Effect of cisapride on portal haemodynamics in patients with liver cirrhosis using duplex Doppler ultrasonography.

PURPOSE: Cisapride, a benzimide derivative, is a gastrointestinal prokinetic agent without dopamine-antagonistic or cholinomimetic effects. This study aims at assessing the effect of cisapride oral administration on portal flow in patients with advanced post hepatitic cirrhosis using duplex Doppler ultrasound (US). METHODS: A total of 12 patients with post-hepatitic liver cirrhosis were included in the study. Duplex Doppler sonographic examinations were performed before and after treatment. The subjects received 10 mg cisapride before starting the measurement procedure and then three times a day for 2 days. Portal haemodynamics including vessel diameters (mm), mean flow velocities (cm/s), blood flows (ml/min) were investigated. RESULTS: Mean portal vein diameters, mean portal flow velocity and portal blood flow volume showed decreases of 18.6, 22.1 and 43.6% (P<0.001), respectively. After cisapride administration the portal vein diameter did not change in two patients and the portal vein velocity did not change in three patients. No significant change was found in systolic blood pressure, diastolic blood pressure or pulse rate after the administration of cisapride. CONCLUSION: In this study, it was demonstrated that oral administration of cisapride results in a significant reduction of portal blood flow but there were no changes in heart rate or systolic pressure in patients with cirrhosis of the liver.

Effect of omeprazole on gallbladder contraction in humans.

BACKGROUND/AIMS: Omeprazole causes hypergastrinemia because of the effects of prolonged complete suppression of acid secretion and also gastrin has an excitatory effect on gallbladder contraction. Therefore, we investigated the meal-induced gallbladder emptying in healthy subjects receiving omeprazole and compared them to controls. METHODOLOGY: Twenty healthy volunteers participated in this study. Gallbladder volume was measured by ultrasonography. After basal measurement, the volunteers received saline intravenously (i.v.) 2 cc (no:10) or omeprazole 20 mg i.v. (no:10). After 15 min the gallbladder volume was scanned at 15 min intervals for 60 min for each of the subjects. At the end of the period, all the subjects received a standard test meal (ensure 250 cal/250 mL), after 1 hour the gallbladder volumes were rescanned at 15 min periods for 60 min. RESULTS: Mean gallbladder volume in the omeprazole group was not significantly different during a 45 min period as compared to the baseline value. The residual gallbladder volume at the end of the 15th minute (43.9 +/- 5.6 mL), 30th minute (45.4 +/- 5.9 mL), 45th minute (40.5 +/- 6.1 mL) and 60th minute (40.5 +/- 6.1 mL) showed no significant differences in both the omeprazole group and the controls. Mean gallbladder volumes of both groups after meal intake were significantly lower during the 1-hour period as compared to the baseline value (P < 0.05). The mean volumes did not show any significant differences between the omeprazole group and the control subjects. CONCLUSIONS: Omeprazole did not change the gallbladder volume during fasting and the postprandial period as compared to the control group.

Portal and splanchnic haemodynamics in patients with advanced post-hepatitic cirrhosis and in healthy adults. Assessment with duplex Doppler ultrasound.

PURPOSE: To assess portal and splanchnic haemodynamics, and splanchnic vascular resistance in patients with advanced post-hepatitic cirrhosis and in healthy volunteers, by means of duplex Doppler ultrasound (US). MATERIAL AND METHODS: The duplex Doppler US examination was performed in 16 patients with cirrhosis and in 24 healthy volunteers. We investigated vessel diameters, mean flow velocities, and mean blood flows in the portal vein, the superior mesenteric artery (SMA), and the splenic artery (SA), and measured the resistive index values of SMA and SA. RESULTS: The mean portal venous blood flow in patients with cirrhosis (829 +/- 264 ml/min) was not statistically different from those in the volunteers (734 +/- 194 ml/min). The ratio of the SMA and SA blood flows (621 ml/min) to the portal venous blood flow (734 ml/min) was 0.85 in the control subjects. The mean portal venous blood flow (1261 ml/min) and the portal venous velocity (14.6 cm/s) were higher in the patients with recanalized para-umbilical veins than in the volunteers and in the patients without recanalized para-umbilical veins. The SMA and SA blood flows were significantly increased in patients with cirrhosis compared with volunteers. Splanchnic inflow (the sum of the SMA and SA blood flows) was higher than the portal blood flow in patients with cirrhosis except in the subjects with recanalized para-umbilical veins. SMA and SA resistive index values were significantly higher in these patients than in the volunteers. CONCLUSION: Splanchnic blood flow and splanchnic vascular impedance increased significantly in patients with advanced post-hepatitic cirrhosis. Splanchnic inflow must not exceed portal venous blood flow in patients with recanalized para-umbilical veins. Portal vein velocity and portal venous blood flow measurements alone are not useful parameters for discriminating patients with cirrhosis from healthy subjects.

Effect of verapamil on portal and splanchnic hemodynamics in patients with advanced posthepatitic cirrhosis using duplex Doppler ultrasound.

PURPOSE: To assess the effect of verapamil (80 mg) oral administration on portal and splanchnic hemodynamics in patients with advanced posthepatitic cirrhosis using duplex Doppler ultrasound (US). METHODS: Fourteen patients with post-hepatitic liver cirrhosis were included in the study. Duplex Doppler sonographic examinations were performed before, and 2-3 h after, 80 mg verapamil oral administration. Portal and splanchnic hemodynamics including vessel diameters (mm), mean flow velocities (cm/s), blood flows (ml/min), Doppler indices such as pulsatility and resistive indices (PI and RI), were investigated before and after verapamil administration. RESULTS: After verapamil administration; diameter of portal vein, splenic vein, and superior mesenteric artery (SMA) showed increase of 8%, 10%, and 7% (P < 0.05 to < 0.001), respectively. Increases of 20%, 38%, and 47% were found in blood flows (P < 0.05 to < 0.0001) with respect to the above vessels. Decreases of 17%, 10%, 11%, and 7% were found in SMA PI, SMA RI, splenic artery (SA) PI, and SA RI, respectively (P < 0.05 to < 0.0001). CONCLUSIONS: Verapamil appears to have splanchnic, portal, splenic, portocollateral and probably intrahepatic vasodilator effects in patients with advanced posthepatitic liver cirrhosis. Verapamil should be further investigated in the treatment of patients with advanced liver cirrhosis with prospective studies measuring portal and wedged hepatic pressure.