Factors influencing hospital infection control policies in Italian hospitals.

A study was undertaken to determine the resources available in Italian hospitals for the control of nosocomial infections and the factors favouring a successful approach. During January-May 2000 a questionnaire about infection control was sent to the hospital health director of all Italian National Health System hospitals treating acute patients and with more than 3500 admissions in 1999. An active programme was defined as a hospital infection control committee (HICC) meeting at least four times in 1999, the presence of a doctor with infection control responsibilities, a nurse employed in infection control and at least one surveillance activity and one infection control guideline issued or updated in the past two years. There was a response rate of 87.5% (463/529). Almost fifteen percent (69/463) of hospitals had an active programme for Infection Control and 76.2% (353/463) had a HICC. Seventy-one percent (330/463) of the hospitals had a hospital infection control physician and 53% (250/463) had infection control nurses. Fifty-two percent (242/463) reported at least one surveillance activity and 70.8% (328/463) had issued or updated at least one guidance document in the last two years. The presence of regional policies [odds ratio (OR) 8.7], operative groups (OR 4.2), at least one full-time nurse (OR 4.6) and a hospital annual plan which specified infection control (OR 2.1) were statistically associated with an active programme in the multivariate analysis.

Evidence for both inhibitory and excitatory effects of morphine on gastric secretion in the rat.

The relationship between a wide range of doses of i.p. morphine and the effects of gastric secretion in several rat experimental models was investigated. In unoperated rats, morphine 5-15 mg/kg dose-dependently decreased gastric acidity, but an excitatory effect was observed with 0.5-1.5 mg/kg. A dose-dependent inhibition was also obtained in conscious pylorus-ligated rats with morphine 5-15 mg/kg, whereas no significant effects were found at lower doses. By contrast, acid concentration was enhanced with morphine 0.5-15 mg/kg in anaesthetized pylorus-ligated rats and in stomach lumen perfused rats. The changes of pepsin concentration correlated with the changes in gastric secretory volume. An increase in the volume was associated with a decrease in pepsin concentration, while pepsin amount per stomach was dose-dependently increased in all the conditions under which morphine increased gastric acidity. All the effects of morphine on acid and pepsin secretion were prevented by naloxone 1 mg/kg i.p. Overall results indicate that morphine may induce both excitatory and inhibitory effects on gastric secretion in the rat: these effects depend on the dose of morphine and the experimental conditions.

Effects of morphine on gastric ulceration, barrier mucus and acid secretion in pylorus-ligated rats.

The effects of intraperitoneal (IP) or intracerebroventricular (ICV) administration of morphine on acid and pepsin secretion, gastric ulceration and gastric bound mucoproteins were investigated in pylorus-ligated rats. Morphine, administered IP, produced a dose-dependent inhibition of the gastric secretion volume, acidity, pepsin output and bound mucoproteins. By contrast, the effect of morphine on gastric ulcers was not dose-dependent: a significant increase in gastric lesions was obtained with morphine 5 mg/kg IP. Naloxone IP prevented the effects of morphine on gastric secretory volume, acidity and pepsin output, but not on gastric mucus and ulcer score. ICV administration of morphine induced a dose-dependent inhibition of secretory volume, acidity and ulcer score, whereas no modification of gastric mucus was observed. Naloxone ICV prevented the effects of ICV morphine. Overall results suggest that morphine inhibits gastric secretion through both central and peripheral opioid receptors, whereas the inhibitory effect of morphine on bound mucus appears to be exerted on mucus synthesis through peripheral opioid receptors. This inhibitory effect on barrier mucus accounts at least in part for the gastric ulcerogenic action of morphine.

Pharmacological evidence of morphine-induced inhibition of gastric mucus synthesis in rats.

The effects of morphine, administered at graded doses by either intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) routes, have been investigated on acid and pepsin outputs, secretory volume, ulcer score, free and bound gastric mucus, in pylorus-ligated rats. Morphine i.c.v. induced a dose-dependent inhibition of secretory volume, acid and pepsin outputs and ulcer score, without modification of either free or bound mucoproteins. Naloxone i.c.v. had no effect per se, but prevented the inhibitory effects of i.c.v. morphine. Morphine i.p. produced a dose-dependent inhibition of gastric secretory volume, acid and pepsin outputs, as well as both free and wall-bound mucoproteins. By contrast, the effect of i.p. morphine on ulcer score was not dose-dependent: the dose of 5 mg/kg induced significant exacerbation of gastric lesions. Naloxone at 0.8 mg/kg i.p. had no effect per se, whereas at the dose of 4 mg/kg it significantly increased bound gastric mucus. The dose of 0.8 mg/kg antagonized the effects of morphine on gastric secretory volume, acidity, pepsin and ulcer score, but not on gastric mucus. These results indicate that morphine affects gastric acidity through central and peripheral opiate receptors, whereas gastric mucus synthesis appears to be regulated through peripheral opioid pathways.