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肝脏缺血再灌注损伤后的微血管变化。米索前列醇的保护作用。

Microvascular changes in liver after ischemia-reperfusion injury. Protection with misoprostol.

作者信息

Lim S P, Andrews F J, Christophi C, O'Brien P E

机构信息

Department of Surgery, Monash Medical School, Alfred Hospital, Prahran, Victoria, Australia.

出版信息

Dig Dis Sci. 1994 Aug;39(8):1683-90. doi: 10.1007/BF02087776.

Abstract

Morphological changes in the hepatic microvasculature were studied in experimentally induced ischemia-reperfusion injury in the rat using a vascular casting technique. Partial hepatic ischemia was induced for 90 min followed by 24 hr reperfusion. Microvascular casting was performed after 24 hr reperfusion by either intraarterial or intravenous infusion of acrylic resin (Mercox). After corrosion of the tissue, the cast was examined by scanning electron microscopy. Casts of normal livers showed good patency with no evidence of unfilled areas. The mean diameter of sinusoids was 14 +/- 3 microns with those in zone 1 slightly smaller than those in zone 3. Liver casts from rats subjected to ischemia and reperfusion resulted in gross disruption of normal architecture. The common characteristics seen in both prograde and retrograde casts were clusters of closed sinusoids around zones 2 and 3 of the liver acini, which resulted in cavities of various sizes. Varicosities were observed in some areas. The mean diameter of sinusoids in areas of patent microvascular structure (10 +/- 2 microns) was significantly smaller compared to those in normal livers (P < 0.001). Misoprostol given at 1 min before reperfusion markedly reduced the microvascular injury. The hepatic microvascular was generally intact with mild focal unfilled areas. The majority of the sinusoids were of normal size and no clusters of blind ending sinusoids were detected. The present study shows that hepatic ischemia-reperfusion results in extensive microvascular injury in the liver. The protective effects of misoprostol against this injury may occur at the vascular level.

摘要

采用血管铸型技术,研究了实验性诱导大鼠缺血再灌注损伤时肝微血管的形态学变化。诱导部分肝脏缺血90分钟,然后再灌注24小时。再灌注24小时后,通过动脉内或静脉内注入丙烯酸树脂(Mercox)进行微血管铸型。组织腐蚀后,通过扫描电子显微镜检查铸型。正常肝脏的铸型显示通畅良好,没有未填充区域的迹象。肝血窦的平均直径为14±3微米,1区的血窦略小于3区的血窦。经历缺血再灌注的大鼠肝脏铸型导致正常结构的严重破坏。在顺行和逆行铸型中都观察到的共同特征是围绕肝腺泡2区和3区的闭合肝血窦簇,这导致了各种大小的腔隙。在一些区域观察到静脉曲张。与正常肝脏相比,有微血管结构通畅区域的肝血窦平均直径(10±2微米)明显更小(P<0.001)。再灌注前1分钟给予米索前列醇可显著减轻微血管损伤。肝微血管总体完整,有轻度局灶性未填充区域。大多数肝血窦大小正常,未检测到盲端肝血窦簇。本研究表明,肝脏缺血再灌注会导致肝脏广泛的微血管损伤。米索前列醇对这种损伤的保护作用可能发生在血管水平。

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