Akiyama M, Takahashi K, Azuma K, Sasaki K, Mizuma K, Totsuka M, Hayasaka H
Jpn J Surg. 1984 Jan;14(1):85-93. doi: 10.1007/BF02469608.
We investigated intestinal blood circulation after re-opening of a fixed-time occlusion of the superior mesenteric artery (SMA) in rabbits. The SMA root was occluded for 60 minutes, after which blood pressure and SMA flow were monitored for one hundred minutes under the administration with fluid infusion of three anti-shock agents; dopamine, phenoxybenzamine and dexamethasone. The intestinal wall tissue circulation in parallel with SMA flow was also studied. Blood pressure and SMA flow decreased after release of the SMA occlusion (SMAO), as compared those during pre-occlusive time in the control group. Fluid infusion alone did not improve blood pressure and SMA flow. Pre-administration of dexamethasone with fluid infusion improved blood pressure, SMA flow and the survival rate. Phenoxybenzamine with fluid infusion improved SMA flow, despite the low blood pressure. Circulatory damage to the intestinal wall was more extensive than that to SMA flow. These findings suggest that the severity and mortality of SMAO shock was not caused by plasma loss but rather by toxic metabolites and endotoxin from the ischemic intestine.
我们研究了家兔肠系膜上动脉（SMA）定时闭塞再开放后的肠血液循环。将SMA根部闭塞60分钟，之后在输注三种抗休克药物（多巴胺、酚苄明和地塞米松）的情况下监测血压和SMA血流100分钟。同时还研究了与SMA血流平行的肠壁组织循环。与对照组闭塞前相比，SMA闭塞（SMAO）解除后血压和SMA血流下降。单纯输液并不能改善血压和SMA血流。输液前给予地塞米松可改善血压、SMA血流和存活率。尽管血压较低，但输液时给予酚苄明可改善SMA血流。肠壁的循环损伤比SMA血流的损伤更广泛。这些发现表明，SMAO休克的严重程度和死亡率不是由血浆丢失引起的，而是由缺血肠段产生的有毒代谢产物和内毒素所致。
