Hemodynamic Properties of Portal Hypertansion in a Portal Vein Stenotic Rat Model.
- Author:
Tae Nyeun KIM
;
Jeong Ill SUH
;
Byeong Ik JANG
;
Moon Kwan CHUNG
;
Hyun Woo LEE
- Publication Type:Original Article
- Keywords:
Portal hypertension;
Hyperdynamic circulation
- MeSH:
Animals;
Arterial Pressure;
Cardiac Output;
Collateral Circulation;
Constriction, Pathologic;
Hemodynamics*;
Hypertension, Portal;
Ligation;
Liver;
Microspheres;
Models, Animal*;
Portal Pressure;
Portal Vein*;
Rats*;
Splanchnic Circulation;
Spleen;
Vascular Resistance
- From:Korean Journal of Medicine
1997;53(1):18-25
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Hemodynamic measurements of chronic portal hypertension were done to study the mechanisms that maintain high portal pressure despite well developed collateral circulations. METHODS: A prehepatic portal hypertensive rat model was produced by partial portal vein ligation. Cardiac output, organ blood flow and porto-systemic shunt were measured by radioisotope labeled microsphere methods, and vascular resistance was calculated by standard equation. RESULTS: There was a significant reduction in the weight of the liver and increase in the weight of the spleen in the portal stenotic rats. Porto-systemic shunting, representing development of the collateral circulations, was 96.7+/-0.6% in the portal stenosis group compared with 0.9+/-0.2% in the control group (p<0.01). Portal pressure was significantly increased in the portal stenosis group compared with the control group(12.8+/-1.4 vs. 6.5+/-0.6mmHg; p<0.01). Mean arterial pressure was significantly decreased in portal stenosis group compared with control group(101.4+/-2.5 vs, 129.9+/-3.9mmHg; p<0.01). In the portal stenosis group, cardiac output(135.7+/-8.0 vs. 111.0+/-4.2ml/min; p<0.01) and splanchnic organ blood flow (28.97+/-2.03 vs. 17.90+/-1.27ml/min, p<0.01) were significantly increased, with concomitant decrease in total peripheral vascular resistance(58.0+/-3.3 vs. 88.2+/-4.8 dyne sec/cm5 X 105; p<0.01) and splanchnic vascular resistance(2.54+/-0.20 vs. 5.47+/-0.33 dyne sec/cm5 X 105; p<0.01), However, the portal venous resistance was not significantly different in both groups of rats (3.57+/-0.31 vs. 3.03+/-0.38 dyne sec/cm5 X 105; p>0.05). CONCLUSION: The hemodynamic results of this study indicate that hyperdynamic status of systemic and splanchnic circulation was present in chronic portal hypertension and that the primary factor contributing to the persistently elevated portal venous pressure was the markedly increased portal venous inflow.
