BACKGROUND: The addition of epinephrine to local anesthetics has been known to prolong the duration of neural blokade and to increase the intensity of analgesia, but underlying mechanisms are unclear. This study was designed to investigate electrophysiologically the analgesic effects of epinephrine and its interaction with tetracaine. METHODS: Whole cell patch clamp recordings were made from acutely dissociated neurons from adult rat dorsal root ganglion (DRG). Using voltage clamp method, we compared the IC50 values of tetracaine for Na+ and Ca2+ channel suppression in the absence and presence of a fixed dose of epinephrine. Action potentials evoked by current pulses were also investigated to evaluate the effect of tetracaine and epinephrine on the excitability of DRG neurons. RESULTS: Clinical doses of epinephrine did not alter the dose-response curves of tetracaine for peak Na+ and Ca2+ channel current, but the amplitude of action potential spikes was reduced and firing rates evoked by sustained current pulse increased. The addition of epinephrine did not affect the changes of action potential parameters caused by tetracaine alone. CONCLUSIONS: The ability of epinephrine to increase the intensity of analgesia induced by tetracaine seems more likely due to an analgesic action at the level of spinal cord rather than a direct analgesic action at a level of primary sensory neurons. Local vasoconstriction and stimulation of descending inhibitory system via alpha-adrenergic pathway may play a role.
Action Potentials ; Adult ; Analgesia ; Anesthetics, Local ; Animals ; Diagnosis-Related Groups ; Epinephrine* ; Fires ; Ganglia, Spinal* ; Humans ; Inhibitory Concentration 50 ; Neurons ; Rats ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerve Roots* ; Tetracaine* ; Vasoconstriction

No abstract available.
Diabetes Mellitus, Type 2* ; Humans

Esophageal perforation continues to be associated with high mortality - 20% to 30% - despite advances in surgical techniques. Traditional surgery has been the mainstay of treatment for perforation, but recent advances in endoscopic closure devices has increased therapeutic options for selected patients. Our patient had a fishbone-induced esophageal perforation. He was treated successfully with endoscopic clipping, antibiotics and parenteral nutrition. We report this case and provide a review of the relevant literature.
Anti-Bacterial Agents ; Esophageal Perforation ; Foreign Bodies ; Humans ; Parenteral Nutrition

BACKGROUND: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglia (SCG), and these nerves may influence the cerebral blood flow. The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats that were subjected to focal cerebral ischemia/reperfusion injury. METHODS: Eighty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of two groups (the ropivacaine group and a control group). In all the animals, brain injury was induced by middle cerebral artery (MCA) reperfusion that followed MCA occlusion for 2 hours. The animals of the ropivacaine group received 30microl of 0.75% ropivacaine, and their SCG. Neurologic score was assessed at 1, 3, 7 and 14 days after brain injury. Brain tissue samples were then collected. The infarct ratio was measured by 2.3.5-triphenyltetrazolium chloride staining. The terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeled (TUNEL) reactive cells and the cells showing caspase-3 activity were counted as markers of apoptosis at the caudoputamen and frontoparietal cortex. RESULTS: The death rate, the neurologic score and the infarction ratio were significantly less in the ropivacaine group 24 hr after ischemia/reperfusion injury. The number of TUNEL positive cells in the ropivacaine group was significantly lower than those values of the control group in the frontoparietal cortex at 3 days after injury, but the caspase-3 activity was higher in the ropivacaine group than that in the control group at 1 day after injury. CONCLUSIONS: The study data indicated that a superior cervical sympathetic ganglion block may reduce the neuronal injury caused by focal cerebral ischemia/reperfusion, but it may not prevent the delayed damage.
Amides ; Animals ; Apoptosis ; Blood Vessels ; Brain ; Brain Injuries ; Caspase 3 ; DNA Nucleotidylexotransferase ; Ganglia, Sympathetic ; Humans ; In Situ Nick-End Labeling ; Infarction ; Male ; Middle Cerebral Artery ; Neurons ; Neuroprotective Agents ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Superior Cervical Ganglion