Anesthesiology
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alpha 2-Adrenergic agonists such as clonidine produce behavioral analgesia and cardiovascular depression in animals, but clonidine's site of action in clinical analgesia and cerebrospinal fluid (CSF) pharmacokinetics have not been defined. ⋯ These data support previous studies in animals and provide the scientific rationale for this novel analgesic therapy. In comparison to the potent opioid alfentanil, epidural clonidine produces a similar degree of analgesia but less respiratory depression.
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The severity of spontaneous myocardial hypercarbic acidosis during cardiac arrest previously has been predictive of the likelihood of restoring spontaneous circulation. The present study investigated whether hypercarbia itself impairs cardiac resuscitation. Since coronary perfusion pressure is the overriding determinant of cardiac resuscitability, we used a porcine model of cardiac arrest in which coronary perfusion pressure was controlled. ⋯ Hypercarbia, in this experimental setting, was therefore a quantitative determinant of both myocardial resuscitability and the restoration of spontaneous circulation.
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Intraspinal clonidine injection produces analgesia free of respiratory depression, but also decreases blood pressure and causes sedation. Spinal neostigmine injection alone increases blood pressure in animals and enhances clonidine-induced analgesia. ⋯ These data are consistent with neostigmine's counteraction of clonidine-induced hypotension by a spinal muscarinic mechanism and support investigation of spinal alpha 2-adrenergic-cholinergic combinations for pain therapy.
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Spinal cord perfusion pressure may be reduced when sodium nitroprusside is used to control proximal aortic hypertension during thoracic aortic clamping. The effect of esmolol infusion on spinal cord perfusion pressure during thoracic aortic clamping is unknown. This study compares spinal cord perfusion pressure following control of proximal hypertension with either sodium nitroprusside or esmolol during thoracic aortic clamping. ⋯ Esmolol was associated with greater spinal cord perfusion pressure, but adverse hemodynamic effects, when compared with nitroprusside during thoracic aortic cross-clamping. When only surviving dogs (4 control, 5 esmolol, 6 nitroprusside) are considered, the incidence of neurologic deficit was greater in nitroprusside-treated dogs than in either control or esmolol-treated dogs. No difference in outcome was present when all dogs are considered.