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2003 HPB  
Aim: To investigate a correlation between ICAM-1 expression with early (ACR1) and delayed (ACR2) post-transplant acute cellular rejection (ACR). Methods: Biopsies were taken 90 min post-reperfusion (85 allografts). Routine postoperative biopsy at day 7 was taken, additional biopsy was taken at the end of week 2 or 3 when there is a suspicion of ongoing rejection. Rejection was graded according to the Royal Free novel scoring system. ICAM-1 expression was demonstrated by immuonocytochemistry
more » ... nique. Results: In post-reperfusion biopsies, 44/85 had mild ICAM-1 expression, of these only 14% developed moderate-severe ACR1 that required medical intervention. 23/85 had moderate ICAM-1 expression, of these 57% had moderate-severe ACR1. 18/85 had intense expression, in this group all allografts (100%) had moderate-severe ACR1. There was a signi®cant correlation between post-reperfusion ICAM-1 expression and the development of early acute 0.0001. In delayed rejection 44/85 allografts had mild ICAM-1 rejection, p expression, of these 9/44 had no post-transplant biopsy as the patients were doing well and 15/44 (34%) had moderatesevere ACR2. 23/85 allografts had moderate ICAM-1 expression, of these 3/23 had no post-transplant biopsy and 13/23 (57%) had moderate-severe ACR2. 18/85 had intense ICAM-1 expression, of these 4/18 had no posttransplant biopsy and 13/18 (72%) had moderate-severe ACR2. There was a signi®cant correlation between post-reperfusion ICAM-1 0.05. Conclusion: ICAM-1 expression (as expression and late acute rejection, p early as 90 minutes post-reperfusion) correlates signi®cantly with early and late rejection episodes. Perhaps this can lead the way to prophylactic treatment to prevent ACR before it becomes fully manifested. Background/aims: Impaired microcirculation in fatty liver has been proposed as an important factor in decreased tolerance of the liver to ischaemia-reperfusion injury. The present study aimed to investigate the effect of ischaemic preconditioning (IPC) on hepatic microcirculation (HM) in a rabbit model of hepatic steatosis. Methods: NZ female rabbits were fed a 2% cholesterol diet for 8 and 12 weeks to induce moderate and severe hepatic steatosis. All animals were subjected to 60 min of liver lobar ischaemia followed by 7 h of reperfusion with (IPC, n = 12) or without IPC (Control, n = 12). Arterial blood pressure, oxygen saturation and heart rate were monitored continuously. HM was assessed by laser Doppler¯owmeter. At the end of the reperfusion, indocyanine green (ICG, 0.5 mg/kg) clearance was measured directly by near infrared spectroscopy. Results: In moderate steatosis, HM in the control group decreased signi®cantly after 7 h of reperfusion (94.0 AE 5.0 vs 73.3 AE 3.3¯ux unit, p < 0.01, baseline vs 7 h), while there was no signi®cant deterioration in HM during the reperfusion period in the IPC group. There were signi®cant differences in HM between control and IPC groups at the 7th hour of reperfusion (73.3 AE 3.3 vs 118.3 AE 16.2¯ux unit, p < 0.05). The rates of ICG clearance were 57.8 AE 13.5% and 44.4 AE 4.0% in control and IPC groups, respectively. In severe steatosis, HM in the IPC group remained unchanged as compared with baseline, but it decreased signi®cantly in the control group at the end of reperfusion (85.6 AE 4.2 vs 65.8 AE 4.3¯ux unit, p < 0.05). The IPC group showed better ICG clearance as compared with control group (66.2 AE 3.9% vs 46.3 AE 11.6%), but the differences were not statistically signi®cant. Conclusions: The data suggest that IPC has a protective effect on the hepatic microcirculation in fatty liver during ischaemia-reperfusion injury.
pmid:18333003 pmcid:PMC2020607 fatcat:xj3aiojz6na7hmvbw2xywcscyq