Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation

医学 原位肝移植 肝移植 微循环 肝循环 人肝 移植 肝功能 内科学 病理 门静脉 生物化学 化学
作者
Gero Puhl,Klaus‐D. Schaser,Daniel Pust,Katrin Köhler,Brigitte Vollmar,Michael D. Menger,P. Neuhaus,Utz Settmacher
出处
期刊:Liver Transplantation [Lippincott Williams & Wilkins]
卷期号:11 (5): 555-563 被引量:65
标识
DOI:10.1002/lt.20394
摘要

Microcirculatory disturbances are an initial causative determinant in hepatic ischemia/reperfusion injury. The aim of this study was to assess sinusoidal perfusion during human liver transplantation using orthogonal polarization spectral imaging and to evaluate the significance of intraoperative microcirculation for early postoperative graft function. Hepatic microcirculation was measured in 27 recipients undergoing full-size liver transplantation and compared to a group of 32 healthy living-related liver donors. The microvascular parameters were correlated with postoperative aspartate aminotransferase and bilirubin levels. Hepatic perfusion following liver transplantation was found to be significantly decreased when compared with the control group. Volumetric blood flow within the individual sinusoids increased due to sinusoidal dilatation and enhanced flow velocity. Regression analysis of postoperative aspartate aminotransferase and bilirubin with microvascular parameters revealed significant correlations. The extent of volumetric blood flow increased within the first 30 minutes after reperfusion and showed a significant correlation with postoperative aspartate aminotransferase release and bilirubin elimination. In conclusion, postischemic hepatic microvascular perfusion was analyzed in vivo, demonstrating significant microvascular impairment during liver transplantation. Sinusoidal hyperperfusion appears to confer protection against postischemic liver injury, as given by the correlation with aspartate aminotransferase and bilirubin levels. Thus, these findings may have therapeutic importance with respect to mechanisms mediating postischemic reactive hyperemia.
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