Department of Studies in Biochemistry, University of Mysore, Manasagangothri, Mysore 570006, Karnataka, India.
Biochemistry (Mosc). 2012 Jun;77(6):639-47. doi: 10.1134/S0006297912060119.
Unlike Naja naja, Bungarus caeruleus, Echis carinatus, and Daboia/Vipera russellii venoms, Ophiophagus hannah venom is medically ignored in the Indian subcontinent. Being the biggest poisonous snake, O. hannah has been presumed to inject several lethal doses of venom in a single bite. Lack of therapeutic antivenom to O. hannah bite in India makes any attempt to save the victim a difficult exercise. This study was initiated to compare O. hannah venom with the above said venoms for possible interference in hemostasis. Ophiophagus hannah venom was found to actively interfere in hemostatic stages such as fibrin clot formation, platelet activation/aggregation, and fibrin clot dissolution. It decreased partial thromboplastin time (aPTT), prothrombin time (PT), and thrombin clotting time (TCT). These activities are similar to that shown by E. carinatus and D. russellii venoms, and thus O. hannah venom was found to exert procoagulant activity through the common pathway of blood coagulation, while N. naja venom increased aPTT and TCT but not PT, and hence it was found to exert anticoagulant activity through the intrinsic pathway. Venoms of O. hannah, E. carinatus, and D. russellii lack plasminogen activation property as they do not hydrolyze azocasein, while they all show plasmin-like activity by degrading the fibrin clot. Although N. naja venom did not degrade azocasein, unlike other venoms, it showed feeble plasmin-like activity on fibrin clot. Venom of E. carinatus induced clotting of human platelet rich plasma (PRP), while the other three venoms interfered in agonist-induced platelet aggregation in PRP. Venom of O. hannah least inhibited the ADP induced platelet aggregation as compared to D. russellii and N. naja venoms. All these three venoms showed complete inhibition of epinephrine-induced aggregation at varied doses. However, O. hannah venom was unique in inhibiting thrombin induced aggregation.
与印度次大陆医学上忽略的 Naja naja、Bungarus caeruleus、Echis carinatus 和 Daboia/Vipera russellii 毒液不同，Ophiophagus hannah 毒液在印度次大陆被医学忽视。作为最大的毒蛇，O. hannah 被认为在单次咬伤中注入了几致死剂量的毒液。印度缺乏针对 O. hannah 咬伤的治疗性抗蛇毒血清，这使得任何拯救受害者的尝试都变得非常困难。本研究旨在比较 O. hannah 毒液与上述毒液，以研究其对止血的可能干扰。结果发现，Ophiophagus hannah 毒液可积极干扰纤维蛋白凝块形成、血小板激活/聚集和纤维蛋白凝块溶解等止血阶段。它降低部分凝血活酶时间（aPTT）、凝血酶原时间（PT）和凝血酶凝固时间（TCT）。这些活性与 E. carinatus 和 D. russellii 毒液相似，因此 O. hannah 毒液通过血液凝固的共同途径发挥促凝活性，而 N. naja 毒液增加 aPTT 和 TCT，但不增加 PT，因此被发现通过内在途径发挥抗凝活性。O. hannah、E. carinatus 和 D. russellii 的毒液缺乏纤溶酶原激活特性，因为它们不能水解偶氮酪蛋白，而它们都通过降解纤维蛋白凝块显示纤溶样活性。尽管 N. naja 毒液不水解偶氮酪蛋白，但与其他毒液不同，它对纤维蛋白凝块显示出微弱的纤溶样活性。E. carinatus 毒液诱导富含血小板的人血浆（PRP）凝固，而其他三种毒液干扰 PRP 中激动剂诱导的血小板聚集。与 D. russellii 和 N. naja 毒液相比，O. hannah 毒液对 ADP 诱导的血小板聚集的抑制作用最小。所有这三种毒液在不同剂量下均完全抑制肾上腺素诱导的聚集。然而，O. hannah 毒液在抑制凝血酶诱导的聚集方面是独特的。
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