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目的：探讨眼镜蛇毒的心脏毒素对大鼠主动脉的毒性反应．方法：以内皮完整和去内皮后的主动脉环的收缩反应为检测指标．结果：心脏毒素（ＣＴＸ）１０μｍｏｌ·Ｌ－１致使去内皮后的血管环产生短暂舒张反应及紧接着的持续收缩反应．去内皮或加入一氧化氮（ＮＯ）合成酶抑制剂ＬＮＡＭＥ，虽能防止ＣＴＸ引起的舒张却不影响随后的收缩．ＣＴＸ本身虽会引起血管环的收缩，却又能量效性地抑制苯福林及高钾激素的收缩幅度，ＣＴＸ引起的收缩有强烈的外钙依赖性．钙浓度１ｍｍｏｌ·Ｌ－１产生最高效应然后随钙浓度增加而逐减，外钙浓度增至７ｍｍｏｌ·Ｌ－１或先加入钙拮抗剂则可完全抑制ＣＴＸ孕育后乙酰胆碱所引起的短暂舒张．虽有显著减少却能受高钙（５ｍｍｏｌ·Ｌ－１）的保护．结论：ＣＴＸ明显地影响血管收缩功能．首先产生内皮依赖性的短暂舒张反应，随后致使血管平滑肌收缩终致细胞坏死，并使其它激动剂引起的收缩幅度减少．这些现象均与钙协调有密切的关系
Objective: To investigate the toxicity of cobra venom toxin on rat aorta. Methods: The endothelium integrity and endothelium after the aortic ring contraction reaction as a detection index. Results: Cardiac toxin (CTX) 10 μmol·L-1 resulted in a transient vasorelaxation and subsequent sustained contractile response to the endothelial loop. Endothelium or add nitric oxide (NO) synthase inhibitor L NAME, although it can prevent CTX-induced relaxation without affecting the subsequent contraction. Although CTX itself causes contraction of the vascular rings, it can energetically inhibit the contraction of phenylephrine and high-potassium hormones, and CTX-induced contractions have a strong extracellular calcium-dependent behavior. Calcium concentration 1mmol·L-1 produce the highest effect and then decreased with increasing calcium concentration, external calcium concentration increased to 7mmol·L-1 or added calcium antagonist can completely inhibit CTX induced short-term diastolic acetylcholine. Although significantly reduced but can be high calcium (5mmol · L-1) protection. Conclusion: CTX significantly affects vasoconstrictive function. First, there is an endothelium-dependent transient relaxation that subsequently leads to necrosis of the vascular smooth muscle cells and a reduction in the amplitude of contraction induced by other agonists. These phenomena are closely related with the coordination of calcium