Endothelin-1 induces direct constriction of hepatic sinusoids.
Endothelin-1 induces direct constriction of hepatic sinusoids.
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内皮素-1 诱导肝窦直接收缩。
DOI：
10.1152/ajpgi.1994.266.4.g624
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Clemens,MG
中科院分区：
文献类型：
--
作者：
Zhang,JX;PegoliJr,W;Clemens,MG
我们研究了肝脏微血管内皮素（ET）的反应和伊藤细胞（脂肪储存细胞）作为周细胞在这种反应中可能发挥的作用，使用离体大鼠肝脏在高功率活体显微镜下。在改良的压力控制系统中，用Krebs缓冲液加大鼠红细胞（RBC，10%）灌注肝脏，在ET-1（单独10（-9 M），硝普钠（NP，10（-5 M））输注之前和期间，在100倍物镜（总放大倍数x 2，533）下观察Ito细胞部位的血窦。+ ET-1或苯丙氨酸（PE，10（-7）M）。ET-1和PE分别降低门静脉血流量（25%和51%）和增加流入压力（28%和43%）。PE对任何正弦参数没有影响，除了降低测量的正弦RBC速度（P < 0.05）; ET-1使正弦直径减小25%，计算的正弦压力梯度和阻力分别增加116%和350%，但不改变RBC速度。NP显著抑制ET-1引起的变化。这些结果表明，ET-1诱导一个特定的正弦收缩，破坏正常的腺泡流动动力学，和正弦收缩colocalizes与伊藤细胞，这表明收缩可能介导的至少部分ET-1对伊藤细胞的作用，这可以抑制一氧化氮供体。
We studied the hepatic microvascular response to endothelin (ET) and the possible role of Ito cells (fat-storing cells) acting as pericytes in this response using isolated rat livers under high-power intravital microscopy. Livers were perfused in a modified pressure-controlled system with Krebs buffer plus rat erythrocytes (RBC, 10%), and sinusoids at the site of Ito cells were observed under a x 100 objective (total magnification x 2,533) before and during infusion of ET-1 (10(-9 M) alone, sodium nitroprusside (NP, 10(-5) M). plus ET-1, or phenylephrine (PE, 10(-7) M). Both ET-1 and PE decreased portal flow (25 and 51%) and increased inflow pressure (28 and 43%), respectively. PE had no effect on any sinusoidal parameters except that it decreased measured sinusoidal RBC velocity (P < 0.05); ET-1 decreased sinusoidal diameter by 25% and increased the calculated sinusoidal pressure gradient and resistance by 116 and 350%, respectively, but did not alter RBC velocity. NP significantly inhibited changes induced by ET-1. These results demonstrate that ET-1 induces a specific sinusoidal constriction that disrupts normal acinar flow dynamics, and the sinusoidal constriction colocalizes with Ito cells, suggesting that the constriction may be mediated at least in part by ET-1 action on Ito cells, which can be inhibited by a nitric oxide donor.