The objective of this study was to determine the scolicidal effects of saline in different concentrations using different exposure times and to examine whether hypertonic saline can be used to irrigate the abdomen when there is a free intraperitoneal perforation of hydatid disease. Various concentrations of saline solutions (0.09%, 3.0%, 6.5%, 10%, 15%, 20%, 25%, 30%) were added to concentrated echinococcus granulosus sediments for the following times: 1, 2, 3, 4, 5, 10, 15, 30, 45, and 60 minutes. Normal (0.09%), 3.0%, and 6.5% saline resulted in high viability ratios after 60 minutes' exposure. Complete lethality for 10%, 15%, 20%, 25%, and 30% saline occurred at the end of 75, 10, 6, 3, and 3 minutes, respectively. During the second part of the study, 20 Sprague-Dawley rats were used for abdominal saline irrigation in four groups: 30% NaCl for 3 minutes; 20% NaCl for 6 minutes; intravenous isotonic dextrose water and furosemide plus 30% NaCl irrigation for 3 minutes; the same prophylactic therapy plus 20% NaCl irrigation for 6 minutes. Sodium and chloride values rose significantly (20-30%) shortly after hypertonic saline irrigation in each group (p < 0.01). Support with isotonic dextrose and furosemide before irrigation did not have any beneficial effect on biochemical values or mortality. The 24- and 48-hour mortality rates were 70% and 90%, respectively. These studies illustrate that the scolicidal effect of hypertonic saline is limited in low concentrations, but an increase in the concentration can augment its adverse effects. Peritoneal irrigation with hypertonic saline should be avoided for intraabdominal perforated hydatid disease. Therefore, we concluded that hypertonic saline is not a good scolicidal agent to prevent recurrence of hydatid disease.

Per-operative 50 mg/kg magnesium sulphate infusion is effective in reducing post-operative pain in patients undergoing LC.

NAC treatment had beneficial effects in sodium taurocholate-induced AP in rats. It reduced pancreatic tissue necrosis and lipid peroxidation. In our study, the mechanism underlying the beneficial effects of NAC seemed to be its antioxidant activity, either by increasing hepatic GPx activity, or by a direct scavenging effect on free radicals, thus enhancing the production of and/or inhibiting the degradation of nitric oxide.

The 5-hydroxytryptamine (5-HT) receptors mediating contraction in human isolated mesenteric arteries were characterized. Endothelium-denuded human isolated mesenteric arteries were used. 5-HT induced concentration-dependent contractions in mesenteric arteries (Emax, 127.37 +/- 7.61% of 80 mM KCl maximal contraction; pD2, 6.73 +/- 0.09 [-logEC50]). Sumatriptan, a selective 5-HT1B/1D receptor agonist, induced concentration-dependent contractions in some of the arteries (Emax, 61.82 +/- 10.04%; pD2, 6.56 +/- 0.21, n = 9) but not in the others (Emax < 5%, n = 13), suggesting that functional 5-HT1B/1D receptors exist in some but not in all mesenteric arteries. GR127935 (a selective 5-HT1B/1D receptor antagonist, 3 nM) inhibited sumatriptan-induced contractions in arteries in which sumatriptan responses were strong in an insurmountable manner. GR127935 (10 nM) also inhibited 5-HT responses and shifted the concentration-response curve of 5-HT to the right significantly (p < 0.05; pD2s were 6.54 +/- 0.18 and 5.93 +/- 0.11 in the presence of vehicle and GR127935, respectively). Ketanserin (0.01-1 microM) competitively antagonized 5-HT responses in human mesenteric arteries: pA2 value was 8.40 +/- 0.25 (slope of Schild regression, 1.43 +/- 0.18; r2, 0.98). Tropisetron (5-HT3 receptor antagonist) and prazosin (alpha1-adrenoceptor antagonist) did not affect the contractions induced by 5-HT. These results suggest that 5-HT2A and 5-HT1B/1D receptors, but not 5-HT3 and alpha1-adrenoceptors, are involved in the 5-HT-induced contractions in human isolated mesenteric arteries. Sumatriptan-induced and 5-HT1B/1D receptor-mediated responses vary greatly among patients.

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