On the basis of our results, the rate of multidrug-resistant UTIs may be very high in some ICUs in patients admitted with sepsis. This antimicrobial susceptibility/resistance should be determined, and a special antimicrobial treatment protocol should be planned based on the results for each ICU. The use of antibiotics for treating UTIs should be guided only through this protocol because of the different spectra of pathogens and susceptibility patterns in each ICU.

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Abstract:In this work we have studied the influences of nicotinic agents on the antinociception of morphine in formalin test. Nicotine (0.001-0.1 mg/kg) induced antinociception in mice in a dose-dependent manner in the early phase of formalin test, and also potentiated the morphine effect. The nicotinic receptor antagonist, mecamylamine (0.5 mg/kg), but not hexamethonium decreased the antinociception induced by nicotine (0.1 mg/kg) in both phases. The muscarinic receptor antagonist atropine ( 5 and 10 mg/kg) also decreased the response of nicotine. Mecamylamine, hexamethonium or atropine did not alter morphine antinociceptive response, while naloxone decreased responses induced by nicotine or morphine. The antagonists by themselves did not elicit any response in formalin test, however, high doses of mecamylamine tend to increase pain response. It is concluded that central cholinergic and opioid receptor mechanisms may be involved in nicotine-induced antinociception.Nicotine has many effects on the central nervous system as alters spontaneous activity, brain excitability, heart rate and blood pressure and causes convulsions, antidiuresis and antinociception (Martin et al. 1983). Nicotine is also known to release a number of neurotransmitters (Balfour 1982). In the central nervous system, nicotinic receptor stimulation enhances release of norepinephrine from the hippocampus (Hall & Turner 1972;Goodman 1974) and dopamine from the limbic system (Imperato et a/. 1986) and striatal slices (Goodman 1974; Giorguieff et al. 1979). It also increases the release of acetylcholine from the cortex (Chiou et a/. 1970; Nordberg ef al. 1989). Muscarinic receptors have been suggested to be involved in analgesia (Chen 1958;Herz 1962;Harris et al. 1968). Nicotine-induced antinociception has been suggested to have different mechanisms than cholinergic-induced antinociception, even different mechanisms for the antinociceptive action of nicotine have been indicated (Tripathi et a/. 1982). There is also good evidence that nicotine is involved in activating opioid system(s) (Balfour 1982;Davenport et al. 1990 However, some investigators (Sahley & Berntson 1979) suggested that nicotine antinociception is mediated through the release of acetylcholine, others (Phan et a/. 1973) did not find evidence for antagonism by atropine in mice. The mechanisms of nicotine-induced antinociception are not fully understood. Our previous study showed that nicotine could attenuate naloxone-induced jumping in morphine-dependent mice (Zarrindast & Farzin 1996). In the present investigation, the possible role of cholinergic and opioid receptor mechanisms in nicotine-or morphine-induced antinociception have been studied. Materials and MethodsAnimals. Male Swiss albino mice weighing 20-25 g were used in groups of 10 in a light-controlled room (lights on 7 a m -7 p.m.) constant temperature (21 k2"C) . Animals had free access to food and water except during the experiments. Groups of 7-14 mice were used. The experimental protocol was approved by the Research a...

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