论文部分内容阅读
目前,有许多证据表明含铝的抗酸剂能保护胃粘膜免受各种致溃疡及坏死因子造成的损伤。这种保护作用不被H_2一受体阻断剂减轻,而且,发现酸化的抗酸剂比有酸中和能力的抗酸剂效果更好,这就清楚说明抗酸剂的细胞保护作用不是靠中和胃酸作用完成。目前,抗酸剂的细胞保护机理还不清楚。本文作者研究比较了氢氧化铝和氢氧化镁及三种H_2一受体阻断剂(西咪替丁,雷尼替丁,法莫替丁)在保护胃粘膜避免受乙醇诱导坏死方面的作用。大鼠分别喂上述药物,1小时后胃内灌注100‰乙醇2ml,灌注乙醇3小时时观察胃粘膜受损的情况。对照组大鼠胃粘膜坏死达42±2％,在光镜和电镜下显示上皮细胞脱落坏死,血管内皮细胞坏死,毛细血管破裂,血小板粘聚和血栓形成,45％的粘膜有出血及深层坏死。预先用氢氧化铝和或氢氧化
At present, there is a lot of evidence that aluminum-containing antacids protect the gastric mucosa from damage caused by various types of ulcers and necrosis factors. This protection was not mitigated by H 2 -receptor blockers, and acidified antacids were found to perform better than antacids with acid neutralization, clearly demonstrating that antacids did not rely on cytoprotection Neutralization of stomach acid effect. At present, the mechanism of cell protection of antacids is unclear. The authors compared the effects of aluminum hydroxide and magnesium hydroxide and three H 2 -receptor blockers (cimetidine, ranitidine and famotidine) on protecting the gastric mucosa from ethanol-induced necrosis . Rats were fed the above drugs, 1 hour after gastric perfusion 100 ‰ ethanol 2ml, ethanol 3 hours when observed gastric mucosal damage. Gastric mucosal necrosis of rats in control group reached 42 ± 2%, showing epithelial cell detachment and necrosis, endothelial cell necrosis, capillary rupture, platelet aggregation and thrombosis under light and electron microscopes, bleeding and deep necrosis in 45% of mucous membranes . Pre-treated with aluminum hydroxide and / or hydroxide