BACKGROUND: Whether long-term octreotide treatment given to portal hypertensive rats could prevent or ameliorate peripheral vasodilatation and thereby modify sodium retention was investigated. METHODS: Starting at the time of partial portal vein ligation or sham operation, rats received a 4-day course of either octreotide (15 micrograms/kg in 5% dextrose in water) or placebo (5% dextrose in water) subcutaneously every 8 hours. RESULTS: In portal hypertensive rats, octreotide induced a 13% increase in mean arterial pressure (P < 0.01) and a 19% increase in total peripheral resistance (P < 0.01). Octreotide treatment induced a decrease in extracellular sodium space (22Na injection) (34.2 +/- 0.5 vs. 36.7 +/- 0.4 mL/100 g; P < 0.01) without changes in serum sodium level. In addition, octreotide treatment significantly reduced portal pressure as well as glucagon levels and plasma renin activity. In contrast, octreotide treatment had no effect on mean arterial pressure and extracellular sodium space in shamoperated rats. CONCLUSIONS: Long-term octreotide treatment ameliorated peripheral vasodilatation and sodium retention only in portal hypertensive rats. These findings suggest that in portal hypertension sodium retention can be modified by pharmacological agents that affect peripheral vasodilatation. The specificity of octreotide's effect sheds additional light into the vasodilatory syndrome associated with portal hypertension in liver diseases.
BACKGROUND: Whether long-term octreotide treatment given to portal hypertensiverats could prevent or ameliorate peripheral vasodilatation and thereby modify sodium retention was investigated. METHODS: Starting at the time of partial portal vein ligation or sham operation, rats received a 4-day course of either octreotide (15 micrograms/kg in 5% dextrose in water) or placebo (5% dextrose in water) subcutaneously every 8 hours. RESULTS: In portal hypertensiverats, octreotide induced a 13% increase in mean arterial pressure (P < 0.01) and a 19% increase in total peripheral resistance (P < 0.01). Octreotide treatment induced a decrease in extracellular sodium space (22Na injection) (34.2 +/- 0.5 vs. 36.7 +/- 0.4 mL/100 g; P < 0.01) without changes in serum sodium level. In addition, octreotide treatment significantly reduced portal pressure as well as glucagon levels and plasma renin activity. In contrast, octreotide treatment had no effect on mean arterial pressure and extracellular sodium space in shamoperated rats. CONCLUSIONS: Long-term octreotide treatment ameliorated peripheral vasodilatation and sodium retention only in portal hypertensiverats. These findings suggest that in portal hypertensionsodium retention can be modified by pharmacological agents that affect peripheral vasodilatation. The specificity of octreotide's effect sheds additional light into the vasodilatory syndrome associated with portal hypertension in liver diseases.
Authors: M Sàbat; C Guarner; G Soriano; O Bulbena; M T Novella; J Ortiz; E Ricart; C Villanueva; J Rosello; J Rodríguez; J Balanzó Journal: Dig Dis Sci Date: 1998-10 Impact factor: 3.199