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.

Action of somatostatin analogue (octreotide) on experimental hepatic encephalopathy in rats.

BACKGROUND/AIMS: We investigated the effect of a somatostatin analogue (octreotide) on hepatic encephalopathy in a rat model. Fulminant hepatic failure was induced by thioacetamide twice daily for 3 consecutive days. METHODOLOGY: Animals with hepatic encephalopathy grade III were divided into 2 groups. The groups received saline (control) or octreotide. In both groups the distance traveled in the open field activity, neurological score and mortality time were evaluated before and after the treatment. RESULTS: In the control group the motor activity was 13.7 +/- 6.4 and 12.9 +/- 5.5 cm/10 min, the neurological score was 8.4 +/- 0.9 and 8.5 +/- 1.3 before and after the treatment, respectively. In the octreotide group the motor activity was 11.4 +/- 5.0 and 10.4 +/- 3.5 cm/10 min, the neurological score was 8.8 +/- 1.5 and 8.6 +/- 0.9 before and after the treatment, respectively. Mortality times in the saline and octreotide group were 76.1 +/- 28.1 and 89.7 +/- 46.5 min, respectively. All parameters of this study were statistically not significant. CONCLUSIONS: This study demonstrated that somatostatin analogue, octreotide does not effect hepatic encephalopathy in an experimental rat model.

Does nimesulide induce gastric mucosal damage? "A double-blind randomized placebo-controlled trial".

BACKGROUND/AIMS: In this study, it was aimed to examine the effect of nimesulide, a selective inhibitor of cox-2 enzyme, to the gastric mucosa and to correlate its effect with aspirin. METHODOLOGY: This study was planned as double-blind, randomized and placebo-controlled. Mean age of voluntary persons (n = 32) was 42.3 +/- 2.7. Divided into 3 groups of volunteers were given randomized placebo (n = 10), aspirin (n = 10) (500 mg aspirin, Bayer) and nimesulide (n = 12) (100 mg mesulid, Pfizer) with 50 mL of water after 12 hours fasting period at 08.00 am. Gastroduodenoscopy was performed to the volunteers 3 hours after each therapy. RESULTS: Endoscopic scores of groups were; placebo: 0.20 +/- 0.13, aspirin: 2.8 +/- 0.46, nimesulide: 1.41 +/- 0.51. Lesion scores both in the aspirin group when compared with nimesulide and placebo groups (P < 0.00002, < 0.03), and in the nimesulide group when compared with the placebo group (P < 0.01) were significantly high. The positivity of Helicobacter pylori of groups was found; 67% in placebo, 72% in aspirin, 71% in nimesulide and there was no statistically significant difference in the groups. CONCLUSIONS: It was shown that nimesulide causes significantly serious gastric mucosal lesion when compared with placebo. The lesion score of nimesulide was found less than aspirin. According to the findings, nimesulide should be given carefully just as other analgesics due to the probability of causing gastric lesion.

The effect of cola consumption on oral mucosa in rats.

Drinks that contain phosphoric acid have been shown to have erosive effects and cola drinks are strongly acidic (pH 2.5). Gingivitis may be caused by dietary acids. Therefore, this study analyses the interaction of Coca Cola consumption and oral mucosal damage. Thirty rats were divided into three groups of 10. The animals received saline (pH 7.0) or HCl acid buffered to pH 2.6 or Coca Cola (pH 2.6) per os with 24-h free access to these solutions. A biopsy was taken from the front of the gingiva and the tongue. Histopathological analysis showed no specific lesion and there were no differences among saline, Coca Cola and HCl groups. Flow cytometric analysis was used to assess proliferative activity. In the HCl acid and Coca Cola groups, cell cycle analysis showed that the effects of Coca Cola and HCl acid in inducing oral mucosal damage are similar. In both Coca Cola [G0/G1, 70.38+/-7.9; S, 28.06+/-10.13; G2/M, 1.62+/-2.80; proliferative index (PI), 28.68+/-7.981 and HCI (G0/G1, 67.7+/-18.9; S, 27.8+/-17.5; G2/M, 4.4+/-3.8; PI, 30.9+/-20.98), the rat cell population G0/G1 and G2/M phases were found to be low (p < 0.05) and the cell population S and PI phases were found to be significantly elevated compared with the control group (p < 0.05) (G0/G1, 86.92+/-8.69; S, 9.8+/-1.21; G2/M, 3.25+/-2.87; P1, 13.2+/-8.7). This result was reflected in the proliferative index, which is used as a measure of the regeneration index. The data show that Coca Cola and HCl acid have similar proliferative and regenerative effects on oral mucosa, and it is possible that their regenerative effects are caused as a result of an irritant effect.

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.