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

[背景/目的]合成非肽型内皮素受体；据报道SB209670 （SB）抑制血管收缩；但其对缺血后肝脏微循环（PILMC）的影响尚不清楚。阐明SB对PILMC的影响是本研究的目的。【材料与方法】活体荧光显微镜观察SB对缺血后肝细胞形态的影响，分析SB对肝细胞PILMC的影响，以及对缺血后天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、乳酸脱氢酶（LDH）释放的影响。[结果]与非缺血肝相比，SB对肝窦血管收缩、白细胞粘附及灌注率的抑制作用显著高于NaCl，达到94.1%；Vs. 83.8%, 1.54/acini Vs. 5.12/acini, 93.3% Vs. 70。但未见血管收缩和白细胞粘附于窦后小静脉。SB也没有阻止肝酶的释放和空泡化肝细胞数量的增加。[结论]SB对缺血后的肝窦微循环紊乱有保护作用，但对缺血再灌注肝损伤却没有预防作用，这可以证明是由于其在窦后小静脉中的冲突作用所致。

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.