Anesthesiology
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Most animal models of pancreatitis are short-lived or very invasive. A noninvasive animal model of pancreatitis developed in highly inbred rats by Merkord with symptoms persisting for 3 weeks was adopted in the current study to test its validity as a model of visceral pain in commercially available rats. ⋯ These results indicate that animals with the dibutyltin dichloride-induced experimental pancreatitis expressed serum, histologic, and behavioral characteristics similar in duration to those present during acute attacks experienced by patients with chronic pancreatitis. These findings and responsivity to morphine suggest the utility of this model developed in a commercially available strain of rats for study of persistent visceral pain.
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Activation of peripheral excitatory amino acid receptors decreases the duration of local anesthesia.
Postsurgical wound infiltration with the -methyl-d-aspartate receptor antagonist ketamine and bupivacaine can significantly prolong the duration of local anesthesia. One possible mechanism for this effect is that increased glutamate concentrations, caused by tissue damage, sensitize nociceptive primary afferent fibers through activation of peripheral excitatory amino acid receptors. ⋯ These results suggest that shortened lidocaine block durations observed after glutamate injection into the masseter muscle result from sensitization of afferent fibers as well as increases of peak extracellular water content and blood flow in masseter muscle. These effects of glutamate are mediated in part through activation of peripheral excitatory amino acid receptors.
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The authors investigated whether the sedative, or hypnotic, action of the general anesthetic dexmedetomidine (a selective alpha -adrenoceptor agonist) activates endogenous nonrapid eye movement (NREM) sleep-promoting pathways. ⋯ The authors propose that endogenous sleep pathways are causally involved in dexmedetomidine-induced sedation; dexmedetomidine's sedative mechanism involves inhibition of the LC, which disinhibits VLPO firing. The increased release of GABA at the terminals of the VLPO inhibits TMN firing, which is required for the sedative response.