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OBJECTIVE: To evaluate the cardiovascular response to short-term prone positioning in neonates. STUDY DESIGN: In this prospective study, we continuously monitored heart rate (HR), stroke volume (SV) and cardiac output (CO) by electrical velocimetry in hemodynamically stable neonates in each of the following positions for 10 min: supine, prone and back-to-supine position. Skin blood flow (SBF) was also continuously assessed on the forehead or foot using Laser Doppler technology. Systemic vascular resistance (SVR) index was calculated as mean blood pressure (BP)/CO. Data were analyzed using repeated measures analysis of variance. RESULTS: Thirty neonates (gestational age: 35±4 weeks; postmenstrual age: 36±3 weeks) were enrolled. HR did not change in response to positioning. However, in prone position, SV, CO and SBF decreased and SVR index increased from 1.5±0.3 to 1.3±0.3 ml kg(-1) (mean ±s.d., P<0.01), 206±44 to 180±41 ml kg(-1) min(-1) (P<0.01), 0.54±0.30 to 0.44±0.29 perfusion units (P<0.01) and 0.25±0.06 to 0.30±0.07 mm Hg ml(-1) kg(-1) min(-1) (P<0.01), respectively. After placing the infants back-to-supine position, SV, CO, SBF and SVR index returned to baseline. The above pattern of cardiovascular changes was consistent in vast majority of the studied neonates. CONCLUSIONS: Short-term prone positioning is associated with decreased SV, CO and SBF and increased calculated SVR index.

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Pulmonary edema and local anesthetic toxicity are potential complications of the use of large volumes of infiltrate during lipoplasty. In most patients, these unfavorable developments are prevented by physiologic and pharmacologic mechanisms. The latter may be inadequate in some patients, however, and it is imperative to identify and monitor those patients to minimize their high risk for fluid overload or CNS toxicity.

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An electrical-equivalent circuit model of the cerebrovascular system is proposed, components of which directly relate to cerebrospinal fluid (CSF) compartment compliance and the determination of intracranial pressure (ICP). The model is based on three premises: 1) Under normal, physiologic conditions, the conversion of pulsatile arterial to nonpulsatile venous flow occurs primarily as a result of arterial compliance. Nonpulsatile venous flow is advantageous because less energy is required to maintain constant flow through the venous system, which comprises 75-80% of total blood volume. 2) Dynamic CSF movement across the foramen magnum is the primary facilitator by which intracranial arterial expansion occurs. Interference of the displacement of CSF during systole results in pulsatile venous flow and increased venous flow impedance. 3) Tissue hydrostatic pressure (here defined as ICP) is a dependent variable which is a function of capillary hydrostatic pressure and the osmotic/oncotic pressure gradient created by the blood-brain-barrier (BBB). An interference of transcranial CSF movement results in a decrease in cerebral blood flow (CBF) due to inertial effects impeding pulsatile venous flow. Feedback regulation in response to this decreased CBF leads to arteriolar vasodilatation (decreased resistance), thereby lowering the pressure difference between internal carotid and capillary pressures. Assuming no changes in the BBB potential, ICP increases linearly as capillary pressure increases.

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OBJECTIVE: We evaluated a combined technique designed for procedures requiring intraoperative language mapping. We planned to induce general anesthesia with endotracheal intubation and hyperventilation and then to awaken and extubate the patient for speech testing. After the latter, endotracheal reintubation and general anesthesia were planned. METHODS: With the patient under intravenously induced sedation, we topically anesthetized the airway with lidocaine that was delivered through a spraying catheter. Fiberoptic endotracheal intubation was then performed on the awake patient, using a modified endotracheal tube. General anesthesia with intravenous propofol or sodium thiopental was induced, the patient's head was attached to a Mayfield holder, and the pin and operative sites were infiltrated with 0.5% bupivacaine with epinephrine. In anticipation of speech mapping, general anesthesia was discontinued and lidocaine was injected into the catheter that was spirally attached to the endotracheal tube. After speech mapping, the awake patients were endotracheally intubated, guided with the fiberoptic laryngoscope or tube changer, and general anesthesia was induced and maintained until termination of the surgery. RESULTS: We did not observe any complications, such as coughing or head movements, during the preparation for general anesthesia, awakening and endotracheal extubation for speech mapping, and post-testing reintubation or induction of general anesthesia. CONCLUSION: The combined technique that we describe abolished the potential discomfort of surgical stimulation on a sedated patient, reduced the duration of wakefulness, and provided a secure airway and the means to hyperventilate our patients before dural opening.

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PURPOSE: Our objective was to anatomically define the anastomoses between cervical and carotid arterial distributions (the carrefour) in the rabbit and to assess the contribution of these collaterals to cortical blood flow (CBF) during cerebral ischemia. METHODS: Angiography was carried out in six rabbits with basilar artery occlusion using selective contrast injection into the right subclavian, external carotid, and internal carotid arteries. Anastomoses were corroborated with methacrylate vascular casts prepared in five additional rabbits. CBF was measured in eight rabbits by H2 clearance after basilar artery occlusion and again after bilateral common carotid artery occlusion. Cortical DC potential was measured during ischemia in these rabbits and in another 19 rabbits after additional occlusion of the cervical collateral arteries. RESULTS: A network of anastomoses between superficial and ascending cervical, superior intercostal, vertebral, and occipital arteries was found by angiography and corrosion casts. Additional communications in the ophthalmic, ethmoidal, and cerebellar arterial distributions are described. These pathways were found to supply a mean of 15 +/- 7 mL/100 g per minute residual CBF during three-vessel ischemia, or 24% of the preischemic CBF. Ischemic depolarization of DC potential occurred in seven of the eight rabbits with collateral CBF at a mean latency of 2.64 +/- 0.59 minutes and at 1.71 +/- 0.09 minutes in those without. CONCLUSION: The suboccipital collateral network of the rabbit resembles that of humans and can contribute significantly to CBF during ischemia. The results suggest that this model may be useful for evaluating methods of optimizing hemodynamic control of the anastomoses in situations such as those encountered during endovascular therapy.

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The laryngeal nerves are at risk during thyroid surgery, and several techniques have been described for their intraoperative identification to minimize potential damage. Nerve protection is based on the electromyographic recording from the muscles innervated by the laryngeal nerves, and that electrical activity is picked up by various techniques. We evaluated an electrode attachment to the endotracheal tube that provides a stable method for continuous recording of the laryngeal electromyogram. In addition, we tested various modalities of electrical stimulation in the region where the nerves are located, identified the most reliable evoked electromyographic activity, and characterized the wave form and latency. The results, obtained in 28 patients scheduled for thyroid and parathyroid surgery, indicate that the technique of recording from electrodes attached to the endotracheal tube is safe and reliable. Insulated bipolar forceps or a monopolar electrode was used to deliver low-voltage pulses (1 to 3 V) at 1 to 2 pulses/s generated by either battery-operated or optically isolated stimulators. The most unequivocal recordings were obtained with the monitoring equipment set to the nerve-conduction velocity modality, with the sweep set at 2 msec/cm. The technique clearly differentiated the evoked electromyographic responses obtained from the superior or recurrent laryngeal nerve and was easily performed with no perioperative complications.

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To determine if the previously reported limitation of i.v. lidocaine in facilitating recovery from cerebral ischemia was related to an effect on ischemic depolarization, we recorded cortical DC potential, electrocorticogram (ECoG) or EEG, and evoked potentials in rabbits subjected to either 3 or 5 min of complete ischemia. Three control animals undergoing 3 min of ischemia and all animals subjected to 5 min of ischemia were continuously monitored under anesthesia for 24 h, at which time the brains were processed for neocortical histology. Complete ischemia was produced by occlusion of the basilar artery and cervical collateral vessels followed by transient snare occlusion of the brachiocephalic trunk. In control animals of either ischemic duration, the onset of ischemic depolarization occurred at 102 +/- 5 s (n = 18). In animals receiving 0.2 mg/kg/min lidocaine infusion, the negative DC shift was delayed to 182 +/- 28 s (n = 7) in animals with 3-min ischemia and 195 +/- 15 s (n = 9) in lidocaine animals with 5 min ischemia (p < .01 and p < .0005 respectively, compared to controls of the same ischemic duration). In 3-min ischemia, lidocaine also reduced the amplitude of the DC shift from 8.9 +/- 0.4 mV to 4.6 +/- 1.1 mV (p < .005), whereas in 5-min ischemia there was no significant difference in the amplitude of the shift between lidocaine and control animals (11.1 +/- 1.4 and 12.7 +/- 1.0 mV, respectively). Lidocaine shortened the isoelectric EEG duration and hastened the recovery of evoked potentials in animals with 3-min ischemia; with 5-min ischemia, however, there was no significant difference in the recovery of either type of electrical activity between control and lidocaine-treated animals. Significant correlations were found between the recovery of cortical electrical activity (both spontaneous and evoked) and the amplitude or integral of the ischemic depolarization shift (p < .001 in each case). Postischemic epileptiform bursts accompanied by negative DC shifts occurred in 3/7 controls and 4/7 lidocaine animals after reperfusion for > 12 h following 5-min ischemia. There was no significant difference in the degree of cortical neuronal injury or status spongiosus found between lidocaine and control animals subjected to 5-min ischemia and 24 h reperfusion. Cortical injury in control animals with 3-min ischemia was negligible and not significantly different from sham-operated animals.(ABSTRACT TRUNCATED AT 400 WORDS)

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To evaluate physiologic responses to mild perianesthetic hypothermia, we measured tympanic membrane and skin-surface temperatures, peripheral vasoconstriction, thermal comfort, and muscular activity in nine healthy male volunteers. Each volunteer participated on three separate days: 1) normothermic isoflurane anesthesia; 2) hypothermic isoflurane anesthesia (1.5 degrees C decrease in central temperature); and 3) hypothermia alone (1.5 degrees C decrease in central temperature) induced by iced saline infusion. Involuntary postanesthetic muscular activity was considered thermoregulatory when preceded by central hypothermia and peripheral cutaneous vasoconstriction. Tremor was considered normal shivering when electromyographic patterns matched those produced by cold exposure in unanesthetized individuals. During postanesthetic recovery, central temperatures in hypothermic volunteers increased rapidly when residual end-tidal isoflurane concentrations were less than or equal to 0.3% but remained 0.5 degree C less than control values throughout 2 h of recovery. All volunteers were vasodilated during isoflurane administration. Peripheral vasoconstriction occurred only during recovery from hypothermic anesthesia, at end-tidal isoflurane concentrations of less than approximately 0.4%. Spontaneous tremor was always preceded by central hypothermia and peripheral vasoconstriction, indicating that muscular activity was thermoregulatory. Maximum tremor intensity during recovery from hypothermic anesthesia occurred when residual end-tidal isoflurane concentrations were less than or equal to 0.4%. Three patterns of postanesthetic muscular activity were identified. The first was a tonic stiffening that occurred in some normothermic and hypothermic volunteers when end-tidal isoflurane concentrations were approximately 0.4-0.2%. This activity appeared to be largely a direct, non-temperature-dependent effect of isoflurane anesthesia. In conjunction with lower residual anesthetic concentrations, stiffening was followed by a synchronous, tonic waxing-and-waning pattern and spontaneous electromyographic clonus, both of which were thermoregulatory. Tonic waxing-and-waning was by far the most common pattern and resembled that produced by cold-induced shivering in unanesthetized volunteers; it appears to be thermoregulatory shivering triggered by hypothermia. Spontaneous clonus resembled flexion-induced clonus and pathologic clonus and did not occur during hypothermia alone; it may represent abnormal shivering or an anesthetic-induced modification of normal shivering. We conclude that among the three patterns of muscular activity, only the synchronous, tonic waxing-and-waning pattern can be attributed to normal thermoregulatory shivering.

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The effects of a cholinergic antagonist (scopolamine) and agonist (physostigmine) on the auditory middle latency evoked responses (MLRs) were studied in 7 normal male volunteers. Scalp recordings were made from a central (Cz) electrode referenced to linked ear lobes on one channel and to a non-cephalic, sternovertebral reference on a second channel. Three components were statistically analyzed for changes in latency and amplitude: Pa, with peak positivity in the 25-40 msec latency range, Nb, with peak negativity 40-50 msec, and P1, with peak positivity 50-65 msec. Control recordings included responses to click rates of 1, 5, 8 and 10/sec; as has been previously reported, P1 showed a marked decrease and disappeared at the faster rates of stimulation whereas Pa showed no change in amplitude. Intravenous injections of scopolamine resulted in a rapid and complete disappearance of P1 and a slight increase in Pa; concurrently, the subjects reported feeling drowsy but were awake with eyes open through the recordings. Subsequent injections of physostigmine resulted in a rapid reversal of the scopolamine effects so that the subjects became alert, Pa decreased, and P1 reappeared and increased to control amplitudes. Rapid click rates caused P1 to diminish, as in the control period, indicating a common P1 recovery cycle in both the control and physostigmine conditions. These data are discussed in terms of the hypothesis that the P1 generator system is comprised of a cholinergic brain-stem-thalamic component of the ascending reticular activating system.

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We recently reported that the continuous infusion of a low dose of lidocaine accelerated the recovery of the electroencephalogram and somatosensory evoked potentials after 20 min of incomplete cerebral ischemia in a single carotid artery preparation in the rabbit. In contrast, the recovery of the electroencephalogram and the auditory evoked potentials was minor on a comparable animal preparation subjected to 5 min of almost complete global ischemia. In the present study, we tested the hypothesis that the facilitatory effect of lidocaine on neuroelectrical recovery is of importance only during a certain combination of duration and severity of an ischemic episode. Similar to the previous studies, the rabbits had one carotid and both vertebral arteries permanently occluded and the other carotid artery reversibly clamped during the ischemic test. In the halothane-anesthetized animals, we monitored mean arterial pressure, carotid stump pressure, cerebral blood flow, auditory evoked potentials, and the electroencephalogram, before and for 90 min after 3 min of complete ischemia. The amplitude of the P1 wave (latency of 10 ms) of the auditory evoked potentials recovered more rapidly than on the previous 5 min preparation and returned towards the control amplitude more completely (p <0.05) in the lidocaine group. More importantly, the amplitude of the P2 wave (latency of 25 ms) recovered only 11% in the control group and 55% (p <0.05) in the lidocaine-infused animals. Comparable effects were observed in the early recovery of electroencephalographic activity during reperfusion. The present findings support the hypothesis that lidocaine may facilitate the recovery of the electroencephalogram and the evoked potentials only when an ischemic episode is below a certain combined level of duration and severity. The accelerating effect of lidocaine on postischemic neuroelectrical recovery was observed using a low dose of the drug, and it was not associated with changes in hemodynamic or cerebrovascular parameters or of blood composition. The latter suggests that the reported action may be related to some specific property of the local anesthetic action of lidocaine, such as blockade of axonal Na channels.

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In the present experiments, we tested the effect of a continuous infusion of low-dose lidocaine on the time course of neuroelectrical recovery after an episode of almost complete ischemia in our single carotid artery model in the rabbit. In this preparation, carotid clamping elicited suppression of the electroencephalogram in less than 15 s, a drop in carotid stump pressure below 15 mm Hg, and evidence of minimal cerebral collateral perfusion in postmortem studies. We monitored mean arterial pressure, cerebral blood flow, carotid stump pressure, electroencephalogram, and auditory evoked potentials during three periods: control (30 min), ischemia (5 min), and reperfusion (90 min). Low-dose lidocaine (0.05 mg/kg/min) was continuously infused throughout the three periods. We specifically measured two peaks of the auditory evoked potentials and the most important finding was that the early wave (P1) partially recovered: to 35-40% in the control and to 64% in the lidocaine group (p <0.05 after 90 min). In contrast, the recovery of the later wave (P2) was very incomplete in both groups, and reached only 25-30% of the control amplitude. Similarly, the electroencephalogram of all of the rabbits failed to return to the control pattern but more animals in the lidocaine group (p <0.05) showed fewer pathological waves at the end of reperfusion. The present results indicate that a low dose of lidocaine had a small but significant action on electrical recovery after brief, almost complete global ischemia, confirming our previous observations on a rabbit model where the ischemic episode was less severe and the recovery more complete. These findings suggest that a low dose of lidocaine can accelerate the time course of neuroelectrical recovery after global ischemia and that the magnitude of this action depends very critically on the duration and severity of the ischemic event.

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Skin-surface temperature gradients (forearm temperature - fingertip temperature) have been used as an index of thermoregulatory peripheral vasoconstriction. However, they have not been specifically compared with total finger blood flow, nor is it known how long it takes fingertip temperature to fully reflect an abrupt change in finger blood flow. Steady-state skin-temperature gradients were compared with total fingertip blood flow in 19 healthy volunteers. There was an excellent correlation between steady-state skin-surface temperature gradients and total fingertip blood flow measured with venous-occlusion volume plethysmography: gradient = 0.2-5.7.log(flow), r = 0.98. The half-time for fingertip cooling after complete arterial obstruction (in 8 volunteers) was 6.6 +/- 1.2 min. The authors conclude that skin-temperature gradients are an accurate measure of thermoregulatory peripheral vasoconstriction.

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The use of high-dose lidocaine for cerebral protection during ischemia has produced varied results. Our study uses a new, single carotid artery preparation in the rabbit to produce incomplete global ischemia by graded carotid occlusion; specific electroencephalographic changes are used as the end point for the extent of blood flow reduction sustained during 20 minutes. We monitored arterial pressure, intracranial pressure, and internal carotid blood flow that were recorded with an electromagnetic flowmeter after surgical ligation of the opposite internal and the two vertebral arteries, and we studied the electroencephalogram and somatosensory-evoked potentials elicited by stimulation of the sciatic nerve. Low-dose lidocaine (0.2 mg/kg/min) infused throughout the experiment significantly accelerated the time course of the return of electroencephalographic and evoked-potential amplitudes toward control. Deep halothane anesthesia alone elicited the slowest recovery, suggesting that the action of lidocaine was independent of its general anesthetic effect. There were very small differences among the groups in the measured arterial pressure, intracranial pressure, and cerebral blood flow, suggesting that lidocaine changed recovery rate without markedly modifying any characteristic of the postischemic cerebral perfusion. The protective effect of lidocaine may be the result of a specific blockade of Na+ channels or a decrease in excitatory neurotransmitter release, either of which would cause a delay in the onset of the events that lead to neuronal damage during ischemia.

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Narcotics and nitrous oxide (N2O) inhibit thermoregulatory responses in animals. The extent to which N2O/fentanyl anesthesia lowers the thermoregulatory threshold in humans was tested by measuring peripheral cutaneous vasoconstriction using skin-surface temperature gradients (forearm temperature-fingertip temperature) and the laser Doppler perfusion index. Fifteen unpremedicated patients were anesthetized with N2O (70%) and fentanyl (10 micrograms/kg iv bolus followed by 4 micrograms.kg-1.h-1 infusion) during elective, donor nephrectomy. Patients were randomly assigned to undergo additional warming (humidified respiratory gases, warmed intravenous fluids, and a heating blanket over the legs; n = 5) or standard temperature management (no special warming measures; n = 10). Significant vasoconstriction was prospectively defined as a skin-surface temperature gradient between forearm surface and finger-tip surface greater than or equal to 4 degrees C, and the thermoregulatory threshold was defined as the esophageal temperature at which such vasoconstriction occurred. Vasoconstriction did not occur in the patients who received additional warming and thus remained nearly normothermic [average minimum esophageal temperature = 35.8 +/- 0.4 degrees C (SD)] but did in six hypothermic patients at a mean esophageal temperature of 34.2 +/- 0.5 degrees C. Four hypothermic patients developed a passive thermal steady state without becoming sufficiently cold to trigger vasoconstriction. Thus, active thermoregulation occurs during N2O/fentanyl anesthesia but does not occur until core temperatures are approximately 2.5 degrees C lower than normal. The thermoregulatory threshold during N2O/fentanyl anesthesia is similar to that previously determined during halothane (34.4 +/- 0.2 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)

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Although suppression of thermoregulatory mechanisms by anesthetics is generally assumed, the extent to which thermoregulation is active during general anesthesia is not known. The only thermoregulatory responses available to anesthetized, hypothermic patients are vasoconstriction and non-shivering thermogenesis. To test anesthetic effects on thermoregulation, the authors measured skin-surface temperature gradients (forearm temperature--finger-tip temperature) as an index of cutaneous vasoconstriction in unpremedicated patients anesthetized with 1% halothane and paralyzed with vecuronium during elective, donor nephrectomy. Patients were randomly assigned to undergo maximal warming (warm room, humidified respiratory gases, and warm intravenous fluids; n = 5) or standard temperature management (no special warming measures; n = 5). Skin-surface temperature gradients greater than or equal to 4 degrees C were prospectively defined as significant vasoconstriction. Normothermic patients [average minimum esophageal temperature = 36.4 +/- 0.3 degrees C (SD)] did not demonstrate significant vasoconstriction. However, each hypothermic patient displayed significant vasoconstriction at esophageal temperatures ranging from 34.0 to 34.8 degrees C (average temperature = 34.4 +/- 0.2 degrees C). These data indicate that active thermoregulation occurs during halothane anesthesia, but that it does not occur until core temperature is approximately equal to 2.5 degrees C lower than normal. In two additional hypothermic patients, increased skin-temperature gradients correlated with decreased perfusion as measured by a laser Doppler technique. Measuring skin-surface temperature gradients is a simple, non-invasive, and quantitative method of determining the thermoregulatory threshold during anesthesia.

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Spontaneous post-anesthetic tremor that resembles shivering is common during recovery from anesthesia. Risks to postoperative patients include an increase in metabolic rate of up to 400%, hypoxemia, wound dehiscence, dental damage, and disruption of delicate surgical repairs. The etiology of spontaneous post-anesthetic tremor is most commonly attributed to normal thermoregulatory shivering in response to intraoperative hypothermia. However, the mechanism of this tremor remains unknown, hampering prevention and treatment. The present study was designed to determine whether mechanisms other than thermoregulation contribute to the tremor. The electromyograms (EMGs) of eight muscles were observed in nine women during recovery from isoflurane anesthesia. Signals from each muscle were compared to those of pathologic clonus induced by plantar flexion in unanesthetized patients with spinal cord transections and to those of cold-induced shivering in normal, unanesthetized subjects. Two distinct EMG patterns were identified: 1) regular, bursting signals of 5-7 Hz similar to those produced by pathologic clonus in patients with spinal cord transections; and 2) tonic, irregular signals of 5-15 Hz which had poorly defined bursts that did not demonstrate the synchronous 4-8-cycle/min waxing and waning pattern typical of normal shivering. EMG activity occurred most often at expired isoflurane concentrations of 0.1-0.19%, and was not related to rectal temperature. During the later part of recovery when isoflurane concentrations were less than or equal to 0.1%, hypothermic patients frequently demonstrated no clinical or EMG evidence of muscular activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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The consequences of the use of ketamine for immobilization have been examined on the concentration of whole blood serotonin, concentrations of neurotransmitters and metabolites in CSF and brain, and specific binding of ligands related to neurotransmitters in brain. Vervet monkeys (Cercopithecus aethiops sabaeus) were examined under conditions which compared ketamine with physical restraint and with halothane. It was found that ketamine, used acutely in monkeys for restraint, had no influence on the concentration of serotonin in whole blood or the concentration of 5-hydroxyindoleacetic acid or homovanillic acid in the CSF. In rats, untreated animals were compared with those treated with ketamine alone, or in conjunction with pentobarbital. Treatment with ketamine had no influence on the specific binding of ketanserin, imipramine, prazosin or dihydroalprenolol in brain of rat, nor any influence on the concentrations of serotonin, 5-hydroxyindoleacetic acid, norepinephrine, epinephrine, dopamine, or dihydroxyphenylacetic acid in brain. A moderately increased concentration of homovanillic acid was observed in several areas of the brain of the rat after ketamine alone or paired with pentobarbital.

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The effects of intravenous ketamine (1 mg/kg) on cerebral cortical blood flow and O2 uptake were evaluated in 13 anesthetized, ventilated rabbits. Blood flow was measured either directly (Group 1) or by the H2 clearance method (Group 2). In those animals of Groups 1 and 2 with normal control arterial pH (pHa), ketamine produced a significant increase in cerebral cortical blood flow of 18 and 34%, respectively, but had no effect on cerebral cortical O2 uptake. However, in rabbits with low control pHa, ketamine caused an increase in blood flow (30%) accompanied by a significant increase in O2 uptake (22%). Ketamine produced nonsignificant changes in mean arterial blood pressure and arterial blood gases, except for a significant reduction in pressure in animals with low pHa. It is concluded that ketamine is a cerebral vasodilator without cerebral metabolic effect when mean arterial blood pressure and arterial PCO2, PO2, and pH are held constant at physiologic levels. The vasodilator effect of ketamine is probably due to direct dilating action or activation of a cholinergic cerebral vasodilator system.

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