Vorobioff J, Bredfeldt J E, Groszmann R J
Am J Physiol. 1983 Jan;244(1):G52-7. doi: 10.1152/ajpgi.1983.244.1.G52.
Two dissimilar hemodynamic hypotheses, the "backward flow" theory and the "forward flow" theory, have been advanced to define splanchnic hemodynamics in portal hypertension. An animal model with portal hypertension and high-grade portal-systemic shunting, the portal vein-stenotic rat, was studied to determine whether a hemodynamic picture compatible with either theory would develop. Splanchnic and systemic hemodynamics and portal-systemic shunting were measured by radioactive microsphere techniques. The portal-hypertensive rats (portal pressure, 12.8 +/- 0.5 vs. 8.3 +/- 0.4 mmHg) with greater than 95% portal-systemic shunting had a 60% increase in portal venous inflow (23.46 +/- 2.54 vs. 14.97 +/- 1.61 ml/min; P less than 0.01) with a concomitant 50% decrease in splanchnic arteriolar resistance (3.86 +/- 0.43 vs. 7.60 +/- 0.80 dyn . s . cm-5 . 10(5); P less than 0.001) compared with control rats. Cardiac index (391 +/- 17 vs. 250 +/- 20 ml . min-1 . kg-1) was elevated 50% (P less than 0.001), and total peripheral resistance (7.1 +/- 0.4 vs. 11.7 +/- 0.8 dyn . s . cm-5 . 10(4)) was decreased 60% (P less than 0.001). The resistance to portal blood flow in portal vein-stenotic rats (4.77 +/- 0.57 dyn . s . cm-5 . 10(4)) was similar to the resistance to portal blood flow in control rats (4.82 +/- 0.43 dyn . s . cm-5 . 10(4)), indicating that the hyperdynamic portal venous inflow, not resistance, provided the main impetus for maintaining the elevated portal venous pressure. The splanchnic hemodynamic observations directly support the forward flow theory of portal hypertension. The relation between splanchnic arteriolar resistance and total peripheral resistance (r = 0.67; P less than 0.01) indicated that the systemic hemodynamic parameters were secondarily altered by the splanchnic hemodynamic changes. This animal model of chronic portal hypertension gave evidence for a generalized splanchnic arteriolar vasodilation occurring in the presence of high-grade portal-systemic shunting.
两种不同的血流动力学假说，即“逆流”理论和“顺流”理论，已被提出用于定义门静脉高压症时的内脏血流动力学。我们研究了一种门静脉高压和高度门静脉-体循环分流的动物模型——门静脉狭窄大鼠，以确定是否会出现与这两种理论之一相符的血流动力学情况。通过放射性微球技术测量内脏和全身血流动力学以及门静脉-体循环分流情况。门静脉高压大鼠（门静脉压力为12.8±0.5 mmHg，而对照组为8.3±0.4 mmHg），其门静脉-体循环分流大于95%，门静脉血流流入量增加了60%（23.46±2.54 vs. 14.97±1.61 ml/min；P<0.01），同时内脏小动脉阻力降低了50%（3.86±0.43 vs. 7.60±0.80 dyn·s·cm⁻⁵·10⁵；P<0.001）。心脏指数（391±17 vs. 250±20 ml·min⁻¹·kg⁻¹）升高了50%（P<0.001），总外周阻力（7.1±0.4 vs. 11.7±0.8 dyn·s·cm⁻⁵·10⁴）降低了60%（P<0.001）。门静脉狭窄大鼠对门静脉血流的阻力（4.77±0.57 dyn·s·cm⁻⁵·10⁴）与对照大鼠对门静脉血流的阻力（4.82±0.43 dyn·s·cm⁻⁵·10⁴）相似，这表明门静脉血流高动力性增加而非阻力增加是维持门静脉压力升高的主要推动力。内脏血流动力学观察结果直接支持门静脉高压的顺流理论。内脏小动脉阻力与总外周阻力之间的关系（r = 0.67；P<0.01）表明，全身血流动力学参数是由内脏血流动力学变化继发改变的。这种慢性门静脉高压动物模型证明在高度门静脉-体循环分流情况下会发生全身性内脏小动脉血管舒张。
