Cryptococcal cellulitis in a lung-transplant recipient.
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Cellulitis↗
Biomedical subjects
N Sandor
Publications and source records attributed to N Sandor.
Effects of remifentanil on neutrophil adhesion, transmigration, and intercellular adhesion molecule expression.
BACKGROUND: Anaesthetic drugs are used for pain therapy and anaesthesia. Neutrophils play a significant role during the process of inflammation. The aim of the current study was to investigate the effects of remifentanil and fentanyl on neutrophil migration through endothelial cell monolayers, and on adhesion molecule expression. METHODS: After isolation of polymorphonuclear neutrophils (PMNL) we used a currently described migration assay. PMNL and/or endothelial cell monolayers (ECM) were pre-treated with remifentanil using clinically relevant, as well as higher and lower concentrations or relevant concentrations of fentanyl. RESULTS: Concentrations of remifentanil (50 ng/mL) similar to the relevant plasma concentration were able to inhibit PMNL migration through ECM significantly (migration compared to the control 82+/-7% SD; P<0.05), when both cell types were treated with the synthetic narcotic remifentanil. Fentanyl (30 ng/mL) showed a stronger inhibitory effect (migration compared to the control 67+/-9.2%; P<0.05). Endothelial cell adhesion molecule expression was reduced after either remifentanil or fentanyl. CONCLUSION: The results of the present investigation indicate that remifentanil influences interaction of ECM against human neutrophils. Compared to fentanyl, remifentanil seems to exhibit minor inhibitory effects on neutrophil migration.
Analgesics, Opioid↗
Cerebrocortical and medullary blood flow changes after general opiate receptor blockade during hemorrhagic shock in cats.
The effect of centrally induced opiate receptor blockade on regional cerebral blood flow (rCBF) was studied in anesthetized, ventilated cats during the course of hemorrhagic shock. The blood flow of the medulla and the parietal cortex was measured with the H2-gas clearance technique. Hemorrhagic shock was produced by lowering the systemic mean arterial pressure to 60 mmHg for 120 min by blood withdrawal. Central opiate receptor blockade was induced by 10 micrograms/kg intracerebroventricularly (i.c.v.) injected naloxone at the 60th min of the bleeding period. Cortical blood flow showed no improvement after i.c.v. naloxone administration. Medullary blood flow, however, increased significantly and approached the pre-bleeding control flow values following central opiate receptor blockade. The results indicate involvement of endogenous opioid mechanisms in the regulation of rCBF during hemorrhage and may provide an explanation for the previously described beneficial effects of naloxone in hemorrhagic shock.
Animals↗