)00137-5.

Abstract

Bites by the Indian cobra (Naja naja naja) are common in India and Sri Lanka because of its close association with humans. Cobra venoms are complex and contain several toxic components, including neurotoxins that cause post-synaptic neuromuscular blockade with respiratory paralysis and even death. Bites may also cause extensive local necrosis by mechanisms not fully elucidated. Although no significant coagulopathy has been reported, N.n. naja venom can form blood clots in vitro by activating prothrombin as demonstrated by thrombin-specific chromogenic substrate. Scanning electron microscopy demonstrates that the clots formed by venom lack the thin fibrin strands of normal blood clots formed by thromboplastin or glass contact. Rheometry shows that clots formed by venom have abnormally low elasticity over an extended period and then, as the platelets contract, a retarded and more feeble increase in elasticity. Purified N.n. naja venom PLA2 inhibits platelet aggregation in PRP and explains the decreased clot retraction and retarded and compromised elasticity build up. The present study shows that the PLA2 and the prothrombin activator from N.n. naja venom have effects on haemostasis and blood clotting, although such effects are not observed systemically in envenomed humans.

摘要

由于印度眼镜蛇(Naja naja naja)与人类关系密切,其咬伤在印度和斯里兰卡很常见。眼镜蛇毒液成分复杂,含有多种有毒成分,包括神经毒素,可导致突触后神经肌肉阻滞,引发呼吸麻痹甚至死亡。咬伤还可能通过尚未完全阐明的机制导致广泛的局部坏死。虽然尚未有显著凝血功能障碍的报道,但如凝血酶特异性显色底物所示,N.n. naja毒液可通过激活凝血酶原在体外形成血凝块。扫描电子显微镜显示,毒液形成的血凝块缺乏由凝血活酶或玻璃接触形成的正常血凝块中的细纤维蛋白丝。流变学表明,毒液形成的血凝块在较长时间内弹性异常低,然后随着血小板收缩,弹性增加延迟且更为微弱。纯化的N.n. naja毒液磷脂酶A2抑制富血小板血浆中的血小板聚集,并解释了血凝块回缩减少以及弹性增加延迟和受损的原因。本研究表明,N.n. naja毒液中的磷脂酶A2和凝血酶原激活剂对止血和血液凝固有影响,尽管在被蛇毒中毒的人类中未观察到全身性此类影响。

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