Bailey R W, Bulkley G B, Hamilton S R, Morris J B, Haglund U H, Meilahn J E
Ann Surg. 1987 Jun;205(6):597-612. doi: 10.1097/00000658-198706000-00001.
Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such that cardiac output was reduced to 38 +/- 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. "Blinded" gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric "stress ulceration" syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal "stress ulceration" is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the "shock liver" syndrome, gastric "stress ulceration" is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis.
急性胃黏膜出血性溃疡在低血容量性或心源性休克患者中很常见。虽然这些病变显然与局部胃缺血有关，但对介导缺血本身的潜在机制关注甚少。为此，对麻醉的猪施加持续性心源性休克（轻度出血和心包填塞），使心输出量降至基线水平的38±1%并持续4小时，随后解除填塞，回输失血，并复苏2小时。在休克期间，由于严重且不成比例的胃血管收缩，出现了严重的局部胃缺血。对实验后取出的胃进行“盲法”大体和显微镜评估，发现有严重的黏膜缺血性坏死、出血和溃疡，而假手术的猪则无病变。因此，该模型的特征模拟了胃“应激性溃疡”综合征的基本特征。事先用酚苄明证实完全阻断α-肾上腺素能受体并不能显著改变这些特征。相反，事先切除肾素-血管紧张素轴，无论是用替普罗肽抑制血管紧张素转换酶还是双侧肾切除，都能显著且实质性地改善缺血、血管痉挛和黏膜损伤。在这个心源性休克模型中，急性胃黏膜“应激性溃疡”是由选择性内脏血管痉挛导致的不成比例的严重局部胃缺血引起的，这种血管痉挛不受交感神经阻滞的影响，但事先切除肾素-血管紧张素轴可消除。与非闭塞性小肠缺血、缺血性结肠炎和“休克肝”综合征一样，胃“应激性溃疡”是多内脏器官功能衰竭综合征的另一个组成部分，似乎主要由内脏血管床对肾素-血管紧张素轴的显著敏感性介导。
