| Research Abstract |
For the last decade, alpha-2 adrenergic agonists such as clonidine have been extensively used for clinical anesthesia to provide better patients' care in perioperative periods. When given clonidine preoperatively as a premedicant for patients undergoing anesthesia and surgery it Would reduce requirements of inhalational and intravenous anesthetic agents, and opioids, provide stable hemodynamics, and enhance the action of vasopressors such as phenylephrine. When clonidine given intrathecally, it would produce a potent spinal antinociception and prolonged spinal anesthesia with local anesthetics. To elucidate some of mechanism(s) and roles for clinical efficacy of alpha-2 adrenoceptor agonists, we have done several studies, Using the cranial window technique, we found that clonidine produces cerebral vasoconstriction via activation of alpha-2 adrenoceptors of the pial vessels in a dose-related manner. When alpha-2 adrenoceptor agonists, clonidine, dexmedetomidine and tizanidine, were given into the epidural space or intravenously in rats, they produced almost 5 times greater antinociception with epidural administration as compared with those with their intravenous administration. The rank of order for their spinal antinociceptive action was identical with those of alpha-2 adrenergic receptor binding affinity of spinal' cord and brain. Brain alpha-2-adrenoceptors are up-regulated in morphine dependent guinea pigs and clonidine could reduced opiate withdrawal sings in morphine-dependent animals. We also found that patients given clonidine as premedicant showed a significantly augmented responses to ephedrine in propofol anesthesia to reduce epinephrine test dose for epidural anesthesia. Also we found that clonidine premedication modifies responses to alpha1- and beta-_2 adrenoceptor agonists and baroreflex sensitivity.
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