Intraoperative transcranial Doppler monitoring.
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Cerebrovascular Circulation↗
Biomedical subjects
A M Lam
Publications and source records attributed to A M Lam.
Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia.
BACKGROUND: Although inhalation anesthetic agents are thought to impair cerebral autoregulation more than intravenous agents, there are few controlled studies in humans. METHODS: In the first group (n = 24), dynamic autoregulation was assessed from the response of middle cerebral artery blood flow velocity (Vmca) to a transient step decrease in mean arterial blood pressure (MABP). The transient hypotension was induced by rapid deflation of thigh cuffs after inflation for 3 min. In the second group (n = 18), static autoregulation was studied by observing Vmca in response to a phenylephrine-induced increase in MABP. All patients were studied during fentanyl (3 micrograms.kg-1.h-1)/nitrous oxide (70%) anesthesia, followed by, in a randomized manner, isoflurane, desflurane, or propofol in a low dose (0.5 MAC or 100 micrograms.kg-1.min-1) and a high dose (1.5 MAC or 200 micrograms.kg-1.min-1). The dynamic rate of regulation (dROR) was assessed from the rate of change in cerebrovascular resistance (MABP/Vmca) with the blood pressure decreases using computer modeling, whereas the static rate of regulation (sROR) was assessed from the change in Vmca with the change in MABP. RESULTS: Low-dose isoflurane delayed (dROR decreased) but did not reduce the autoregulatory response (sROR intact). Low-dose desflurane decreased both dROR and sROR. During 1.5 MAC isoflurane or desflurane, autoregulation was ablated (both dROR and sROR impaired). Neither dROR nor sROR changed with low- or high-dose propofol. CONCLUSIONS: At 1.5 MAC, isoflurane and desflurane impaired autoregulation whereas propofol (200 micrograms.kg-1.min-1) preserved it.
Adult↗
Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans.
BACKGROUND: The effect of volatile anesthetics on cerebral blood flow depends on the balance between the agent's direct vasodilatory action and the indirect vasoconstrictive action mediated by flow-metabolism coupling. To compare the intrinsic action of volatile anesthetics, the effect of halothane, isoflurane, and desflurane on flow velocity in the middle cerebral artery during propofol-induced isoelectricity of the electroencephalogram was examined. METHODS: In 21 ASA physical status 1-2 patients, anesthesia was induced with 2.5 mg/kg propofol, 3 micrograms/kg fentanyl, and 0.1 mg/kg vecuronium and maintained with a propofol infusion to preserve an isoelectric electroencephalogram. End-tidal carbon dioxide and blood pressure were maintained constant throughout the study period. A transcranial Doppler was used to measure blood flow velocity in the middle cerebral artery, and a catheter was inserted in a retrograde direction into the jugular bulb for oxygen saturation measurements. After 15 min of isoelectric electroencephalogram, arterial and jugular venous blood samples were drawn, and flow velocity in the middle cerebral artery was recorded. Patients were randomly allocated to receive 0.5 MAC halothane, isoflurane, or desflurane, and after 15 min of equilibration, all variables were measured again. The concentration of the volatile agent was increased to 1.5 MAC, and after 15 min of equilibration, the measurements were repeated. RESULTS: Halothane, isoflurane, and desflurane significantly increased flow velocity in the middle cerebral artery (baseline 28 +/- 4, 30 +/- 4, and 29 +/- 3 cm/s, respectively) at 0.5 MAC (19 +/- 1.5%, 21 +/- 2%, and 23 +/- 3%, respectively; P < 0.05) and at 1.5 MAC (48 +/- 3%, 75 +/- 7%, and 74 +/- 4%, respectively; P < 0.05). Changes in the cerebral arteriovenous oxygen content difference are consistent with these findings. CONCLUSIONS: Halothane, isoflurane, and desflurane have intrinsic, dose-related cerebral vasodilatory effects. Whereas all three agents are similar at 0.5 MAC, isoflurane and desflurane have greater vasodilatory effects than halothane at 1.5 MAC.
Adult↗
Nitrous oxide increases cerebral blood flow velocity during pharmacologically induced EEG silence in humans.
We examined the effect of nitrous oxide on cerebral blood flow velocity (Vmca), arteriovenous oxygen content difference and cerebral use of glucose during propofol-induced electrical silence of the electroencephalogram (EEG) in 10 patients undergoing anesthesia for nonneurosurgical procedures. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 3 micrograms/kg (followed by an infusion of 2 micrograms/kg/h), vecuronium 0.1 mg/kg, and maintained with a propofol infusion (250-300 micrograms/kg/min) sufficient to induce EEG silence. A transcranial Doppler was used to measure the Vmca and a jugular bulb catheter was inserted for oxygen saturation and glucose use measurements. After a 15-period of isoelectric EEG and normocapnia (PaCO2 38 +/- 1 mm Hg), baseline arterial and jugular bulb venous blood gases were drawn, and mean arterial pressure (MAP), heart rate (HR), and Vmca were recorded. Nitrous oxide was then introduced and equilibrated to an end-tidal concentration of 70% for 15 min, after which MAP, HR, Vmca, arterial and jugular bulb venous blood gases were measured again. Nitrous oxide increased Vmca (29 +/- 4 to 35 +/- 4 cm/s, p < 0.01), cerebral use of oxygen (166 +/- 13 to 190 +/- 12 vol%-cm/s, p < 0.05) and glucose (245 +/- 38 to 290 +/- 48 g%-cm/s, p < 0.05) by approximately 20%. Occasional bursts of EEG activity were observed in eight patients studied during the N2O stage. We conclude that in patients with propofol-induced isoelectric EEG, the increase seen in Vmca with the introduction of N2O is mainly due to cerebral stimulation and increase in cerebral metabolic rate.
Adult↗
Accuracy of continuous jugular bulb venous oximetry during intracranial surgery.
We compared readings obtained from the Baxter-Edwards continuous jugular bulb venous oximetry catheter with those obtained from blood gas analysis of simultaneously drawn samples from the catheter in 12 patients undergoing neurosurgical procedures. Within the range studied (SjvO2, 42-95%), the 111 (median, nine samples per patient; range five to 17) oximetric catheter readings correlated well with hemoglobin oxygen saturation values obtained from in vitro analysis of simultaneously drawn blood samples from the catheter (y = 0.93x + 3.4, r = 0.94, p < 0.001). Fiberoptic light signal was suboptimal (signal quality index = 3 or 4) on fewer than five occasions per patient during an average surgical procedure duration of seven h, and these occurrences were generally corrected by flushing the catheter. We conclude that the Baxter-Edwards jugular bulb oximetric catheter provides an accurate measure of SjvO2 during neurosurgical procedures.
Adult↗
Comparison of static and dynamic cerebral autoregulation measurements.
BACKGROUND AND PURPOSE: Cerebral autoregulation can be evaluated by measuring relative blood flow changes in response to a steady-state change in the blood pressure (static method) or during the response to a rapid change in blood pressure (dynamic method). The purpose of this study was to compare the results of the two methods in humans with both intact and impaired autoregulatory capacity. METHODS: Using intraoperative transcranial Doppler sonography recordings from both middle cerebral arteries, we determined static and dynamic autoregulatory responses in 10 normal subjects undergoing elective surgical procedures. The changes in cerebrovascular resistance were estimated from the changes in cerebral blood flow velocity and arterial blood pressure in response to manipulations of blood pressure. Static autoregulation was determined by analyzing the response to a phenylephrine-induced rise in blood pressure, whereas rapid deflation of a blood pressure cuff around one thigh served as a stimulus for testing dynamic autoregulation. Both measurements were performed in patients with intact autoregulation during propofol anesthesia and again in the same patients after autoregulation had been impaired by administration of high-dose isoflurane. RESULTS: There was a significant reduction in autoregulatory capacity after the administration of high-dose isoflurane, which could be demonstrated using static (P < .0001) and dynamic (P < .0001) methods. The correlation between static or steady-state and dynamic autoregulation measurements was highly significant (r = .93, P < .0001). CONCLUSIONS: These data show that in normal human subjects measurement of dynamic autoregulation yields similar results as static testing of intact and pharmacologically impaired autoregulation.
Adult↗
Effects of the valsalva maneuver on cerebral circulation in healthy adults. A transcranial Doppler Study.
BACKGROUND AND PURPOSE: Knowledge is limited about the effects of the Valsalva maneuver on cerebral circulation because of the poor temporal resolution of traditional cerebral blood flow measurements. The purpose of this study was to investigate changes in cerebral blood flow during the Valsalva maneuver and to explore its potential use for the evaluation of cerebral autoregulation. METHODS: Using transcranial Doppler ultrasonography, we simultaneously recorded systemic arterial blood pressure in the radial artery and flow velocities in both middle cerebral arteries in 10 healthy adults during the Valsalva maneuver. Gosling's pulsatility index was calculated for all phases of the Valsalva maneuver. Autoregulatory capacities were estimated from the change in cerebrovascular resistance (flow velocity in relationship to blood pressure) during phase II and changes in the velocity-pressure relationship in phase IV relative to phase I. RESULTS: The characteristic changes in blood pressure (phases I to IV) were seen in all subjects, accompanying distinct changes in cerebral blood flow velocity. The relative changes in mean velocity during phases II and IV were significantly greater than those in mean blood pressure. Compared with the baseline value, velocity decreased by 35% in phase IIa, then rose by 56.5% in phase IV (corresponding changes in blood pressure were -10.2% and +29.8%, respectively). During phase II, the pulsatility and cerebrovascular resistance decreased by 19.9%. The increase in cerebral blood flow velocity in phase IV was significantly higher than in phase I (P < .0004), and there was no corresponding significant difference in blood pressure. CONCLUSIONS: These results demonstrated that in healthy humans the Valsalva maneuver causes characteristic changes in systemic blood pressure as well as in flow velocity in the middle cerebral artery, reflecting the sympathetic and cerebral autoregulatory responses, respectively. Analysis of these changes may provide an estimate of autoregulatory capacity.
Adult↗
Anesthetic-dependent pial arteriolar response to ethanol.
Anesthetic agents are often administered in the presence of ethyl alcohol, both in research and in the clinical setting. The authors tested the hypothesis that anesthetic agents may affect cerebrovascular responses to ethanol. A closed cranial window preparation in the rat was used to compare the response of pial arterioles to topically applied ethanol (0.01% to 1% vol/vol) in the presence of alpha-chloralose/urethane (50 and 600 mg/kg, respectively) or halothane (0.5% to 1%) anesthesia. Heart rate, mean arterial blood pressure, and blood gas levels were maintained stable and within the physiological range throughout each experiment. Ethanol induced significant vasoconstriction in alpha-chloralose/urethane-anesthetized animals (multivariate analysis of variance (MANOVA), p = 0.039); conversely, ethanol induced significant vasodilation of the pial arterioles in halothane-anesthetized animals (MANOVA, p = 0.017). These responses were significantly different from one another (MANOVA, p = 0.001). Thus, the choice of anesthetic agent alters the cerebrovascular response to ethanol, and care should be taken to ascertain the influence of anesthesia in both research and clinical settings.
Anesthetics↗
Laparoscopic surgery for stress incontinence.
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Female↗
Evoked potential monitoring during posterior fossa aneurysm surgery: a comparison of two modalities.
The purpose of this study was to compare and assess the ability of two different evoked potential (EP) modalities, median nerve somatosensory evoked potentials (SSEP) and brainstem auditory evoked potentials (BAEP) in monitoring for cerebral ischaemia and in predicting neurological outcome during posterior fossa aneurysm surgery. During 70 procedures, patients were monitored with both SSEP and BAEP. Temporary occlusion of an artery was used in 52 patients and permanent occlusion in 21 patients. A change was defined as a greater than 50% decrease in amplitude and/or an increase in latency greater than 1 msec of the N20 (cortical waveform) for SSEP monitoring and of the fifth peak for BAEP monitoring. Neurological assessment of the patient was performed immediately on emergence, after 24 hr and at the time of discharge. In total, 14 patients had an SSEP change which predicted a neurological deficit in eight patients (57%). Ten patients had a change in BAEP; six had a neurological deficit (60%). Five patients had a change in both, two had a deficit (40%). The incidence of false negative results (a neurological deficit but no EP change) for both modalities was 20% (SSEP 47%, BAEP 60%). The incidence of false positive results (an EP change but no deficit) was 13% overall (SSEP 11%, BAEP 7%). All patients who had a permanent EP change developed a neurological deficit. We did not find a difference in the ability of SSEP compared with BAEP in predicting neurological deficits but, using both modalities, the incidence of false negative results was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials.
Intraoperative monitoring of somatosensory-evoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexus-evoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 +/- 6 (SD) yr, weight 68 +/- 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg.kg-1 and fentanyl 3 micrograms.kg-1 and was followed by succinylcholine 1 mg.kg-1. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 micrograms.kg-1.hr-1, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide +/- 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 +/- 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 +/- 4% vs 48 +/- 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isoflurane-nitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxide-isoflurane anaesthesia but less than the predicted additive effect.
Adult↗
The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation.
Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FIO2) was varied to give four different levels of arterial oxygen tension (PaO2 100-200, 201-300, 301-400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2(25) and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 +/- 1.1 mmHg at PaO2 of 100 mmHg to 30.6 +/- 1.4 and 33.6 +/- 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 +/- 3% at PaO2 of 100 mmHg to 60 +/- 3 and 65 +/- 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia, General↗
Therapeutic time window and dose response of the beneficial effects of ketamine in experimental head injury.
BACKGROUND AND PURPOSE: The aim of this study was to determine the time and dose response of the therapeutic effects of the N-methyl-D-aspartate receptor antagonist ketamine in experimental head injury. METHODS: Sixty-six male Sprague-Dawley rats were divided into eight groups. Groups A, B, and C were surgically prepared but received no trauma. Groups D through H received a nonpenetrating impact to the left cranium. Group A (n = 7) received no treatment. Groups B (n = 4) and C (n = 5) received 60 and 120 mg/kg IP ketamine, respectively. Group D (n = 8) received no treatment. Groups E (n = 8) and F (n = 7) received 120 and 180 mg/kg IP ketamine, respectively, 1 hour after head trauma. Groups G (n = 7) and H (n = 9) were treated with 180 mg/kg IP ketamine 2 and 4 hours after head trauma, respectively. Neurological severity score (NSS, 0 through 25 from no injury to severe injury) was determined at 1, 24, and 48 hours after head trauma. After death at 48 hours, cortical slices were taken adjacent to the lesion on the traumatized hemisphere and from comparable sites in the contralateral hemisphere for determination of tissue specific gravity and water content. Brains were then placed in 4% formaldehyde, and the volume of hemorrhagic necrosis was measured 4 days later. NSS was compared within and between groups using the Kruskal-Wallis test for repeated measurements and Mann-Whitney U test for post hoc testing. Water content, specific gravity, and hemorrhagic necrosis were compared within and between groups using two-way ANOVA followed by Fisher's protected least significant difference procedure. A value of P < .05 was considered statistically significant. RESULTS: Head trauma alone increased NSS, decreased specific gravity, increased water content, and caused cerebral infarction in the injured hemisphere. Ketamine given in two time-dose regimens, 180 mg/kg IP at 2 hours (group G) and 120 mg/kg IP at 1 hour (group F) after trauma, improved NSS from 11.6 +/- 1.7 and 14.4 +/- 0.8 at 1 hour to 4.4 +/- 1.3 and 8.0 +/- 1.4 (mean +/- SEM) at 48 hours, respectively (P < .03). Compared with the untreated group (group D), 180 mg/kg IP ketamine given at 2 and 4 hours after head trauma decreased the volume of hemorrhagic necrosis from 37.1 +/- 9.5 mm3 to 10.1 +/- 3.8 and 15.3 +/- 3.6 mm3, respectively (P < .05). Brain tissue specific gravity and water content at 48 hours were not significantly different between treated and untreated groups. There was no difference in rectal and temporalis muscle temperature between groups. CONCLUSIONS: We conclude that 180 mg/kg IP ketamine was effective in ameliorating neurological dysfunction after head trauma in rats when the administration time was delayed for 1 hour to 2 hours but not after 4 hours. When given at 1 hour after head trauma, ketamine at 120 mg/kg but not 60 mg/kg is effective in reducing neurological damage after head trauma.
Analysis of Variance↗
Nitrous oxide-isoflurane anesthesia causes more cerebral vasodilation than an equipotent dose of isoflurane in humans.
To compare the cerebral vascular and metabolic effect of an isoflurane-nitrous oxide mixture to an equipotent dose of isoflurane at 1.1 minimum alveolar anesthetic concentration (MAC), and to study the interaction between nitrous oxide and isoflurane anesthesia, we measured right middle cerebral artery blood flow velocity (V mca) and cerebral arteriovenous oxygen content difference (AVDO2) in six healthy patients during normocapnia and normothermia under the following sequence of steady-state anesthetic conditions: Condition A, 0.5 MAC of isoflurane, Condition B, 0.5 MAC of isoflurane + 0.6 MAC of N2O, Condition C, 1.1 MAC of isoflurane + 0.6 MAC of N2O, and Condition D, 1.1 MAC of isoflurane. The study entry sequence was randomized. V mca and AVDO2 during 1.1 MAC of isoflurane (Condition D) was 48 +/- 7 cm/s and 3.9 +/- 0.6 vol%, respectively. Substituting 0.6 MAC of isoflurane with an equipotent concentration of N2O (Condition B) resulted in an increase in both V mca and AVDO2 of approximately 20% (P < 0.05). These findings suggest that the increase in flow was accompanied by an even greater increase in metabolic rate. Adding 0.6 MAC of N2O to 1.1 MAC of isoflurane (Condition C) also increased V mca (P < 0.05). We conclude that N2O is a more potent cerebral vasodilator than an equipotent dose of isoflurane alone in humans.
Adult↗
Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury.
The effect of succinylcholine (SCh) on intracranial pressure (ICP) was studied in 10 mechanically ventilated patients (Glasgow coma scale score 3-10, median 6) being treated for increased ICP in an intensive care unit. Mean arterial blood pressure (MAP), ICP, processed electroencephalogram (EEG), and mean middle cerebral artery blood flow velocity (V mca) were monitored. Baseline measurements after saline injection were obtained for 5 min. SCh (1 mg/kg) was administered intravenously and the above variables were monitored for 15 min. Neither saline nor SCh cause any significant change in cerebral perfusion pressure, MAP, V mca, EEG, or ICP. We conclude that in brain-injured patients, SCh did not alter cerebral blood flow velocity, cortical electrical activity, or ICP.
Adult↗
A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures.
We examined the intraoperative use of jugular venous bulb catheters in 100 consecutive patients undergoing neurosurgical procedures. The catheters were successfully placed after induction of anesthesia in 99 patients using an aseptic technique. The efforts were abandoned after four attempts in the remaining patient. The mean time of insertion was 94 s (SD 108, range 15-420). Carotid artery puncture on two occasions controlled by firm pressure was the only complication. Arterial blood pressure, PaCO2, PaO2, and jugular venous bulb oxygen saturations (SjVO2) were intermittently measured at set intervals throughout the operation. We defined cerebral venous desaturation as 1) none (SjVO2 > 50%), 2) mild (45% < SjVO2 < 50%), and 3) severe (SjVO2 < 45%). We graded the usefulness of the catheter as 1) not useful (NU), SjVO2 > 50% and PaCO2 > 25 mm Hg; 2) useful (U1), SjVO2 > 50% and PaCO2 < 25 mm Hg; intervention, no increase in PaCO2; 3) useful (U2), SjVO2 < 50% and PaCO2 < 25 mm Hg; intervention, increase PaCO2 to improve SjVO2; 4) useful (U3), SjVO2 < 50% and PaCO2 > 25 mm Hg; intervention, nonventilatory action to increase SjVO2 (e.g., infusion of mannitol). Mild desaturation was detected in 24 patients and severe desaturation was present in 17 patients. We found SjVO2 monitoring to be useful in 60 of 99 patients studied. It was useful for detecting and treating cerebral venous desaturation in 13 of 18 patients with intracranial hematomas (subdural, epidural, and intracerebral hematomas), 9 of 18 patients with intracerebral tumors, 27 of 45 patients with cerebral aneurysms, and 6 of 8 patients with other intracranial pathology.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Ketamine alters calcium and magnesium in brain tissue following experimental head trauma in rats.
We previously reported that the N-methyl-D-aspartate receptor antagonists dizocilpine maleate and ketamine improved the neurological severity score (NSS) after head trauma in rats. Other investigators have reported increased calcium and decreased magnesium following head trauma in untreated rats. The present study was designed to determine whether ketamine influences the concentrations of calcium and magnesium in brain tissue following head trauma. Eighty-six male Sprague-Dawley rats (180 +/- 15 g) were divided into eight groups. Groups A (no head injury) and C (head injury) received no treatment. Groups B (no head injury) and D-H (head injury) received ketamine. In groups D, E, and F, ketamine, 180 mg/kg i.p., was given 1, 2, and 4 h after head trauma, respectively. In groups G and H, ketamine, 120 and 60 mg/kg, respectively, was given 1 h after head trauma. After we killed the rats at 48 h, cortical slices were taken to measure tissue calcium and magnesium content by the inductively coupled plasma atomic emission spectroscopy method. In the contused hemispheres, calcium increased and magnesium decreased (p < 0.0001). Among the head-injured groups, the increase in brain tissue calcium was smaller in groups receiving 60 mg/kg of ketamine at 1 h or 180 mg/kg of ketamine at 1, 2, or 4 h than in the group not receiving ketamine. The decrease in brain tissue magnesium was smaller in the groups receiving 180 mg/kg of ketamine at 1 and 2 h than in the group not receiving ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The diagnosis and management of a perianesthetic cerebral aneurysmal rupture aided with transcranial Doppler ultrasonography.
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Female↗