Anesthesiology
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Comparative Study
Does the choice of local anesthetic affect the catecholamine response to stress during epidural anesthesia?
Previous work has established that 2-chloroprocaine epidural anesthesia has no effect on circulating plasma epinephrine concentrations in young, healthy, resting volunteers, and results in a decrease in norepinephrine concentration only when a level of analgesia to pinprick of C-8 is reached. The current study was performed to evaluate the possibility that this finding is unique to 2-chloroprocaine. ⋯ Epidural anesthesia with all three local anesthetic agents tested resulted in an incomplete sympathectomy in the resting state in healthy young men, judged by plasma catecholamine concentrations and cardiovascular variables minimally changed from resting baseline. Lidocaine epidural anesthesia did not attenuate the catecholamine response to CPT, indicating decreased blockade of sympathetic efferent neural traffic compared with bupivacaine and chloroprocaine epidural anesthesia.
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Supraventricular dysrhythmias are common during anesthesia, but have been incompletely investigated. Mechanisms may involve altered automaticity of subsidiary pacemakers and participation of vagal reflexes. The following hypotheses were tested: (1) shifts from the sinoatrial (SA) node to subsidiary pacemakers require intact vagal reflexes and (2) halothane sensitizes the heart to epinephrine-induced atrial pacemaker shifts. ⋯ Pacemaker shifts account for atrial dysrhythmias in the conscious state and during 1.25 MAC halothane with epinephrine, and require vagal participation. Halothane sensitizes the heart to epinephrine-induced atrial dysrhythmias. Atropine and halothane facilitate His bundle beats during exposure to epinephrine.
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In vitro studies have shown that isoflurane, enflurane, and halothane inhibit the hypoxic pulmonary vasoconstriction (HPV) with essentially the same potency. The aim of this study is to compare the effects of sevoflurane and isoflurane on HPV in constant-flow perfused rabbit lungs. ⋯ Sevoflurane inhibits the HPV response in a dose-related manner, and its potency is similar to that of isoflurane in vitro. Cyclooxygenase products do not mediate the inhibition of HPV by sevoflurane.
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To reduce the incidence of misleading assessments, and to derive criteria for critical spinal cord ischemia during thoracic or thoracoabdominal aortic aneurysm repair, the authors epidurally stimulated and recorded somatosensory evoked potentials (ESEP) below and above, respectively, the spinal segment at risk (electrospinogram). ⋯ Epidural somatosensory evoked potentials appeared to be a reasonable intraoperative predictor of postoperative neurologic outcome, and informs surgeons and anesthesiologists about the impending danger at an early state of the operation.
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Atrial dysrhythmias precede ventricular dysrhythmias during epinephrine-anesthetic sensitization, and may be caused by an altered relationship between automaticity of primary and subsidiary pacemakers. The following hypotheses were tested: (1) epinephrine-induced pacemaker shifts with enflurane or isoflurane require intact vagal reflexes and (2) these anesthetics sensitize the atrial myocardium to epinephrine-induced dysrhythmias. ⋯ With enflurane, epinephrine-induced atrial pacemaker shifts in chronically instrumented dogs are caused by direct depression of SA node automaticity or a relative increase of automaticity in subsidiary atrial pacemakers. With isoflurane, pacemaker shifts are caused by reflex-induced vagal suppression of SA node automaticity and escape of latent pacemakers. Enflurane sensitizes the atrial myocardium to dysrhythmias when combined with muscarinic blockade; isoflurane does not sensitize the atrium.