Role of humoral factors in the intestinal hyperemia associated with chronic portal hypertension.

Role of humoral factors in the intestinal hyperemia associated with chronic portal hypertension.
复制标题

体液因素在慢性门脉高压相关肠道充血中的作用。

DOI:
10.1152/ajpgi.1984.247.5.g486
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发表时间:
1984
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Granger,DN
Granger,DN
中科院分区:
--
文献类型:
--
作者:
Benoit,JN;Barrowman,JA;Harper,SL;Kvietys,PR;Granger,DN

文献摘要

被引文献

相似文献

本研究采用大鼠门静脉狭窄模型,探讨了神经、代谢、生理和体液因素在慢性门静脉高压症肠充血中的作用。与对照组相比,门静脉狭窄大鼠的肠血流量和脾髓压力增加,而体循环动脉压和总血管阻力降低。总血管阻力的减少完全是由于毛细血管前阻力的下降,并伴随着肠毛细血管压力的增加,超过了急性门静脉压力升高到同一水平所产生的。在门脉高压大鼠中,15微米微球的动静脉分流高出4倍。门脉高压大鼠的动脉血交叉灌注对照肠道制剂产生了30%的血流量增加。门脉高压大鼠的血浆胰高血糖素水平比对照组高3倍。动脉内输注胰高血糖素(以达到门脉高压动物中测量的浓度的速率)使肠血管阻力降低20%。这些研究的结果表明,体液因素,包括胰高血糖素,是主要负责充血与门静脉高压症。
The role of neural, metabolic, physical, and humoral factors in the intestinal hyperemia associated with chronic portal hypertension was examined by use of the rat portal vein stenosis model. Intestinal blood flow and splenic pulp pressure were increased, while systemic arterial pressure and total vascular resistance were reduced in portal vein-stenosed rats as compared with controls. The reduction in total vascular resistance was entirely due to a fall in precapillary resistance and was accompanied by an increase in intestinal capillary pressure, which exceeded that produced by acute portal pressure elevation to the same level. Arteriovenous shunting of 15-micron microspheres was four times higher in portal-hypertensive rats. Cross-perfusion of control intestinal preparations with arterial blood from portal-hypertensive rats produced a 30% increase in blood flow. Plasma glucagon levels in portal-hypertensive rats were three times higher than in controls. Intra-arterial infusion of glucagon (at a rate that achieved the concentration measured in portal-hypertensive animals) produced a 20% reduction in intestinal vascular resistance. The results of these studies indicate that humoral factors, including glucagon, are primarily responsible for the hyperemia associated with portal hypertension.