Hepato-gastroenterology · 1996
Effects of canrenoate potassium, an aldosterone antagonist on portal hemodynamics in patients with compensated liver cirrhosis.
Клиническое исследованиеКонтролируемое клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Koda M, Murawaki Y, Kawasaki H, Ikawa S
Аннотация
BACKGROUND/AIMS: Long-term administration of spironolactone is reported to reduce portal pressure in cirrhotic patients. We examined the effects of acute administration of canrenoate potassium, an aldosterone antagonist, on portal hemodynamics in compensated cirrhotic patients using noninvasive duplex Doppler ultrasonography.
MATERIALS AND METHODS: Baseline values were obtained in the fasting state, and then 200mg of canrenoate potassium in 10ml of saline solution was intravenously administered to 22 patients, whereas 10ml of saline solution was administered as a placebo to 8 patients.
RESULTS: The portal cross-sectional area, portal blood velocity and portal blood flow decreased by 5.3 +/- 9.2, 10.4 +/- 8.7% and 13.0 +/- 12.4%, respectively at the nadir 60min after administration and these decreases persisted until 120min. Placebo did not affect these parameters of portal hemodynamics. Eleven responders, who had a more than 10% drop in portal blood flow 60min after administration, had significantly higher levels of plasma aldosterone than 8 non responders who had less than 10% drop. The reduction rate of portal blood flow was closely correlated with plasma aldosterone level.
CONCLUSIONS: These findings suggest that aldosterone antagonist directly causes a reduction in portal blood flow, probably through inhibition of aldosterone-induced vasoconstrictive action.
MATERIALS AND METHODS: Baseline values were obtained in the fasting state, and then 200mg of canrenoate potassium in 10ml of saline solution was intravenously administered to 22 patients, whereas 10ml of saline solution was administered as a placebo to 8 patients.
RESULTS: The portal cross-sectional area, portal blood velocity and portal blood flow decreased by 5.3 +/- 9.2, 10.4 +/- 8.7% and 13.0 +/- 12.4%, respectively at the nadir 60min after administration and these decreases persisted until 120min. Placebo did not affect these parameters of portal hemodynamics. Eleven responders, who had a more than 10% drop in portal blood flow 60min after administration, had significantly higher levels of plasma aldosterone than 8 non responders who had less than 10% drop. The reduction rate of portal blood flow was closely correlated with plasma aldosterone level.
CONCLUSIONS: These findings suggest that aldosterone antagonist directly causes a reduction in portal blood flow, probably through inhibition of aldosterone-induced vasoconstrictive action.