Comerota A J, Stewart G J, White J V
Am J Surg. 1985 Oct 8;150(4A):39-44.
The cause of postoperative DVT is considered to be changes in blood coagulation, stasis of blood within the veins, and injury to the vein wall. The coagulation changes have been investigated and documented and involve platelet activation, stimulation of the coagulation cascade, and blunting of endogenous fibrinolytic activity. Stasis has been objectively identified by retention of contrast material in soleal sinuses and marked changes in venous flow velocity in patients in the supine position and in those under general anesthesia. Vein wall injury is more controversial, but has been shown to be directly related to venodilation. Such dilation of veins occurs in response to operative trauma, hence venous endothelial damage most likely plays a part in the milieu responsible for postoperative DVT. The prophylaxis provided by the combination of dihydroergotamine and heparin appears to affect each of the three limbs of Virchow's triad. Heparin achieves its prophylactic benefit by activating antithrombin III. Activated antithrombin III affects numerous sites in the coagulation cascade. It has been shown that 1 micrograms of antithrombin III inhibits the formation of 1 unit of thrombin; however, in the presence of heparin, 1 micrograms of activated antithrombin III inhibits 750 units of thrombin. Dihydroergotamine increases venous smooth muscle tone without affecting arteriolar smooth muscle. Hence, it has the effect of preventing stasis without increasing blood pressure. It also affects the platelet membrane, prostaglandin synthesis, and blood distribution, although these findings need to be elucidated. The combination of dihydroergotamine and heparin seems to have a synergistic prophylactic effect in preventing postoperative DVT. Heparin modifies the coagulation changes, whereas dihydroergotamine minimizes stasis and potentially prevents the endothelial damage caused by excessive operative venodilation. Such a combination of effects can explain the synergistic prophylactic efficacy found when dihydroergotamine and heparin were employed in combination in the multicenter trial [42].
术后深静脉血栓形成的原因被认为是凝血功能改变、静脉内血液淤滞以及静脉壁损伤。凝血功能改变已得到研究和记录，涉及血小板活化、凝血级联反应的刺激以及内源性纤维蛋白溶解活性的减弱。通过造影剂在比目鱼肌窦内的滞留以及仰卧位患者和全身麻醉患者静脉血流速度的显著变化，已客观证实了血液淤滞。静脉壁损伤存在更多争议，但已表明其与静脉扩张直接相关。这种静脉扩张是对手术创伤的反应，因此静脉内皮损伤很可能在术后深静脉血栓形成的发病机制中起作用。双氢麦角胺与肝素联合使用提供的预防措施似乎对维勒布兰德三联征的三个环节均有影响。肝素通过激活抗凝血酶III发挥预防作用。活化的抗凝血酶III影响凝血级联反应的多个位点。已表明1微克抗凝血酶III可抑制1单位凝血酶的形成；然而，在肝素存在的情况下，1微克活化的抗凝血酶III可抑制750单位凝血酶。双氢麦角胺可增加静脉平滑肌张力，而不影响小动脉平滑肌。因此，它具有预防血液淤滞而不升高血压的作用。它还影响血小板膜、前列腺素合成和血液分布，尽管这些发现尚需阐明。双氢麦角胺与肝素联合使用似乎在预防术后深静脉血栓形成方面具有协同预防作用。肝素改变凝血功能变化，而双氢麦角胺可最大程度减少血液淤滞，并可能预防过度手术静脉扩张引起的内皮损伤。这种联合效应可以解释在多中心试验[42]中双氢麦角胺与肝素联合使用时发现的协同预防效果。
