Smelley Christopher, Specian Robert D, Tang Jiping, Zhang John H
Department of Neurosurgery, Louisiana State University Health Sciences Center in Shreveport, LA 71105, USA.
Brain Res. 2005 Mar 21;1038(2):198-207. doi: 10.1016/j.brainres.2005.01.042.
Severe intracerebral hemorrhage (ICH) produces gastric pathology in about 30% of the patient population, even after the standard treatment of H2 receptor blockers or proton pump inhibitors. This study was undertaken to establish a rat model of ICH-induced gastric ulcer. Adult male Sprague-Dawley rats (300-350 g) were divided into two hemorrhage groups and a sham control group. ICH was produced either by injection of 100 microl of autologous arterial blood or by injection of 4 microl saline containing 0.6 unit of bacterial collagenase VII into the right basal ganglia. Rats were sacrificed at 24, 48, 72 h, and 7 days after ICH to harvest brains and stomachs. Greater degrees of hemorrhage and brain edema were observed in collagenase-induced ICH. Motor behavior decreased significantly after 24 h in both models. The incidence of acute ulceration with destruction of the forestomach epithelium was extremely low at 8.7% in the collagenase injection model and 4.8% in the blood injection rats. Small, pinpoint hemorrhages (petechiae) were noticed in 38% of rats after blood injection and 22% after collagenase injection, in the glandular portion of the gastric mucosa with penetration of red blood cells and inflammatory cells into the gastric mucosa. Enhanced tumor necrosis factor alpha (TNFalpha) and cyclooxygenase 2 (COX-2) expressions were observed in gastric tissues after ICH with more intense staining occurring at 24 and 48 h. Due to the low incidence of ulceration, ICH-induced gastric ulceration in rodents may not appropriate for evaluating the potential human risk of gastric ulceration after ICH.
严重脑出血（ICH）在约30%的患者中会导致胃部病变，即便采用H2受体阻滞剂或质子泵抑制剂进行标准治疗后仍是如此。本研究旨在建立脑出血诱导的胃溃疡大鼠模型。成年雄性Sprague-Dawley大鼠（300 - 350克）被分为两个出血组和一个假手术对照组。通过向右侧基底神经节注射100微升自体动脉血或注射含0.6单位细菌胶原酶VII的4微升生理盐水来制造脑出血。在脑出血后24、48、72小时及7天处死大鼠，以获取脑和胃。在胶原酶诱导的脑出血中观察到更严重的出血和脑水肿。两种模型在24小时后运动行为均显著下降。在前胃上皮破坏的急性溃疡发生率极低，胶原酶注射模型中为8.7%，血液注射大鼠中为4.8%。血液注射后38%的大鼠以及胶原酶注射后22%的大鼠在胃黏膜腺部出现小的点状出血（瘀点），有红细胞和炎性细胞渗入胃黏膜。脑出血后在胃组织中观察到肿瘤坏死因子α（TNFα）和环氧化酶2（COX - 2）表达增强，在24和48小时染色更强烈。由于溃疡发生率低，啮齿动物脑出血诱导的胃溃疡可能不适用于评估人类脑出血后胃溃疡的潜在风险。
