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肝微血管调节机制。十一、血清素对门静脉周围窦状隙入口处小叶内灌注及中央静脉窦状隙出口处容积流量的影响。

Hepatic microvascular regulatory mechanisms. XI. Effects of serotonin on intralobular perfusion and volumetric flowrates at the inlet of periportal and outlet of centrivenous sinusoids.

作者信息

Blankenship L L, Cilento E V, Reilly F D

机构信息

Department of Anatomy, School of Medicine, West Virginia University, Morgantown 26506.

出版信息

Microcirc Endothelium Lymphatics. 1991;7(1-3):57-75.

PMID:1762610
Abstract

A normotensive (1.0 microgram per 100 g b.w.) or hypotensive (10.0 micrograms per 100 g b.w.) dose of serotonin (5-HT) was administered endoportally while changes in microcirculation at the inlet and outlet regions of hepatic lobules were measured on-line using quantitative in vivo microscopy. The number of sinusoids with decreased (cellular) flow also was counted to index intralobular perfusion in video recordings of microvasculature examined off-line. The normotensive and hypotensive doses of 5-HT elicited decreases in intralobular perfusion within periportal and centrivenous sinusoids. Hypoperfusion was accompanied by a transient decrease in volumetric flowrate (Q) at the outlet of centrivenous sinusoids in 40% of normotensive and in 100% of hypotensive rats. At the inlet of periportal sinusoids, Q was depressed in 75% of hypotensive and in 27% of normotensive rats. The remainder of these segments had either an increase or no change in Q at the inlet and outlet. These results suggested that during conditions of 5-HT induced (lobular) hypoperfusion: (a) Q at the inlet is maintained in 73% of normotensive rats by redistribution of intralobular blood flow, and decreased in all but 25% of hypotensive rats as a function of transient reductions in total hepatic (arterial) and/or portal (venous) blood flow(s), and (b) Q at the outlet is depressed in 40% of normotensive rats by apparent increases in flow redistribution and resistance to flow generated during sinusoidal constriction, whereas in all hypotensive rats this mechanism is aggravated by decreased total hepatic (arterial) and/or portal (venous) inflow(s). Therefore, although the initial time course for microvascular responses tended to be similar for normo- and hypo-tensive doses of 5-HT, quantitative differences in regional flow distribution and Q emphasize (a) the importance of intra- and extra-hepatic determinants in the regulation of blood flow within hepatic (unit) lobules, and (b) the presence of microvascular heterogeneity within these lobular units.

摘要

以门静脉内注射的方式给予正常血压剂量(每100克体重1.0微克)或低血压剂量(每100克体重10.0微克)的血清素(5-羟色胺,5-HT),同时使用定量活体显微镜在线测量肝小叶入口和出口区域微循环的变化。离线检查微血管视频记录时,还对血流减少(细胞性)的肝血窦数量进行计数,以作为小叶内灌注的指标。正常血压剂量和低血压剂量的5-HT均可引起门静脉周围和中央静脉肝血窦内小叶内灌注减少。在40%的正常血压大鼠和100%的低血压大鼠中,灌注不足伴随着中央静脉肝血窦出口处体积流量(Q)的短暂下降。在门静脉周围肝血窦入口处,75%的低血压大鼠和27%的正常血压大鼠的Q值降低。这些节段的其余部分在入口和出口处的Q值要么增加,要么没有变化。这些结果表明,在5-HT诱导(小叶)灌注不足的情况下:(a)73%的正常血压大鼠通过小叶内血流重新分布维持入口处的Q值,除25%的低血压大鼠外,所有低血压大鼠的Q值均因肝总(动脉)和/或门静脉(静脉)血流的短暂减少而降低;(b)40%的正常血压大鼠出口处的Q值因肝血窦收缩期间血流重新分布和血流阻力明显增加而降低,而在所有低血压大鼠中,这种机制因肝总(动脉)和/或门静脉(静脉)流入减少而加剧。因此,尽管正常血压和低血压剂量的5-HT引起的微血管反应的初始时间进程往往相似,但区域血流分布和Q值的定量差异强调了:(a)肝内和肝外决定因素在调节肝(单位)小叶内血流中的重要性;(b)这些小叶单位内存在微血管异质性。

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