Benoit J N, Barrowman J A, Harper S L, Kvietys P R, Granger D N
Am J Physiol. 1984 Nov;247(5 Pt 1):G486-93. doi: 10.1152/ajpgi.1984.247.5.G486.
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.
通过使用大鼠门静脉狭窄模型,研究了神经、代谢、物理和体液因素在与慢性门静脉高压相关的肠充血中的作用。与对照组相比,门静脉狭窄大鼠的肠血流量和脾髓压增加,而全身动脉压和总血管阻力降低。总血管阻力的降低完全是由于毛细血管前阻力下降,并伴有肠毛细血管压升高,这超过了急性门静脉压力升高到相同水平时所产生的压力。门静脉高压大鼠中15微米微球的动静脉分流比对照组高4倍。用门静脉高压大鼠的动脉血对对照肠制剂进行交叉灌注,使血流量增加了30%。门静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(以达到门静脉高压动物中测得的浓度的速率)使肠血管阻力降低了20%。这些研究结果表明,包括胰高血糖素在内的体液因素是门静脉高压相关充血的主要原因。