解放军医学院学报
解放軍醫學院學報
해방군의학원학보
Academic Journal of Chinese Pla Medical School
2013年
11期
1178-1181
,共4页
辛宪磊%陈永亮%陈明易%李崇辉%李鸾%冯健%郭少华%张安红
辛憲磊%陳永亮%陳明易%李崇輝%李鸞%馮健%郭少華%張安紅
신헌뢰%진영량%진명역%리숭휘%리란%풍건%곽소화%장안홍
门静脉动脉化%肝动脉结扎%梗阻性黄疸%胆管%大鼠
門靜脈動脈化%肝動脈結扎%梗阻性黃疸%膽管%大鼠
문정맥동맥화%간동맥결찰%경조성황달%담관%대서
portal vein arterialization%hepatic artery ligation%obstructive jaundice%bile duct%rats
目的:探讨部分门静脉动脉化重建胆管血流后对梗阻性黄疸大鼠肝门部胆管、肝功能及胆管上皮的影响。方法40只大鼠随机分为对照组(A)、梗阻性黄疸5 d行胆管再通组(B)、梗阻性黄疸5 d行胆管再通+肝动脉结扎组(C)、梗阻性黄疸5 d行胆管再通+部分门静脉动脉化组(D),每组10只。分别于术后1周应用HE染色观察胆管病理学改变,检测血清ALP、GGT变化,TUNEL染色观察胆管上皮细胞凋亡及坏死情况。结果 A组大鼠肝门部胆管病理学检查未见异常改变;B组大鼠肝门部胆管病理学检查见少量急慢性炎症细胞浸润,少部分胆管上皮细胞脱失;C组大鼠肝门部胆管可见大量急慢性炎症细胞浸润,胆管上皮细胞多量胞质空泡化改变,大量胆管上皮脱失,可见胆管壁坏死,胆管上皮细胞凋亡指数显著升高;D组大鼠肝门部胆管可见少量炎症细胞浸润,散在数个胆管上皮细胞空泡化,少部分上皮脱失,凋亡指数与B组比较无统计学差异。结论梗阻性黄疸情况下行肝动脉结扎会导致肝门部胆管严重的缺血缺氧改变,甚至胆管壁坏死,部分门静脉动脉化明显减轻肝总动脉结扎对梗阻性黄疸大鼠肝门部胆管的损害。
目的:探討部分門靜脈動脈化重建膽管血流後對梗阻性黃疸大鼠肝門部膽管、肝功能及膽管上皮的影響。方法40隻大鼠隨機分為對照組(A)、梗阻性黃疸5 d行膽管再通組(B)、梗阻性黃疸5 d行膽管再通+肝動脈結扎組(C)、梗阻性黃疸5 d行膽管再通+部分門靜脈動脈化組(D),每組10隻。分彆于術後1週應用HE染色觀察膽管病理學改變,檢測血清ALP、GGT變化,TUNEL染色觀察膽管上皮細胞凋亡及壞死情況。結果 A組大鼠肝門部膽管病理學檢查未見異常改變;B組大鼠肝門部膽管病理學檢查見少量急慢性炎癥細胞浸潤,少部分膽管上皮細胞脫失;C組大鼠肝門部膽管可見大量急慢性炎癥細胞浸潤,膽管上皮細胞多量胞質空泡化改變,大量膽管上皮脫失,可見膽管壁壞死,膽管上皮細胞凋亡指數顯著升高;D組大鼠肝門部膽管可見少量炎癥細胞浸潤,散在數箇膽管上皮細胞空泡化,少部分上皮脫失,凋亡指數與B組比較無統計學差異。結論梗阻性黃疸情況下行肝動脈結扎會導緻肝門部膽管嚴重的缺血缺氧改變,甚至膽管壁壞死,部分門靜脈動脈化明顯減輕肝總動脈結扎對梗阻性黃疸大鼠肝門部膽管的損害。
목적:탐토부분문정맥동맥화중건담관혈류후대경조성황달대서간문부담관、간공능급담관상피적영향。방법40지대서수궤분위대조조(A)、경조성황달5 d행담관재통조(B)、경조성황달5 d행담관재통+간동맥결찰조(C)、경조성황달5 d행담관재통+부분문정맥동맥화조(D),매조10지。분별우술후1주응용HE염색관찰담관병이학개변,검측혈청ALP、GGT변화,TUNEL염색관찰담관상피세포조망급배사정황。결과 A조대서간문부담관병이학검사미견이상개변;B조대서간문부담관병이학검사견소량급만성염증세포침윤,소부분담관상피세포탈실;C조대서간문부담관가견대량급만성염증세포침윤,담관상피세포다량포질공포화개변,대량담관상피탈실,가견담관벽배사,담관상피세포조망지수현저승고;D조대서간문부담관가견소량염증세포침윤,산재수개담관상피세포공포화,소부분상피탈실,조망지수여B조비교무통계학차이。결론경조성황달정황하행간동맥결찰회도치간문부담관엄중적결혈결양개변,심지담관벽배사,부분문정맥동맥화명현감경간총동맥결찰대경조성황달대서간문부담관적손해。
Objective To study the effect of partial portal vein arterialization after bile ductflow reconstruction on hepatohilar bile duct, liver function and bile duct epithelium in rats with obstructive jaundice.Methods Forty rats were randomly divided into group A (control group), group B undergoing bile duct recanalization 5 days after obstructive jaundice, group C undergoing bile duct recanalization + hepatic artery ligation 5 days after obstructive jaundice, and group D undergoing bile duct recanalization + partial portal vein arterialization 5 days after obstructive jaundice (10 in each group). Pathological changes in bile duct were observed with HE staining, serum ALP and GGT levels were measured, and apoptosis and necrosis of bile duct epithelial cells were detected with TUNEL staining 1 week after operation.Results No distinct pathological change was observed in hepatohilar bile duct of group A. Filtration of a small number of inflammatory cells and loss of a small number of bile duct epithelial cells were found in group B. The following changes occurred in group C, including acute or chronic infiltration of inflammatory cells on hepatic bileduct wall, cytoplasm vacuolation of bile duct epithelial cells, loss of massive bile duct epithelium, necrosis of bile duct wall, and significantly increased apoptosis index of bile duct epithelial cells. Infiltration of a small number of inflammatory cells, scattered vacuolation of bile duct epithelial cells and loss of some bile duct epithelium were detected in group D with no significant difference in apoptosis index and necrosis of bile duct wall. Conclusion Liver artery ligation leads to severe ischemic and anoxic change in hepatohilar bile duct and even necrosis of bile duct wall while partial portal vein arterialization can significantly alleviate the damage to hepatohilar bile duct caused by liver artery ligation in rats with obstructive jaundice.