摘要:

Hypertension after craniotomy is frequent. To establish an association between vasoactive modulators and postoperative hypertension, we followed the arterial blood pressure and plasma concentrations of selected substances in patients undergoing craniotomy. Twelve consecutive patients scheduled for operation of a supratentorial brain tumor were anesthetized with thiopental, fentanyl, isoflurane, and pancuronium. None of the patients had a history of arterial hypertension or were hypertensive before the operation. Arterial blood pressure and heart rate measurements were obtained preoperatively, after incision, during closure, and four times in the 50-minute interval after stopping isoflurane. At the same time, plasma concentrations of norepinephrine, epinephrine, renin, aldosterone, atrial natriuretic peptide, endothelin, and cortisol were measured. Data are given as mean ± SD (range). The postoperative concentrations of these substances were significantly higher than the baseline concentrations measured preoperatively. Six of the patients developed postoperative hypertension defined as a mean arterial pressure (MAP) > 20% more than the baseline MAP (group H), and six had normal blood pressure postoperatively (group N). The mean value of the maximal postoperative MAPs measured in groups H and N, respectively, was 118 ± 16 mm Hg (range: 96–132) and 103 ± 9 mm Hg (range: 92–115) (P= .01). Only renin levels were higher intraoperatively in group H when compared to group N. However, postoperative levels of catecholamines, aldosterone, renin, and endothelin levels were higher in group H patients. The results suggest that in addition to an increased discharge of the sympathetic system, activation of the renin-angiotensin aldosterone system may also play an important role in the development of postoperative hypertension after craniotomy.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Volatile anesthetics reduce excitatory synaptic transmission in the mammalian brain. In the present study, the effect of sevoflurane on synaptic glutamate release, free cytosolic Ca2+([Ca2+]i), and glutamate uptake was investigated using isolated presynaptic terminals prepared from human cerebral cortex. The tissue was obtained from standard temporal lobe specimens removed because of epilepsy. The glutamate release and [Ca2+]iwas measured as the fluorescence of nicotinamide adenine dinucleotide phosphate (NADPH) and fura-2, respectively. The uptake of radiolabeled glutamate was measured in a &bgr;-scintillation counter. Membrane depolarization with 4-aminopyridine for three minutes evoked a Ca2+-dependent glutamate release of 3.4 ± 0.5 nmol/mg. Sevoflurane 2.5 and 4.0% attenuated the evoked release by 45 and 55%, respectively. The evoked increase in [Ca2+]iwas not significantly altered by the anesthetic agent. The uptake studies were performed in the high-affinity area, and Kmwas calculated to 19.3 ± 5.7 × 10−6M and Vmaxto 5.7 ± 1.0 &mgr;mol g−1min−1. The Kmand Vmaxvalues were not significantly altered by sevoflurane 2.5%. These results demonstrate that sevoflurane in the human brain reduces Ca2+-dependent glutamate release. The exact mode of action is still to be resolved.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Cerebral edema commonly accompanies brain tumors and frequently leads to lethal intracranial compartmental shifts and elevated intracranial pressure. Therapeutic modalities for tumor–associated cerebral edema include diuretics, osmotherapy, and corticosteroids. Recently, hypertonic saline (HS) has received attention as an osmotic agent in the treatment of cerebral edema from diverse causes. The effects of continuous HS infusion in brain tumor–associated edema have not been previously reported. Therefore, we tested the hypothesis that HS given as a continuous intravenous infusion ameliorates tumor-associated edema in a rat model of brain tumor. 9L gliosarcoma, propagated as a solid flank tumor, was implanted intracranially over the left hemisphere in adult female Fischer 344 rats (180–220 g). On day 11 after implantation, rats were divided in a blinded, randomized fashion into groups that received no treatment or continuous infusion of 0.9% saline (NS) (0.3 mL/h) and in a subsequent series that included NS + intravenous furosemide 2.5 mg/kg every six hours, NS + intravenous mannitol 2.5 g/kg every six hours, or continuous infusion 7.5% HS (chloride:acetate 50:50) (0.3 mL/h). Hemispheric water content ipsilateral (IH) and contralateral to tumor implantation was determined at day 13 by wet-to-dry weight ratio after 48 hours of therapy. Ipsilateral hemispheric water content (mean ± SEM) was significantly increased in rats with intracranial tumor on day 11 (80.3 ± 0.5%) (n = 7) and day 13 (81.4 ± 0.3%) (n = 10), as compared to naive weight-matched rats without tumor implant (79.3 ± 0.1%) (n = 13) (P< .05). After 48 hours of treatment, IH water content was attenuated with continuous HS (n = 15) (79.3 ± 0.2%), mannitol (n = 14) (80.1 ± 0.2%), and furosemide (n = 15) (79.9 ± 0.2%) as compared to NS (n = 7) (80.8 ± 0.5%). Continuous HS infusion attenuated cerebral edema in the affected hemisphere as well as the contralateral noninjured hemisphere to a larger extent than was observed with furosemide or mannitol. These findings suggest a potential new treatment strategy for tumor–associated cerebral edema.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

In patients who experience sudden death from spontaneous subarachnoid hemorrhage, more than 90% present with acute pulmonary edema. The underlying pathogenesis of this complication is poorly understood. In addition, the specific role of the extravasated blood products and the associated elevation in intracranial pressure leading to the systemic and pulmonary effects during subarachnoid hemorrhage are not well established. The authors tested a new model of acute and severe subarachnoid hemorrhage comparing fresh whole autologous blood (n = 20) with 5% albumin (n = 19) injected at two different rates (35 seconds versus 24 minutes) into the cisterna magna of anesthetized, mechanically ventilated rats. Cerebral and systemic hemodynamics and the corresponding pulmonary function were evaluated. The type of fluid injected had no influence on survival or hemodynamic and respiratory parameters. Rapid infusion of either blood or albumin (n = 14) produced an acute and transient rise in intracranial pressure (37.9 ± 3.5 mm Hg) associated with systemic hypertension and increased cerebral perfusion pressure that was sustained in survivors but not in nonsurvivors. Slow infusion (n = 23) produced a more progressive increase in intracranial pressure to 31.2 ± 7.1 mm Hg with a parallel and sustained increase of systemic blood pressure and preserved cerebral perfusion pressure in survivors, but produced a pattern of more severe hypertension followed by hypotension in nonsurvivors. Sixty-four percent of animals (rapid infusion) and 48% of animals (slow infusion) survived the challenge and presented no pulmonary alterations. In contrast, nonsurviving rats developed reduced lung compliance and gas exchange, an increased alveolar–arterial protein concentration ratio (0.36 ± 0.02 versus 0.17 ± 0.03 in survivors;P< .0001), and increased lung weight (5.7 ± 0.3 g versus 2.0 ± 0.1 g;P< .0001), demonstrating a fulminant increased permeability pulmonary edema, leading to death within one hour. These results indicate that the chosen rapid- and slow-injection rates resulted in a similar death rate of 50%. Mortality was similar for blood and albumin administration, pulmonary edema occurred in nonsurvivors in both the rapid- and slow-injection groups, and pulmonary edema is associated with more severe hypertension in the slow-injection group. Furthermore, these results suggest that the development of neurogenic pulmonary edema that is characterized by an acutely increased capillary permeability to proteins is independent of the degree of intracranial pressure increase or the type of fluid administrated.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Brain arteriovenous malformation (BAVM) resection can result in an acute increase in cerebral blood flow (CBF) of unclear etiology. This observational study investigated the relationship between changes in CBF and cardiac output (CO) in patients undergoing microsurgical resection of BAVMs. In 20 patients undergoing a BAVM resection during an isoflurane-based anesthesia, we measured CBF and systemic cardiovascular parameters immediately before and after BAVM resection. CBF was measured on the hemisphere ipsilateral to the lesions and on the contralateral side, using intravenous cold133Xe washout. Cardiac output was measured using thermodilution technique via a pulmonary artery catheter. There was an increase in global CBF after resection (25 ± 8 versus 31 ± 13 mL/100 g/min, preresection versus postresection, mean ± SD,P= .002), ipsilateral CBF (25 ± 8 versus 31 ± 13 mL/100 g/min,P= .002), and contralateral CBF (24 ± 7 versus 30 ± 13 mL/100 g/min,P= .003). There was no change in CO, mean systemic arterial pressure, central venous pressure, or pulmonary artery diastolic pressure. The change in CBFGLOBALwas not correlated with changes in CO (r= .154,P= .517). BAVM resection resulted in global increases in CBF that was not substantially related to changes in CO or other systemic parameters.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

After the reported successful use of dexmedetomidine to sedate patients in the intensive care unit without respiratory depression, we began to use dexmedetomidine for interventional neuroradiologic procedures. We report on five patients who had dexmedetomidine administered for sedation during embolization of cerebral arteriovenous malformations. All patients were comfortably sedated and breathing spontaneously. However, although patients were awake and following simple commands 10 minutes after the discontinuation of the infusion of dexmedetomidine, they were nevertheless unable to undergo cognitive testing. They were still unable to undergo cognitive testing 45 minutes after the infusion was stopped. In contrast, 10 minutes after the discontinuation of the infusion of propofol, all patients were awake, alert, cooperative, and able to undergo cognitive testing without difficulty. In conclusion, on examination of five non-randomly selected case records, we found that dexmedetomidine significantly prevented neurologic and cognitive testing.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean × 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th–90th percentile: 380 &mgr;V, 129–953 &mgr;V; 135 &mgr;V, 38–658 &mgr;V, respectively;P< .05). There were no significant differences in motor evoked potential latency (mean ± standard deviation: 20.9 ± 2.2 msec and 21.4 ± 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22–42%] and 26% [18–41%], respectively) and latencies (mean ± standard deviation: 2.1 ± 0.7% and 2.1 ± 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

This pilot study was designed to determine the feasibility of measuring cerebral blood flow noninvasively after an intravenous bolus of indocyanine green using near-infrared spectroscopy and pulse dye–densitometry. Feasibility aside, this study did not attempt to validate the measured values of cerebral blood flow against an established method of measurement. Twelve healthy volunteers were investigated after peripheral intravenous injection of indocyanine green. Arterial and cerebral changes in indocyanine green concentration were measured using pulse dye–densitometry and near-infrared spectroscopy, respectively. Two methods of calculating cerebral blood flow were used, and a blood flow index was also estimated. Absolute cerebral blood flow was calculated using a modification of the Fick principle and a deconvolution algorithm to derive the impulse residue function. Mean (range) estimated cerebral blood flow for the Fick method was 8.2 mL/100 g/min (4.2–16.2 mL/100 g/min) and 8.3 mL/100 g/min (4.7–15.3 mL/100 g/min) for the impulse residue function method. The impulse residue function method provided a more precise intrasubject estimation of cerebral blood flow compared with the modified Fick principle, with a coefficient of variation of 10.1% versus 25.5%. The blood flow index was 8.6 mg/sec (range: 5.6–17.3 mg/sec) with an intrasubject coefficient of variation of 12.0%. Estimation of cerebral blood flow using near-infrared spectroscopy and pulse dye–densitometry can be made at the bedside after intravenous injection of indocyanine green, and the precision can be improved using a deconvolution algorithm. Notwithstanding the low values obtained for absolute cerebral blood flow, further investigation and validation of this bedside technique is warranted.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Infrared pupillary scans have been used extensively as an objective measure of pupillary reflexes during pharmacological studies of human subjects, but no previous scans have documented the pupillary changes during transtentorial uncal herniation. We present infrared pupillary scans from three patients with brain stem compression secondary to expanding intracranial mass lesions. The scans were made with a portable device permitting infrared pupillometry at the patient's bedside. Portable infrared pupillometry records objective measurements of pupillary light reflexes, which provides information useful for diagnosing transtentorial herniation and affords objective measurements of an important endpoint in the management of patients with head trauma or supratentorial mass lesions.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Toxic epidermal necrolysis is a drug-induced, rare, but life-threatening skin eruption. The main differential diagnoses are drug-induced erythema (hypersensitivity syndrome), acute graft-versus-host disease, staphylococcal scalded skin syndrome, and toxic shock syndrome. Because the therapy for toxic epidermal necrolysis and acute graft-versus-host disease differs largely from the others, it is necessary to make an accurate diagnosis. In addition to a detailed medical history, skin biopsy is mandatory because the skin eruptions are not always unequivocal. Discontinuation of the causing agent is crucial, and treatment in specialized intensive care units or burn units is supportive. Currently there is no specific treatment for toxic epidermal necrolysis. Advantages from corticosteroids, plasmapheresis, intravenous immunoglobulin, cyclophosphamide, cyclosporin, andN-acetylcysteine still remain to be established by controlled trials, or have failed to prove a benefit (thalidomide). The patient presented here demonstrates the difficulties in diagnosing toxic epidermal necrolysis in a critically ill patient. A short overview of the pathogenesis and the management of toxic epidermal necrolysis is provided.

ISSN:0898-4921    

出版商:OVID    

年代:2002

数据来源: OVID