Lauber David Tibor, Tihanyi Dóra Krisztina, Czigány Zoltán, Kovács Tibor, Budai András, Drozgyik Dóra, Fülöp András, Szijártó Attila
Hepato-Pancreatico-Biliary (HPB) Surgical Research Center, 1st Department of Surgery, Semmelweis University, Budapest, Hungary.
Hepato-Pancreatico-Biliary (HPB) Surgical Research Center, 1st Department of Surgery, Semmelweis University, Budapest, Hungary.
J Surg Res. 2016 Jun 15;203(2):451-8. doi: 10.1016/j.jss.2016.03.032. Epub 2016 Mar 25.
Selective portal vein ligation (PVL) is followed by ipsilateral atrophy and contralateral hypertrophy of the liver lobes. Although the atrophy-hypertrophy complex induced by PVL is a well-documented phenomenon, the effect of different degrees of extended portal vein occlusion on liver regeneration is not known. The aim of this study was to assess the effects of different degrees of portal occlusion on portal pressure and liver regeneration.
Male Wistar rats (n = 96; 220-250 g) were randomized into three groups and underwent 70%, 80%, or 90% portal vein ligation, respectively. The portal pressure was measured immediately and 24, 48, 72, 120, and 168 h after PVL (n = 6/group/time point). The hepatic lobes and the spleen were weighed, and liver regeneration ratio was calculated. Changes in liver histology and the mitotic activity were assessed on hematoxylin-eosin stained slides.
Higher degree of portal occlusion triggered a stronger regenerative response (regeneration ratio of PVL 70%168h = 2.23 ± 0.13, PVL 80%168h = 3.11 ± 0.37, PVL 90%168h = 4.68 ± 0.48) PVL led to an immediate increase in portal pressure, the value of which changed proportionally to the mass of liver tissue deprived of portal perfusion (PVL 70%acute = 17 ± 2 mm Hg, PVL 80%acute = 19 ± 1 mm Hg, PVL 90%acute = 26 ± 4 mm Hg). Findings in histology showed necro-apoptotic lesions in the atrophic liver lobes and increased mitotic cell count in the hypertrophic lobes. The mitotic cell count of PVL 90% peaked earlier and at a significantly higher value than of PVL 70% and PVL 80% (PVL 9024h%: 96.0 ± 3.5 PVL 70%48h: 64.0 ± 2.1, PVL 80%48h: 56.3 ± 4.0). The mitotic index after 24 h showed a strong correlation with the acute portal hypertension.
A higher degree of portal vein occlusion leads to a greater regenerative response, presumably triggered by the proportional increase in portal pressure, which supports the role of the so-called "blood-flow" theory of PVL-triggered liver regeneration.
选择性门静脉结扎术(PVL)后会出现肝叶同侧萎缩和对侧肥大。尽管PVL诱导的萎缩-肥大复合体是一个有充分文献记载的现象,但不同程度的门静脉延长闭塞对肝再生的影响尚不清楚。本研究的目的是评估不同程度的门静脉闭塞对门静脉压力和肝再生的影响。
将雄性Wistar大鼠(n = 96;体重220 - 250 g)随机分为三组,分别接受70%、80%或90%的门静脉结扎。在PVL后即刻、24、48、72、120和168小时测量门静脉压力(每组每个时间点n = 6)。称量肝叶和脾脏重量,计算肝再生率。在苏木精-伊红染色切片上评估肝脏组织学变化和有丝分裂活性。
更高程度的门静脉闭塞引发更强的再生反应(PVL 70% 168小时的再生率 = 2.23 ± 0.13,PVL 80% 168小时 = 3.11 ± 0.37,PVL 90% 168小时 = 4.68 ± 0.48)。PVL导致门静脉压力立即升高,其值与失去门静脉灌注的肝组织质量成比例变化(PVL 70%急性 = 17 ± 2 mmHg,PVL 80%急性 = 19 ± 1 mmHg,PVL 90%急性 = 26 ± 4 mmHg)。组织学检查发现萎缩肝叶有坏死-凋亡病变,肥大肝叶有丝分裂细胞计数增加。PVL 90%的有丝分裂细胞计数峰值出现得更早,且显著高于PVL 70%和PVL 80%(PVL 90% 24小时:96.0 ± 3.5,PVL 70% 48小时:64.0 ± 2.1,PVL 80% 48小时:56.3 ± 4.0)。24小时后的有丝分裂指数与急性门静脉高压呈强相关。
更高程度的门静脉闭塞导致更大的再生反应,推测是由门静脉压力的成比例增加引发的,这支持了PVL触发肝再生的所谓“血流”理论的作用。