EARLY VASCULAR INJURY AND INCREASED VASCULAR-PERMEABILITY IN GASTRIC-MUCOSAL INJURY CAUSED BY ETHANOL IN THE RAT
EARLY VASCULAR INJURY AND INCREASED VASCULAR-PERMEABILITY IN GASTRIC-MUCOSAL INJURY CAUSED BY ETHANOL IN THE RAT
复制标题
DOI：
10.1016/s0016-5085(85)80176-1
复制
发表时间：
1985-01-01
期刊：
影响因子：
29.4
通讯作者：
SCHNOOR, J
中科院分区：
文献类型：
--
作者：
SZABO, S;TRIER, JS;SCHNOOR, J
采用血管示踪剂对大鼠灌胃乙醇后血管损伤导致出血性糜坏的假设进行了检验。静脉注射Evans Blue外渗胃壁及胃内容物作为血管通透性的指标。用墨汁和寺院蓝标记血管损伤，从形态学上显示血管损伤。灌胃75%和100%乙醇可在1-3分钟内诱导血管通透性增加，1分钟内分别有13%和17%的腺粘膜血管出现单侧蓝色标记。100%乙醇暴露1 h后，单侧蓝色染色血管的面密度与1 min时相比没有增加，但肉眼可见的出血灶的面密度显著增加，与血管染色的面密度接近。出血性糜烂始终发生在腺粘膜区域，此处的血管呈单侧蓝色。前列腺素f2 . β预处理。半胱胺或半胱胺可减少乙醇诱导的埃文斯蓝外渗和粘膜血管的单侧蓝染色，但不能减少胃表面腺粘膜细胞损伤的组织学证据。由于血管通透性的增加和形态学上可检测到的血管病变始终先于腺粘膜明显可见的出血性糜烂的发生，血管损伤显然是乙醇性胃出血性糜烂发生的早期致病因素。数据还表明，与表面上皮细胞的损伤不同，前列腺素f2 . β预处理可以降低血管损伤的程度。或者是巯基半胱胺。
The hypothesis that vascular injury contributes to the development of hemorrhagic erosions after intragastric administration of ethanol was examined in the rat using vascular tracers. Extravasation of i.v. injected Evans Blue into the gastric wall and into gastric contents was used as an indicator of vascular permeability. India ink and monastral blue, which label damaged blood vessels, were used to demonstrate vascular injury morphologically. Intragastric instillation of 75% and 100% ethanol induced increased vascular permeability within 1-3 min and resulted in monastral blue labeling of vessels in 13% and 17%, respectively, of the glandular mucosa within 1 min. After 1 h of 100% ethanol exposure, the areal density of monastral blue-stained blood vessels did not increase compared with that seen at 1 min, but the areal density of grossly visible hemorrhagic lesions increased strikingly and approximated that of vessel staining. The hemorrhagic erosions consistently occurred in regions of glandular mucosa where vessels were stained with monastral blue. Pretreatment with prostaglandin F2.beta. or cysteamine reduced ethanol-induced Evans Blue extravasation and monostral blue staining of mucosal blood vessels but did not reduce histologic evidence of gastric surface cell damage in the glandular mucosa. As increased vascular permeability and morphologically detectable vascular lesions consistently preceded the development of grossly visible hemorrhagic erosions in the glandular mucosa, vascular injury is apparently an early pathogenetic factor in the development of ethanol-induced gastric hemorrhagic erosions. The data also indicate that the degree of vascular damage, unlike the injury to surface epithelial cells, is reduced by pretreatment with prostaglandin F2.beta. or the sulfhydryl cysteamine.