Effects of α1 and β-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension
Version of Record online: 10 MAR 2008
Journal of Gastroenterology and Hepatology
Volume 7, Issue 5, pages 449–454, October 1992
How to Cite
KOSHY, A., SEKIYAMA, T., HADENGUE, A., CERINI, R., BRAILLON, A. and LEBREC, D. (1992), Effects of α1 and β-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension. Journal of Gastroenterology and Hepatology, 7: 449–454. doi: 10.1111/j.1440-1746.1992.tb01018.x
- Issue online: 10 MAR 2008
- Version of Record online: 10 MAR 2008
- Accepted for publication 23 March 1992.
- collateral circulation;
- portal pressure;
- portal vein stenosis;
- splanchnic circulation.
In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an α1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 ± 1.0 (mean ± s.e.m.) to 10.1 ± 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 ± 2.1 to 11.7 ± 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 ± 16 to 73 ± 9 dyn s/cm5 x 103. Propranolol (4 mg), a β-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 ± 1.2 to 13.3 ± 0.9 mmHg while reducing portal tributary blood flow from 14.6 ± 1.5 to 11.0 ± 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 ± 7 to 103 ± 8 dyn s/cm5 x 103. Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 ± 1.0 to 13.3 ± 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 ± 14 to 74 ± 13 dyn s/cm5 x 103. Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.