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Hepatic arterial buffer response fails to restore hepatic oxygenation after temporary liver dearterialization in canines.

机译:犬的暂时性肝脱盐后,肝动脉缓冲反应无法恢复肝氧合。

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BACKGROUND: Hepatic artery thrombosis is a rare but extremely troublesome condition after liver transplantation. Recently, urgent arterial revascularization has been used as rescue therapy, leading to improved graft and patient survivals. Hepatic artery ligation produces a progressive reduction in portal vein blood flow. Theoretically, a hyperemic response may be expected following hepatic artery reperfusion (hepatic artery buffer response, HABR). In this study, we tested the hypothesis that HABR can maintain adequate liver oxygenation after temporary liver dearterialization. METHODS: Seven dogs (19.7 +/- 1.2 kg) subjected to 60 minutes of hepatic artery occlusion were observed for 120 minutes thereafter. Systemic hemodynamics was evaluated through Swan-Ganz and arterial catheters, and splanchnic perfusion by portal vein and hepatic artery blood flows (PVBF and HABF) via an ultrasonic flowprobe. Liver enzymes (ALT and LDH) and systemic and hepatic oxygen delivery (DO2hepat) were calculated using standard formulae. RESULTS: Hepatic artery occlusion induced a progressive reduction in PVBF and DO2hepat. A complete restoration of HABF after hepatic artery declamping was observed; however, the DO2hepat (33.3 +/- 5.9 to 16.5 +/- 5.9 mL/min) did not return to the baseline levels. CONCLUSION: Temporary hepatic artery occlusion induced a progressive decrease in portal vein blood flow during ischemia, an effect that continued during the reperfusion period. The hepatic artery blood flow was promptly restored after declamping. However, HABR was not able to restore hepatic oxygen delivery to baseline levels during the reperfusion period.
机译:背景:肝动脉血栓形成是一种罕见的但在肝移植后极为麻烦的疾病。最近,紧急动脉血运重建已被用作抢救疗法,从而改善了移植物和患者的存活率。肝动脉结扎会逐渐减少门静脉血流量。从理论上讲,肝动脉再灌注后可能会出现充血反应(肝动脉缓冲反应,HABR)。在这项研究中,我们测试了以下假设:HABR可以在暂时性肝去盐后维持足够的肝脏氧合作用。方法:对七只狗(19.7 +/- 1.2千克)进行60分钟肝动脉闭塞,观察120分钟。通过Swan-Ganz和动脉导管评估全身血流动力学,并通过超声波探头通过门静脉和肝动脉血流(PVBF和HABF)评估内脏灌注。使用标准公式计算肝酶(ALT和LDH)以及全身和肝氧输送(DO2肝)。结果:肝动脉闭塞引起PVBF和DO2肝的逐渐减少。观察到肝动脉放松后HABF完全恢复。但是,DO2hepat(33.3 +/- 5.9至16.5 +/- 5.9 mL / min)未恢复到基线水平。结论:暂时性肝动脉阻塞导致缺血期间门静脉血流量的逐渐减少,这种作用在再灌注期间持续存在。放松后,肝动脉血流迅速恢复。但是,HABR无法在再灌注期间将肝氧输送恢复至基线水平。

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