Increased nitric oxide (NO) release has been implicated in the pathogenesis of the hyperdynamic circulation in portal hypertension. NOS 3 (eNOS) causes NO release from the endothelium in response to physical stimuli, such as increased blood flow and shear stress. We evaluated the functional activity
Circulatory changes induced by portal venous diversion and mesenteric hypertension in rats
β Scribed by Dr. Samuel S. Lee; Kaj Johansen; Didier Lebrec
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 614 KB
- Volume
- 15
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
We studied the hemodynamics in four groups of rats with combinations of mesenteric hypertension and portal diversion. Operations created three groups with mesenteric hypertension and different degrees of portal venous diversion: mesenteric vein stenosis, portal vein stenosis and end-to-side portacaval anastomosis with mesenteric vein stenosis, the fourth group had only portacaval anastomosis. A control group had sham operations. Cardiac output, splanchnic blood flows and portosystemic shunt indices were measured with radioactive microspheres. Mesenteric venous pressures in the mesenteric-stenosed, portal-stenosed, portacaval-shunted and end-to-side portacaval anastomosis with mesenteric vein stenosis rats were, respectively, 13.5 f 0.6, 15.3 -C 0.7, 4.3 -C 0.5 and 13.0 f 0.9 mm Hg, which were all significantly different from controls: 8.3 -C 0.3 mm Hg. Portosystemic shunt indices were also significantly different from each other: controls, 0.4% & 0.02%; mesenteric-stenosed, 5.9% -C 2.3%; and portal-stenosed, 52.1% -C 4.9%. Cardiac output and splanchnic visceral blood flows were significantly increased in the portal-stenosed rats and the two groups with portacaval anastomoses, with the latter two groups having the highest values. The addition of mesenteric stenosis did not change the blood flows because mesenteric-stenosed rats did not differ from controls and end-to-side portacaval anastomosis with mesenteric vein stenosis rats did not differ from rats with portacaval anastomosis alone. These results suggest that mesenteric venous hypertension per se does not affect hemodynamics but that diversion of portal venous blood from the liver is a critical factor in the development of hyperkinetic circulation in portal hypertension. (HEPATOLOGY 1992;
π SIMILAR VOLUMES
and his associates are to be commended upon pursuing an original research idea in the field of portal hypertension. The commonest cause of portal hypertension is an increased resistance to portal blood flow. Another important cause results from an increased blood flow secondary to arteriovenous fist