Possible interactions between gentamicin, cefotaxime, ofloxacin and metronidazole with some non-depolarizing neuromuscular blocking drugs on rat phrenic nerve-hemidiaphragm preparation

The present study was conducted to investigate the neuromuscular blocking activity for gentamicin, cefotaxime, ofloxacin and metronidazole and the possible interaction with the nondepolarizing neuromuscular blockers; atracurium, rocuronium and vecuronium, using the rat phrenic nerve-hemidiaphragm preparation. Gentamicin and cefotaxime exerted concentration dependent neuromuscular blocking activities on the rat phrenic nerve-hemidiaphragm preparation. Also, they potentiated significantly the neuromuscular blocking activity of the used neuromuscular blocking agents, atracurium, rocuronium and vecuronium at most of the used concentrations. On the other hand, ofloxacin and metronidazole had no effect on the rat phrenic nerve hemidiaphragm preparation when used alone or with the used neuromuscular blockers. It was concluded that anesthesiologists should be aware of the neuromuscular blocking activity of gentamicin and cefotaxime when used perioperatively. Also, the use of ofloxacin and metronidazole, which appears to be safe and does not affect the action of neuromuscular blockers, still needs further investigations

Effect of intravenous anesthetics on endothelium-dependent vasodilatation in intact rats

In-vitro studies had shown that ketamine, thiopental and propofol attenuated endothelium-dependent vasodilatation in different species. In this study, the effect of intravenous anesthetics on endothelium-dependent and - independent vasodilatation was examined in intact rats. The effect of acetylcholine and sodium nitroprusside on mean arterial pressure [MAP] was examined in conscious and ketamine, thiopental, propofol and urethane anesthetized rats. MAP was significantly higher in ketamine-anesthetized rats than in conscious rats. There was no significant change in MAP in other anesthetized groups. Also, acetylcholine and sodium nitroprusside induced dose-dependent decrease in MAP in all groups. Ketamine and thiopental potentiated the vasodepressor effect of both acetylcholine and sodium nitroprusside in comparison to the conscious group. Propofol did not have any significant effect on the vasodepressor response to both acetylcholine and sodium nitroprusside. Urethane potentiated the effect of acetylcholine but not that of sodium nitroprusside induced vasodilatation. Ketamine and thiopental, but not propofol, potentiated both endothelium-dependent and independent vasodilatation in intact rats

Evaluation of 5- [phenylselenenyl] acyclouridine [psau], anovel uridine phosphorylase inhibitor

5-[phenylselenenyl] acyclouridine [PSAU] was recently synthesized as a potent and lipophilic inhibitor of uridine phosphorylase [UrdPase], the enzyme responsible for the catabolism of 5-fluoro- 2'-deoxyuridine [FdUrd] in many types of tumors that are deficient or have little thymidine phosphorylase activity. The effect of PSAU on modulating the antitumor efficacy of FdUrd was evaluated in vivo against murine clone tumor 26-10 growth in balb/c mice. Moreover, the profile of important enzyme activities involved in FdUrd metabolism was determined in order to understand the response of the tumors to the combinations of FdUrd and PSAU. Finally, the effect of the inhibitor as a modulator of plasma uridine and uracil concentrations and its effect on the bioavailability of uridine when co-administered with the uridine prodrug 2',3',5' tri-O-acetyluridine [TAU] was also investigated