Anesthesiology
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Changes in basal temperature of > or = 1 degree C (e.g., fever-induced hyperthermia or anesthesia-related hypothermia) are a common occurrence in neurologically impaired patients. The current study tested the hypothesis that temperature changes as small as 1 degree C or 2 degrees C would significantly alter post-ischemic functional neurologic outcome and cerebral histopathology. The hypothesis was tested in a canine model of transient, complete cerebral ischemia. ⋯ Small, clinically relevant changes in temperature (1 degree C or 2 degrees C) resulted in significant alterations in both postischemic neurologic function and cerebral histopathology. Assuming that our results are transferable to humans, the results suggest that, in patients at imminent risk for ischemic neurologic injury, body temperature should be closely monitored. Further, the clinician should aggressively treat all episodes of hyperthermia until the patient is no longer at risk for ischemic neurologic injury.
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Measurement of motor evoked responses to transcranial stimulation (tc-MER) is a technique for intraoperative monitoring of motor pathways in the brain and spinal cord. However, clinical application of tc-MER monitoring is hampered because most anesthetic techniques severely depress the amplitude of motor evoked responses. Because paired electrical stimuli increase tc-MER responses in awake subjects, we examined their effects in anesthetized patients undergoing surgery. METHODS. Eleven patients whose neurologic condition was normal and who were undergoing spinal or aortic surgery were anesthetized with sufentanil-N20-ketamine. Partial neuromuscular blockade (single-twitch height 25% of baseline) was maintained with vecuronium. Single and paired electrical stimuli were delivered to the scalp, and compound action potentials were recorded from the tibialis anterior muscle. The amplitude and latency of the tc-MERs were measured as the interval between paired stimuli was varied between 0 (single stimulus) and 10 ms. All recordings were completed before spinal manipulation or aortic clamping. ⋯ Application of paired transcranial electrical stimuli increases amplitudes and reproducibility of tc-MERs during anesthetic-induced depression of the motor system. The effect may represent temporal summation of stimulation at cortical or spinal sites. The results of this study warrant further clinical evaluation of paired transcranial stimulation.
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Visceral pain is an important component of many clinical pain states. The perispinal administration of drug combinations rather than a single agent may reduce side effects while maximizing analgesic effectiveness. The purpose of this study was to examine the nature of interactions between an alpha 2-adrenergic agonist (clonidine) and a mu-opioid agonist (morphine), a delta-opioid agonist ([D-Pen2, D-Pen5] enkephalin [DPDPE]), or a kappa-opioid agonist (U50,488H). ⋯ Spinal combinations of alpha 2-adrenergic and mu- or delta- but not kappa-opioid agonists may be beneficial in the control of visceral pain.
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Jugular venous catheters and near-infrared spectroscopy can measure cerebral venous blood hemoglobin oxygen saturation (SvO2). We used computer simulation to characterize the relation between Sv02 and cerebral metabolic rate for oxygen (CMR02) during hypothermic cardiopulmonary bypass (CPB). ⋯ High Sv02 observed during hypothermic CPB may indicate impaired oxygen transfer from hemoglobin to brain, not "luxury perfusion." The relation between Sv02 and CMR02 depends dramatically on the temperature of the patient. Sv02 per se may not be reliable index of normal CMR02 during hypothermic CPB.
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Visceral sensations are an important component of many clinical pain states. It is apparent that intrathecal pain relief may be more effective if appropriate combinations of drugs rather than a single agent can be used. The purpose of this study was to examine the relative contribution of opioid receptor subtypes to visceral antinociception using colorectal distension as a visceral pain model. ⋯ The results suggest that spinal mu- and delta- but not kappa-opioid receptors have a significant role in the modulation of visceral nociception induced by colorectal distension. In addition, the results indicate that activation of nonspinal kappa receptors may mediate visceral antinociception.