We evaluated the effect of three carbapenems on gut colonization of mice by Candida albicans. A total of 150 Crl:CD1 (ICR) BR mice were fed chow containing C. albicans or regular chow. Both groups were subsequently treated either with one carbapenem or with normal saline for 10 days. Stool cultures to determine colonization by C. albicans were performed immediately before, at the end, and one week after the end of treatment. Candida-colonized mice that received carbapenems had substantially higher C. albicans concentrations than control animals fed C. albicans, especially if they received ertapenem. Mice fed regular chow and treated with the study antibiotics or saline did not have Candida in their stools. Candida was not detected in the internal organs of any group of mice.
Sir,Remifentanil, which is effective and easily titratable, with a rapid onset and offset of action, and no accumulation, is costeffective as it improves the quality of care, reduces the time spent on mechanical ventilation and reduces the length of stay in the Paediatric Intensive Care Unit (PICU). There have been reports, however, that remifentanil may cause hypotension in anesthetized children and decrease the cardiac index, mainly as a result of a fall in heart rate (1). In this communication, we report a sustained episode of severe bradycardia with suppressed myocardial depression after remifentanil infusion in a child during the weaning process. This is the first report of potentially life-threatening bradycardia after remifentanil infusion in a child.The patient, a 2-year-old boy, had been treated for 6 days in our PICU for a moderate closed head injury, was hemodynamically stable (cardiac frequency, >90 beats/min) and was receiving continuous midazolam and fentanyl infusions. Initial computed tomography (CT) scan showed mild brain edema and a small subdural hematoma; the intracranial pressure was kept below 15 mmHg and the cerebral perfusion pressure above 50 mmHg. After 5 days, the patient's clinical condition had improved significantly and the CT scan was normal. In order to facilitate rapid neurological assessment and to prepare the weaning process, the initial sedative/analgesic regimen was substituted with a continuous infusion of low-dose midazolam (0.1 mg/kg/h) and remifentanil (0.1 mg/kg/min). In less than 5 min, the patient's heart rate had decreased to 58 beats/min. Probable explanations, such as incorrect dilution or incorrect calculation of the infusion rate, were excluded and atropine 0.2 mg/kg was administered intravenously without an effect. The patient was normothermic and the electrocardiogram showed sinus bradycardia. An echocardiogram was performed revealing bradycardia with depressed shortening and ejection fractions (26 and 58%, respectively). Urgent magnetic resonance imaging did not show brain edema, hydrocephalus or any other expanding lesion. Although the arterial pressure remained stable at 96/46 mmHg, the heart rate decreased further to 42 beats/min. In view of the persistent bradycardia, a decision was made to discontinue remifentanil. Within 15 min, the heart rate had returned to its normal readings (more than 80 beats/min) and the myocardial contractility had improved. The patient was successfully extubated and, after uneventful neurological recovery, discharged to the ward.Remifentanil can cause bradycardia, either by parasympathetic activation or by other negative chronotropic effects. As parasympathetic inhibition by atropine does not totally prevent remifentanil's negative chronotropic effect, a direct negative chronotropic effect of remifentanil has been proposed (2). In accordance with this hypothesis, our patient developed severe bradycardia unresponsive to atropine after remifentanil infusion. Others have also reported severe bradycardia after remifentanil infusion in...
Background and Aims Fetal (FA) and perinatal asphyxia (PA) are major causes of neonatal morbidity and death worldwide. Although most studies are focused on the brain, FA and PA are known to be associated with multi-organ disease. Therefore, as part of the systemic impact, we aimed to investigate the hepatic inflammatory response after asphyxia. Methods A clinical relevant rat model was used, inducing global asphyctic insults to reflect the human pathophysiology. At different time points (acute and chronic) after FA and PA, we assessed hepatic inflammation, ceramide signaling and hepatocellular damage. Additionally, we assessed whether the combination of both insults (preconditioning) would have any protective effect on the liver. Results FA induced significant changes in inflammatory cytokines and ceramide metabolism genes with increased interleukin (IL)-1b mRNA at 6h, increased mRNA levels of IL-6, LAG1 homolog ceramide synthase 1 and ceramide transporters at 24h and finally, increased acid sphingomyelinase and sphingomyelin synthase 1 mRNA at 96h. Also PA induced an inflammatory response, with increased IL-6 and IL-10 levels 2h after birth. The combination of FA and PA (preconditioning) attenuated the inflammatory response, reflecting comparable IL-6 and IL-10 levels as control animals. 8 months after birth, no significant differences between groups were observed in hepatic mRNA levels for all cytokines and ceramide enzymes. Nevertheless, markers for hepatocellular damage, AST and ALP, showed increased levels when animals experienced FA and PA. Conclusions FA and PA induce acute changes in hepatic cytokine and ceramide levels which may lead to hepatocellular damage in later life.
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