Anesthesia and analgesia
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Anesthesia and analgesia · Jun 2008
The analgesic drug, tramadol, acts as an agonist of the transient receptor potential vanilloid-1.
Tramadol is an effective analgesic substance widely used in medical practice. Its therapeutic action have been mainly attributed to the activation of mu-opioid receptors as well as to the inhibition of neurotransmitter reuptake mechanisms and various voltage- and ligand-gated ion channels of the nociceptive system. As transient receptor potential vanilloid-1 (TRPV1, "the capsaicin receptor") has been shown to function as a central integrator molecule of pain sensation, our aim in the current study was to define the involvement of TRPV1 in the complex mechanism of action of tramadol. ⋯ Collectively, these findings strongly support the intriguing and novel concept that tramadol acts as an agonist of TRPV1. Considering that activation of TRPV1 on sensory neurons is followed by a local release of vasoactive neuropeptides and a marked desensitization of the afferent fibers (hence termination of pain sensation), our findings may equally explain both the desired analgesic as well as the often-seen, yet "unexpected," local side effects (e.g., initiation of burning pain and erythema) of tramadol.
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Anesthesia and analgesia · Jun 2008
Case ReportsDexmedetomidine sedation leading to refractory cardiogenic shock.
Dexmedetomidine is frequently used for deep sedation during electrophysiology procedures. We report a case where, presumably, the use of dexmedetomidine resulted in a patient's death. ⋯ We postulate that, in certain susceptible individuals, dexmedetomidine may lead to terminal complications. We therefore urge caution about using dexmedetomidine in the electrophysiology laboratory.
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Anesthesia and analgesia · Jun 2008
Subanesthetic doses of propofol induce neuroapoptosis in the infant mouse brain.
Drugs that block N-methyl-d-aspartate glutamate receptors or that promote gamma-aminobutyric acid type A inhibition trigger neuroapoptosis in the developing rodent brain. Propofol reportedly interacts with both gamma-aminobutyric acid type A and N-methyl-d-aspartate glutamate receptors, but has not been adequately evaluated for its ability to induce developmental neuroapoptosis. ⋯ We then administered graduated doses of propofol (25-300 mg/kg i.p.) and found that doses >or=50 mg/kg induce a significant neuroapoptosis response. We conclude that propofol induces neuroapoptosis at 1/4 the dose required for surgical anesthesia.