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Effect of release‐controlled nifedipine on portal hemodynamics in cirrhotic patients

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OBJECTIVE: To evaluate the therapeutic effect of release‐controlled nifedipine on portal hypertension. METHODS: Thirty‐two cirrhotic patients were enrolled to investigate, by using duplex Doppler ultrasonography, differences in portal hemodynamics before and after treatment with release‐controlled nifedipine (30 mg once per day). RESULTS: After taking nifedipine, the diameter, blood velocity and blood flow of the portal vein decreased, but only the change in velocity was statistically significant. After treatment, the congestion index increased, and the blood velocity and blood flow of the splenic vein significantly decreased. The resistance and pulsatile indices of the right hepatic and splenic arteries also decreased markedly. The total hepatic blood flow was elevated slightly and there were no significant changes in mean arterial pressure and heart rate. CONCLUSIONS: The resistance and pulsatile indices of the hepatic and splenic arteries are representative indices of portal resistance. Release‐controlled nifedipine may decrease portal pressure by the following mechanisms: (i) decrease of systemic blood pressure triggers the sympathetic reflex, leading to splanchnic artery constriction and portal blood flow reduction; (ii) dilatation of the portal vein and sinusoids leads to decrease portal resistance; and (iii) dilatation of the collateral veins. Nifedipine has no significant effect on systemic circulation in normotensive cirrhotic patients, therefore it has good prospects as a drug for clinical use in portal hypertension.
Title: Effect of release‐controlled nifedipine on portal hemodynamics in cirrhotic patients
Description:
OBJECTIVE: To evaluate the therapeutic effect of release‐controlled nifedipine on portal hypertension.
METHODS: Thirty‐two cirrhotic patients were enrolled to investigate, by using duplex Doppler ultrasonography, differences in portal hemodynamics before and after treatment with release‐controlled nifedipine (30 mg once per day).
RESULTS: After taking nifedipine, the diameter, blood velocity and blood flow of the portal vein decreased, but only the change in velocity was statistically significant.
After treatment, the congestion index increased, and the blood velocity and blood flow of the splenic vein significantly decreased.
The resistance and pulsatile indices of the right hepatic and splenic arteries also decreased markedly.
The total hepatic blood flow was elevated slightly and there were no significant changes in mean arterial pressure and heart rate.
CONCLUSIONS: The resistance and pulsatile indices of the hepatic and splenic arteries are representative indices of portal resistance.
Release‐controlled nifedipine may decrease portal pressure by the following mechanisms: (i) decrease of systemic blood pressure triggers the sympathetic reflex, leading to splanchnic artery constriction and portal blood flow reduction; (ii) dilatation of the portal vein and sinusoids leads to decrease portal resistance; and (iii) dilatation of the collateral veins.
Nifedipine has no significant effect on systemic circulation in normotensive cirrhotic patients, therefore it has good prospects as a drug for clinical use in portal hypertension.

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