Protection of hepatic microcirculatory disturbance due to the ischemia-reperfusion injury

摘要[背景/目的] SB 209670（SB）是一种人工合成的非肽类内皮素受体，具有抑制血管收缩的作用，但其对缺血后肝脏微循环（PILMC）的影响尚不清楚。本研究的目的是阐明SB对PILMC的影响。[材料与方法]采用活体荧光显微镜观察SB对PILMC、AST、ALT、LDH释放及肝细胞形态的影响。[结果] SB明显抑制肝窦血管收缩、白细胞粘附和恢复灌注率，与非缺血肝比较，SB组分别为94.1%和83.8%，1.54/腺泡和5.12/腺泡，SB组分别为93.3%和70。2%，但不引起窦后微静脉血管收缩和白细胞粘附。SB也不能阻止肝酶的释放和空泡化肝细胞数量的增加。[结论] SB对缺血后肝窦微循环障碍有保护作用，但对缺血再灌注肝损伤无保护作用，可能与SB对肝窦后微静脉的作用冲突有关。

Abstract[Background/Aim] A synthesized non-peptide endothelin receptor; SB209670 (SB) reported to inhibit vasoconstriction; however its effects on the post-ischemic liver microcirculation (PILMC) is still unclear. To clarify the effects of SB on the PILMC was the aim of this study.[Material and Methods] We analyses the effects of SB on not only PILMC, but also release of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) and the hepatocyte morphology after ischemia by intravital fluorescent microscopy. [Results] SB significantly inhibited the sinusoidal vasoconstriction, leukocyte sticking and restored the perfusion rate than NaCl administration in comparison with those of non-ischemic liver, 94.1%; vs. 83.8%, 1.54/acini vs. 5.12/acini and 93.3% vs. 70. 2%, respective, however, it did not the vasoconstriction and leukocyte sticking in the post-sinusoidal venule. SB also did not prevent release of liver enzyme and the increase of the vacuolated hepatocyte number. [Conclusion] SB protects the post-ischemic microcirculatory disturbance in the sinusoid, however it did not prevent ischemic reperfusion liver injury provably due to the conflictive effects in the post-sinusoidal venule.