中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
22期
1525-1528
,共4页
肝脏移植%高血压,门静脉%移植物%损伤
肝髒移植%高血壓,門靜脈%移植物%損傷
간장이식%고혈압,문정맥%이식물%손상
Liver transplantation%Hypertensin,portal%Transplant%Injuries
目的 探讨小体积移植肝损伤机制.方法 采用肝周骨骼化的去神经解剖、肝切除和原位灌注建立巴马小型猪不同移植量肝移植模型.分为3组(n=5):(1)A组:原位肝移植组;(2)B组:右半肝供肝肝部分移植组;(3)C组:右中叶和尾状叶供肝部分肝移植组.移植后观察动物7 d存活率,动态监测门静脉压(PVP)、门静脉血流量(PBF)以及移植肝组织学病理改变.结果 巴马小型猪不同移植量肝移植7 d存活率分别为:A组100%(5/5);B组100%(5/5)和C组20%(1/5).C组移植肝复流后PVP立即升高,高峰达(28.6±2.07)mm Hg,复流后1 h单位肝组织PBF达(3.56±0.11)ml·min-1·g-1.C组移植肝组织病理改变严重,包括肝窦淤血、出血,肝细胞气球样变或肝细胞坏死,内皮细胞脱落,狄氏间隙增宽或消失以及明显的细胞凋亡.结论 小体积肝移植中门静脉过度灌流和急性门静脉高压是移植肝的主要病因学机制.
目的 探討小體積移植肝損傷機製.方法 採用肝週骨骼化的去神經解剖、肝切除和原位灌註建立巴馬小型豬不同移植量肝移植模型.分為3組(n=5):(1)A組:原位肝移植組;(2)B組:右半肝供肝肝部分移植組;(3)C組:右中葉和尾狀葉供肝部分肝移植組.移植後觀察動物7 d存活率,動態鑑測門靜脈壓(PVP)、門靜脈血流量(PBF)以及移植肝組織學病理改變.結果 巴馬小型豬不同移植量肝移植7 d存活率分彆為:A組100%(5/5);B組100%(5/5)和C組20%(1/5).C組移植肝複流後PVP立即升高,高峰達(28.6±2.07)mm Hg,複流後1 h單位肝組織PBF達(3.56±0.11)ml·min-1·g-1.C組移植肝組織病理改變嚴重,包括肝竇淤血、齣血,肝細胞氣毬樣變或肝細胞壞死,內皮細胞脫落,狄氏間隙增寬或消失以及明顯的細胞凋亡.結論 小體積肝移植中門靜脈過度灌流和急性門靜脈高壓是移植肝的主要病因學機製.
목적 탐토소체적이식간손상궤제.방법 채용간주골격화적거신경해부、간절제화원위관주건립파마소형저불동이식량간이식모형.분위3조(n=5):(1)A조:원위간이식조;(2)B조:우반간공간간부분이식조;(3)C조:우중협화미상협공간부분간이식조.이식후관찰동물7 d존활솔,동태감측문정맥압(PVP)、문정맥혈류량(PBF)이급이식간조직학병리개변.결과 파마소형저불동이식량간이식7 d존활솔분별위:A조100%(5/5);B조100%(5/5)화C조20%(1/5).C조이식간복류후PVP립즉승고,고봉체(28.6±2.07)mm Hg,복류후1 h단위간조직PBF체(3.56±0.11)ml·min-1·g-1.C조이식간조직병리개변엄중,포괄간두어혈、출혈,간세포기구양변혹간세포배사,내피세포탈락,적씨간극증관혹소실이급명현적세포조망.결론 소체적간이식중문정맥과도관류화급성문정맥고압시이식간적주요병인학궤제.
Objective To elucidate the mechanisms of graft injury in small-for-size liver transplantation. Methods Animal models were established with skeletonized and denervated anatomic para-hepatic dissection, hepatectomy and perfusion in situ. Chinese Bama miniature pigs were divided into three groups (n=5): Group A, liver transplantation; Group B, partial liver transplantation with right hemi-liver graft and Group C, liver transplantation with right median and caudate lobe graft. Animals were followed for 7 days with regards to survival, dynamical portal venous pressure (PVP), portal blood flow (PBF) and graft histopathological examination. Results Animal survivals were as follows: Group A, 5/5, Group B, 5/5 and Group C, 1/5. PVP rose immediately after reperfusion. PVP in Group C peaked to 28.6±2.07 mm Hg. Portal blood flow (PBF) measured by CDFI showed that the index of PBF per gram liver tissue reached 3.56±showed that severe pathological changes occurred in small-for-size grafts, including sinusoidal congestion, hemorrhage, hepatocytic ballooning change or necrosis, endothelial cell detachment, Disse's space widening or vanishing and significant apoptosis. Conclusion Portal overperfusion and acute portal hypertension are the primary etiological mechanisms of graft injury in small-for-size liver transplantation.
