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内毒素性休克的“血管痉挛”学说已渐为多数人所承认。应用多种血管扩张剂治疗感染中毒性休克的成功报告颇多;使用去甲肾上腺素等血管收缩剂则未能证实可使病死率下降。鉴于该症多见,特就“血管痉挛”学说及血管扩张剂疗法综述如下。实验性犬的内毒素性休克一、症象与病理:静注内毒素(1.75毫克/仟克)后,初因组织释放,肝静脉收缩、回心血量减少,血压迅即下降。数分钟内又迅回升至接近原水平,但1—2小时后又逐渐下降且不能自动回升。同时,血浆容量及酸碱度亦下降;仅补充血容量、纠正酸中毒及电解质紊乱,均不能阻止病情恶化。如无特殊处理,93—94％犬于10±5.5小时内死亡
Endotoxin shock “vasospasm” doctrine has gradually accepted by the majority. The successful application of a variety of vasodilators in the treatment of toxic shock infections has been reported. The use of norepinephrine and other vasoconstrictors failed to confirm that mortality could be reduced. In view of the disease more common, especially on the “vasospasm” theory and vasodilator therapy are summarized below. Experimental dogs with endotoxic shock A symptom and pathology: intravenous endotoxin (1.75 mg / kg), initially due to tissue release, hepatic vein contraction, back to less blood flow, blood pressure decreased rapidly. Within a few minutes and then rapidly rose back to the original level, but gradually decline after 1-2 hours and can not automatically pick up. At the same time, plasma volume and pH also dropped; only to add blood volume, correct acidosis and electrolyte disorders, can not stop the disease progression. Without special treatment, 93-94% of dogs died within 10 ± 5.5 hours