Laboratories of The Mount Sinai Hospital, New York.
J Exp Med. 1939 Oct 31;70(5):453-60. doi: 10.1084/jem.70.5.453.
We have attempted to reproduce in animal experiments a group of pathological findings which we have observed to be associated with shock. In order to simulate the compensatory vasomotor reactions occurring in shock, we have utilized the intraperitoneal injection of adrenalin hydrochloride in dogs, cats, rabbits and guinea pigs. That the effect of adrenalin hydrochloride when injected by this route is of long duration has been shown by the prolonged hyperglycemia which it produces. Our experiments have resulted in the production of a lesion in the digestive tract which is identical in the gross with those which we observed in our human material. The histological changes, however, have been found to differ from those encountered in the latter. These differences have been noted to occur only in the dog and cat, where the initial changes take place in the mucosa, and the alterations in the submucosa appear secondary to these. In the rabbit and guinea pig the histogenesis of the lesions is identical with that observed in man, the lesions first manifesting themselves in changes in the submucosa, congestion, edema and hernorrhage. Only later are similar changes seen in the mucosa, progressing finally to necrosis and ulceration. The cause of the histological differences has been found in the presence of arteriovenous anastomoses which occur in the submucosa in the case of the dog and cat and in the mucosa in the case of the rabbit, guinea pig and man. We have pointed out that variations in blood flow through the intestinal wall may result from the short circuiting of the blood through the arteriovenous anastomoses. This, associated with the vasoconstriction known to occur in shock, may if severe and prolonged, result in necrosis of the intestinal wall. We have experimentally reproduced the same lesion by the injection of adrenalin, which acts in a similar way. The experimentally produced anatomical changes offer additional evidence in support of the clinical occurrence of a vasospasm which is of sufficient severity and duration to cause tissue necrosis.
我们试图在动物实验中重现一组与休克相关的病理发现。为了模拟休克时发生的代偿性血管运动反应，我们在狗、猫、兔和豚鼠中使用了盐酸肾上腺素腹腔注射。通过这种途径注射盐酸肾上腺素的效果持续时间长，这是由它产生的长期高血糖所证明的。我们的实验导致了消化道的损伤，其大体上与我们在人体材料中观察到的损伤相同。然而，组织学变化与后者不同。这些差异仅在狗和猫中观察到，在这些动物中，最初的变化发生在黏膜中，而黏膜下的改变是继发于这些变化的。在兔和豚鼠中，病变的组织发生与在人身上观察到的相同，病变首先表现为黏膜下的改变、充血、水肿和出血。只有在稍后阶段才会在黏膜中看到类似的变化，最终进展为坏死和溃疡。组织学差异的原因是在狗和猫的黏膜下和兔、豚鼠和人的黏膜中存在动静脉吻合。我们已经指出，肠壁血流的变化可能是由于血液通过动静脉吻合短路引起的。这种情况与休克时已知的血管收缩相结合，如果严重且持续时间长，可能会导致肠壁坏死。我们通过注射肾上腺素实验性地重现了相同的病变，肾上腺素的作用方式类似。实验性产生的解剖学变化为临床出现足以导致组织坏死的血管痉挛提供了额外的证据。
