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M H Zornow

Publications and source records attributed to M H Zornow.

At least 19 recordsLinked to original sources
PubMed2001

Lubeluzole inhibits accumulation of extracellular glutamate in the hippocampus during transient global cerebral ischemia.

Increases in extracellular glutamate during cerebral ischemia may play an important role in neuronal injury. Lubeluzole is a novel neuroprotective drug, which in previous in vitro and focal ischemia studies has been shown to inhibit nitric oxide synthesis, to block voltage-gated Na+-ion channels, and to inhibit glutamate release. In this study, we investigated the ability of lubeluzole to inhibit glutamate accumulation during episodes of transient global cerebral ischemia. Twenty-five New Zealand white rabbits were randomized to one of four groups: a normothermic control group; a hypothermic group; a 1.25 mg/kg lubeluzole group; or a 2.5 mg/kg lubeluzole group. The animals were anesthetized, intubated, and ventilated before microdialysis probes were placed in the hippocampus. Lubeluzole was given intravenously 90 min before the onset of ischemia. Esophageal temperature was maintained at 38 degrees C in the control, and lubeluzole treated groups, while the animals in the hypothermia group were cooled to 30 degrees C. A 15-min period of global cerebral ischemia was produced by inflating a neck tourniquet. Glutamate concentrations in the microdialysate were determined using high-performance liquid chromatography (HPLC). During ischemia and early reperfusion, glutamate concentrations increased significantly in the control group and returned to baseline after 15 min of reperfusion. In the lubleuzole 2.5 mg/kg and hypothermia groups, glutamate levels were significantly lower (P<0.05) than in the control group and there was no significant change from baseline levels during the entire experiment. This study suggests that lubeluzole is effective in inhibiting extracellular glutamate accumulation during global cerebral ischemia, and has the potential to produce potent neuroprotection when instituted prior to an ischemic event.

Action Potentials↗
PubMed2001

Designing meaningful industry metrics for clinical productivity for anesthesiology departments.

IMPLICATIONS: Clinical productivity measurements that account for differences in clinical settings and concurrencies provided more precise comparisons between two anesthesiology groups. The data show that different concurrencies confound the current industry standard, "per full-time equivalent" measurements, whereas "per operating room site" and "per case" measurements allowed for more meaningful comparisons.

Anesthesiology↗
PubMed2001

The impact of longer-than-average anesthesia times on the billing of academic anesthesiology departments.

UNLABELLED: Academic anesthesiology departments provide clinical services for surgical procedures that have longer-than-average surgical times and correspondingly increased anesthesia times. We examined the financial impact of these longer times in three ways: 1) the estimated loss in revenue if billing were done on a flat-fee system by using industry-averaged anesthesia times; 2) the estimation of incremental operating room (OR) sites necessitated by longer anesthesia times; and 3) the estimated potential gain in billed units if the hours of productivity of current anesthesia time were applied to surgical cases of average duration. Health Care Financing Administration average times per anesthesia procedure code were used as industry averages. Billing data were collected from four academic anesthesiology departments for 1 yr. Each claim billed with ASA units was included except for obstetric anesthesia care. All clinical sites that do not bill with ASA units were excluded. Base units were determined for each anesthesia procedure code. The mean commercial conversion factor (US$45 per ASA unit) for reimbursement was used to estimate the impact in dollar amounts. In all four groups, anesthesia times exceeded the Health Care Financing Administration average. The loss per group in billed ASA units if a flat-fee billing system were used ranged from 18,194 to 31,079 units per group, representing a 5% to 15% decrease (estimated billing decrease of US$818,719 to US$1,398,536 per group). The number of excess OR sites necessitated by longer surgical and anesthesia times ranged from 1.95 to 4.57 OR sites per group. The potential gain in billed units if the hours of productivity of current anesthesia time were applied to surgical cases of average duration was estimated to be from 13,273 to 21,368 ASA units. Longer-than-average anesthesia and surgical times result in extra hours or additional OR sites to be staffed and loss of potential reimbursement for the four academic anesthesiology departments. A flat-fee system would adversely affect academic anesthesiology departments. IMPLICATIONS: We examined the economic impact of longer-than-average anesthesia times on four academic anesthesiology departments in three ways: the estimated loss in revenue under a flat-fee system, the excess operating room sites staffed, and the potential gain in revenue if the surgeries were of average length. These results should be considered both in productivity measurements and strategies for operating room management.

Accounting↗
PubMed2001

Effects of profound anemia on brain tissue oxygen tension, carbon dioxide tension, and pH in rabbits.

This study sought to determine the maximum tolerable limit of anemia for the brain during halothane anesthesia. Using a multiparameter sensor, we continuously monitored brain tissue oxygen tension (PO2), carbon dioxide tension (PCO2), and pH during profound hemodilution and subsequent transfusion. Twelve New Zealand White rabbits were anesthetized, intubated, and mechanically ventilated at a fraction of inspired oxygen (FiO2) of 21% to produce an arterial carbon dioxide tension (PaCO2) of 35 to 40 mm Hg. The femoral artery was cannulated to continuously monitor arterial blood pressure and to intermittently measure arterial blood gases. The electroencephalogram (EEG) was recorded throughout the course of the study. A fiberoptic sensor was inserted into the brain for the continuous measurement of brain PO2, PCO2, pH, and temperature. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. Severe anemia was induced by repeatedly withdrawing 50-mL aliquots of blood and infusing an equal volume of 6% hetastarch. This procedure was performed four times for each rabbit. After the forth blood draw and fluid infusion, a total of 60 mL of packed red blood cells were transfused. Upon completion of the hemodilution, the hemoglobin concentration was 2.4 +/- 0.3 g/dL (mean +/- SEM). Brain tissue PO2 decreased from 27 +/- 3 mm Hg to a minimum of 12 +/- 2 mm Hg. Brain tissue pH also decreased from 7.22 +/- 0.03 to 7.12 +/- 0.05 and returned to the baseline value with transfusion. Brain PCO2 did not change significantly during the experiment. Cerebral blood flow increased from 37 +/- 3 to 66 +/- 15 mL x 100 g(-1) x min(-1) during hemodilution and returned to baseline after infusion of red blood cells. There was some loss of EEG amplitude and the calculated cerebral metabolic rate (CMRO2) decreased from 4.3 +/- 0.6 to 1.9 +/- 0.3 mL x 100 g(-1) x min(-1) at the most profound level of anemia. This is the first report of which the authors are aware of continuous monitoring of brain tissue pH, PCO2, and PO2 during profound hemodilution and transfusion. Hemodilution results in a decrease in brain tissue PO2. Increases in CBF and oxygen extraction can only partially compensate for the decreased oxygen carrying capacity of the blood. Decreases in brain tissue PO2, pH, CMRO2, and a loss of EEG amplitude suggest that the maximum tolerable limit of hemodilution was achieved in this study.

Anemia↗
PubMed2001

The combination of lamotrigine and mild hypothermia prevents ischemia-induced increase in hippocampal glutamate.

The excessive release of glutamate during cerebral ischemia may play an important role in subsequent neuronal injury. Both lamotrigine and hypothermia have independently been shown to attenuate the release of glutamate. In this study, the authors sought to determine whether these effects were additive. Thirty-five New Zealand White rabbits were randomized to one of six groups: a normothermic control group; a lamotrigine-treated group; two hypothermic groups at 33 degreesC or 34.5 degreesC; or two groups treated with both hypothermia at 33 degreesC or 34.5 degreesC plus lamotrigine. Animals were anesthetized before implanting microdialysis probes in the hippocampus. Esophageal temperature was maintained at 38 degreesC in the control and lamotrigine groups, while the temperatures of animals in the hypothermia and hypothermia-plus-lamotrigine groups were cooled to 33 degreesC or 34.5 degreesC. Two 10 minute periods of global cerebral ischemia were produced by inflating a neck tourniquet. Levels of glutamate in the microdialysate were then determined using high-performance liquid chromatography. Extracellular glutamate concentrations increased only slightly from baseline during the first ischemic period. Glutamate levels during the second ischemic episode in the hypothermia-plus-lamotrigine group (34.5 degreesC) were significantly lower than those in the hypothermia group alone (34.5 degreesC), lamotrigine, or control groups (P < .01). The fact that mild hypothermia (34.5 degreesC) plus lamotrigine (20 mg/kg) together were more effective in inhibiting extracellular glutamate accumulation than hypothermia (34.5 degreesC) or lamotrigine (20 mg/kg) alone, suggests the potential for increased neuroprotection by the addition of lamotrigine to mild hypothermia.

Animals↗
PubMed2000

Effect of a neuronal sodium channel blocker on magnetic resonance derived indices of brain water content during global cerebral ischemia.

Diffusion-weighted magnetic resonance imaging (DWI) with calculation of the apparent diffusion coefficient (ADC) of water is a widely used noninvasive method to measure movement of water from the extracellular to the intracellular compartment during cerebral ischemia. Lamotrigine, a neuronal Na(+) channel blocker, has been shown to attenuate the increase in extracellular concentrations of excitatory amino acids (EAA) during ischemia and to improve neurological and histological outcome. Because of its proven ability to reduce EAA levels during ischemia, lamotrigine should also minimize excitotoxic-induced increases in intracellular water content and therefore attenuate changes in the ADC. In this study, we sought to determine the effect of lamotrigine on intra- and extracellular water shifts during transient global cerebral ischemia. Fifteen New Zealand white rabbits were anesthetized and randomized to one of three groups: a control group, a lamotrigine-treated group, or a sham group. After being positioned in the bore of the magnet, a 12-min 50-s period of global cerebral ischemia was induced by inflating a neck tourniquet. During ischemia and early reperfusion there was a similar and significant decrease of the ADC in both the lamotrigine and control group. The ADC in the sham ischemia group remained at baseline throughout the experiment. Lamotrigine-mediated blockade of voltage-gated sodium channels did not prevent the intracellular movement of water during 12 min 50 s of global ischemia, as measured by the ADC, suggesting that the ADC decline may not be mediated by voltage-gated sodium influx and glutamate release.

Animals↗
PubMed2000

Effects of adenosine agonists and an antagonist on excitatory transmitter release from the ischemic rabbit hippocampus.

The purpose of this study was to determine the effects of adenosine agonists and an antagonist on ischemia-induced extracellular glutamate concentrations in an animal model of transient cerebral ischemia using in vivo cerebral microdialysis. Fifty New Zealand white rabbits were randomly assigned to one of five groups (normothermia, hypothermia, cyclopentyladenosine (CPA), theophylline, or propentofylline). Microdialysis probes were stereotactically placed in the dorsal hippocampus. Twenty minutes before the onset of ischemia, either 1 mg/kg CPA, 5 mg/kg propentofylline, or 20 mg/kg theophylline were administered intravenously. Esophageal temperature was maintained at 38 degrees C, except in the hypothermic animals, which were cooled to 30 degrees C throughout the entire experiment. Two 12-min periods of cerebral ischemia, separated by a 105-min interval of reperfusion, were produced by inflating a neck tourniquet. High-performance liquid chromatography was used to determine the glutamate concentration in the microdialysate. There were no significant increases in glutamate concentrations during the first ischemic period in any of the five groups. During the second ischemic episode, glutamate concentrations in the normothermic group peaked at levels approximately three times higher than the initial values. A similar pattern of changes in glutamate concentrations was observed in the CPA, propentofylline, and theophylline groups. In the hypothermic group, the concentrations of glutamate remained at baseline levels during the entire experiment. Contrary to expectations, neither the adenosine agonists (CPA, propentofylline) nor the antagonist (theophylline) had any effect on extracellular glutamate concentrations in the peri-ischemic period. Although adenosine and its analogs may be cerebroprotective agents, their mechanism of action is not fully understood. The data derived from this study indicates that the acute administration of such agents had no effect on ischemia-induced glutamate release within the hippocampus under these experimental conditions. Based on these results, further work is needed to compare in vivo versus in vitro experimental results in acute and long-term treatment studies with adenosine receptor agonists and antagonists.

Adenosine↗
PubMed2000

Rapid induction of anesthesia with high concentrations of halothane or sevoflurane in children.

STUDY OBJECTIVE: To compare the characteristics of the rapid induction of anesthesia in pediatric patients with high concentrations of sevoflurane or halothane, and to determine the ability of anesthesiologists to correctly identify the anesthetic drug when administered in this fashion. DESIGN: Randomized, prospective, open-label study. SETTING: Academic university hospital. PATIENTS: 78 ASA physical status I and II healthy children scheduled for brief surgical procedures with general anesthesia and medicated with midazolam. INTERVENTIONS: Assessments were made by 5 pediatric anesthesiologists and 18 anesthesiology residents. Sevoflurane or halothane was randomly selected for anesthetic induction. The anesthetic circuit was primed with the drug (8% sevoflurane or 4% halothane) in 50% nitrous oxide and oxygen. The anesthesiologists were blinded as to the anesthetics being administered. After completion of anesthetic induction, the anesthesiologists were asked to identify the anesthetic and to assess the quality and speed of induction. MEASUREMENT AND MAIN RESULTS: The pediatric anesthesiologists correctly identified the anesthetic in 55 of 78 assessments (70.5%). This figure is statistically better than what could be achieved by random guessing (p < 0.001). The residents correctly identified the anesthetic in only 46 of 78 assessments (60.0%). Statistically, this figure is no better than what could be achieved by random guessing (p = 0.06). Speed of induction was subjectively felt to be faster with sevoflurane than halothane but there were no differences in actual induction time (sevoflurane group, 3.7 +/- 2.7 min; halothane group, 3.7 +/- 2.6 min). There were no differences in the quality of induction or the incidence of airway complications. The perceived incidence of tachycardia was significantly higher with sevoflurane than halothane(sevoflurane group, 74%; halothane group 20%). CONCLUSION: The induction of anesthesia with high concentrations of either halothane or sevoflurane can be safely accomplished. Pediatric anesthesiologists can differentiate between halothane and sevoflurane when either drug is given in high initial concentrations. The presence of tachycardia may have served as the primary clue in determining which drug was being used.

Anesthesia↗
PubMed2000

Effects of pentobarbital and isoflurane on conditioned learning after transient global cerebral ischemia in rabbits.

BACKGROUND: The acquisition of a conditioned eyeblink response has been used extensively to study the neurologic substrates of learning and memory. We examined the effects of the anesthetics isoflurane and pentobarbital, or hypothermia (30 degrees C), on the ability of rabbits to acquire an eyeblink conditioned response after 6.5 min of cerebral ischemia. METHODS: New Zealand white rabbits (n = 48) were randomly assigned to sham, normothermic, hypothermic, isoflurane, or pentobarbital groups. In the normothermic, hypothermic, isoflurane, and pentobarbital groups, 6.5 min of global cerebral ischemia was produced. In animals randomized to the isoflurane and pentobarbital groups, a pattern of burst suppression was achieved on the electroencephalogram before the start of the ischemic episode. Animals in the hypothermia group were cooled to 30 degrees C before ischemia. Seven days after ischemia, eyeblink training was started using an audible tone presented for 100 ms as the conditioned stimulus. The unconditioned stimulus was an air puff directed at the cornea. The delay between the end of conditioned stimulus and the start of the unconditioned stimulus (the trace interval) was 300 ms in duration. A conditioned response was defined as an eyeblink that was initiated during the trace interval. Eighty trials per day and 15 days of training were delivered. RESULTS: Neurologic deficits were greatest in the normothermia group, and these animals also had fewer conditioned responses than those in the sham, hypothermia, or pentobarbital groups. Animals in the isoflurane group had an intermediate number of conditioned responses that was not significantly different from the normothermia group. CONCLUSIONS: This study demonstrates that a brief episode of cerebral ischemia results in the impairment of associative learning. Hypothermia and burst-suppressive doses of pentobarbital were able to improve neurobehavioral outcome as measured by ability to acquire a trace conditioned response.

Adjuvants, Anesthesia↗
PubMed2000

Measurement of individual clinical productivity in an academic anesthesiology department.

BACKGROUND: The ability to measure productivity, work performed, or contributions toward the clinical mission has become an important issue facing anesthesiology departments in private practice and academic settings. Unfortunately, the practice and billing of anesthesia services makes it difficult to quantify individual productivity. This study examines the following methods of measuring individual productivity: normalized clinical days per year (nCD/yr); time units per operating-room day worked (TU/OR day); normalized time units per year (nTU/yr); total American Society of Anesthesiologists (ASA) units per OR day (tASA/OR day); and normalized total ASA units per year (ntASA/yr). METHODS: Billing and scheduling data for clinical activities of faculty members of an anesthesiology department at a university medical center were collected and analyzed for the 1998 fiscal year. All clinical sites and all clinical faculty anesthesiologists were included unless they spent less than 20% of their time during the fiscal year providing clinical care, i.e., less than 0.2 clinical full-time equivalent. Outliers, defined as faculty who had productivity greater or less than 1 SD from the mean, were examined in detail. RESULTS: Mean and median values were reported for each measurement, and different groups of outliers were identified. nCD/yr identified faculty who worked more than their clinical full-time equivalent would have predicted. TU/OR day and tASA/OR day identified apparently low-productivity faculty as those who worked a large portion of their time in obstetric anesthesia or an ambulatory surgicenter. tASA/OR day identified specialty anesthesiologists as apparently high-productivity faculty. nTU/yr and ntASA/yr were products of the per-OR day measurement and nCD/yr. CONCLUSION: Each of the measurements studied values certain types of productivity more than others. By defining what type of service is most important to reward, the most appropriate measure or combination of measures of productivity can be chosen. In the authors' department, nCD/yr is the most useful measure of individual productivity because it measures an individual anesthesiologist's contribution to daily staffing, includes all clinical sites, is independent of nonanesthesia factors, and is easy to collect and determine.

Anesthesia Department, Hospital↗
PubMed1999

Effects of hypothermia and lamotrigine on trace-conditioned learning after global cerebral ischemia in rabbits.

Acquisition of the trace-conditioned eye blink response (CR) is mediated by a variety of brain structures, including the cerebellum, the hippocampus, and brain stem nuclei. We examined the effects of a neuronal sodium channel antagonist (lamotrigine) on the ability of rabbits to acquire an eye blink CR after 6.5 min of cerebral ischemia. New Zealand white rabbits (n = 31) were randomly assigned to sham (S), normothermic ischemia (N), hypothermic (30 degrees C) ischemia-(H), or lamotrigine (50 mg/kg) treated (L) groups. In the N, H, and L groups, 6.5 min of global cerebral ischemia was produced using an inflatable neck tourniquet. Trace conditioning was started on the 7th postischemic day. The conditioned stimulus consisted of a tone (85 dB, 6 kHz) presented for 100 ms. The unconditioned stimulus was an air puff (150 ms duration) directed at the cornea. The interval between the end of the conditioned stimulus and the start of the unconditioned stimulus (the trace interval, TI) was 300 ms in duration. A trace-conditioned response was defined as an eye blink that was initiated during the TI. Eighty trials were delivered daily for 15 days. Neurologic deficits were greatest in the N group, and these animals had fewer CRs (149 +/- 157) than animals in the S (509 +/- 214) or H (461 +/- 149) groups (P < 0.05 by analysis of variance). Animals in the L group had a total number of CRs (380 +/- 253) that was intermediate between the S and N groups. Histologic evidence of neural injury was greatest in the N group. This study demonstrates that a brief episode of cerebral ischemia results in the impairment of this test of neurobehavioral function. Both hypothermia and lamotrigine were able to attenuate the impairment of eye blink trace-conditioned responses produced by cerebral ischemia.

Animals↗
PubMed1999

Monitoring brain PO2, PCO2, and pH during graded levels of hypoxemia in rabbits.

Brain ischemia and hypoxia are of concern when they occur following traumatic brain injury because they frequently result in potentially preventable secondary brain damage. In this study, we examined the ability of an implantable catheter (Paratrend 7; Diametrics Medical, St. Paul, MN) to continuously measure brain tissue pH, PCO2, and PO2 during graded levels of hypoxia. Values obtained from this catheter were compared with simultaneous measurements of arterial and sagittal sinus blood. As expected, there was a good correlation between the changes in pH, PCO2, and PO2 in brain tissue and sagittal sinus blood. Brain tissue PO2 was numerically lower than sagittal sinus blood at all inspired levels of oxygen. These data suggest that the Paratrend 7 may be useful in monitoring brain tissue oxygen tension in patients at risk for regional cerebral ischemia and hypoxia.

Animals↗
PubMed1998

Riluzole does not attenuate increases in hippocampal glutamate concentrations in a rabbit model of repeated transient global cerebral ischemia.

UNLABELLED: The aim of the present study was to examine the ability of riluzole to inhibit glutamate release during episodes of transient global cerebral ischemia. New Zealand White rabbits (n = 36) were anesthetized with halothane and mechanically ventilated to maintain normocarbia. Microdialysis catheters were inserted bilaterally into the dorsal hippocampus and perfused with artificial cerebrospinal fluid at 2 microL/min. Animals were randomly assigned to control, hypothermia (30 degrees C), or riluzole (2 or 8 mg/kg; R2 and R8) groups. Two episodes of transient global cerebral ischemia (each lasting 10 min) were produced by inflating the pneumatic tourniquet combined with induced hypotension. Dialysate was collected throughout the periischemic period, and glutamate concentrations were determined by using high-performance liquid chromatography. Peak levels were compared by using the Kruskal-Wallis test. Glutamate concentrations significantly increased by twofold to fourfold during the second ischemic period for the control, R2, and R8 groups. Glutamate concentrations in the hypothermic group were significantly lower than those in the other three groups and remained at baseline levels during the entire experiment. This study demonstrates that the sodium channel blocker riluzole does not inhibit ischemia-induced glutamate accumulation. The previously reported neuroprotective ability of riluzole may be caused by mechanisms other than the presynaptic inhibition of glutamate release during ischemia. IMPLICATIONS: Glutamate, an excitatory neurotransmitter, is released in excessive amounts during brain ischemia and may result in neuronal injury and death. Riluzole, a neuronal sodium channel blocker, has neuroprotective properties in some animal models of brain ischemia, possibly because of its ability to inhibit the release of glutamate from synaptic vesicles. However, this microdialysis study failed to demonstrate any attenuation of glutamate release during transient global ischemia after the administration of either 2 mg/kg or 8 mg/kg of riluzole.

Animals↗
PubMed1998

Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs.

BACKGROUND: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28 degrees C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. METHODS: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37 degrees C (n = 10), 34 degrees C (n = 10), 31 degrees C (n = 11), or 28 degrees C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. RESULTS: Cerebral oxygen metabolism increased after rewarming from 28 degrees C, 31 degrees C, and 34 degrees C CPB but not in the 37 degrees animals; CMRO2 remained lower with 37 degrees C (1.8 +/- 0.2 ml x min[-1] x 100 g[-1]) than with 28 degrees C (3.1 +/- 0.1 ml x min[-1] x 100 g[-1]; P < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37 degrees C animals. With 28 degrees C and 31 degrees C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37 degrees C and remained significantly greater during reperfusion in the 34 degrees C and 37 degrees C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37 degrees C animals. S-100 protein in cerebrospinal fluid was greater in the 37 degrees C (6 +/- 0.9 microg/l) and 34 degrees C (3.5 +/- 0.5 microg/l) groups than the 31 degrees C (1.9 +/- 0.1 microg/l) and 28 degrees C (1.7 +/- 0.2 microg/l) animals. CONCLUSIONS: Hypothermia to 28 degrees C and 31 degrees C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28 degrees C compared with 31 degrees C. In contrast, ischemia during 34 degrees C and particularly 37 degrees C CPB showed greater EAA release and evidence of neurologic morbidity. Cooling to 31 degrees C was necessary to improve acute recovery during global cerebral ischemia on CPB.

Animals↗
PubMed1998

Effects of temperature on cerebral tissue oxygen tension, carbon dioxide tension, and pH during transient global ischemia in rabbits.

BACKGROUND: A decrease in brain temperature (Tbrain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (PO2 brain), carbon dioxide tension (PCO2 brain), and pH (pHbrain) were monitored during short episodes of global cerebral ischemia. METHODS: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (alpha-stat). A sensor to measure PO2 brain, PCO2 brain, pHbrain, and Tbrain was inserted into the brain through a burr hole in the skull. Tbrain was adjusted to 38 degrees C, 34.4 degrees C, and 29.4 degrees C in a random sequence in each animal. PO2 brain, PCO2brain, and pHbrain (all variables are reported at the actual Tbrain) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of Tbrain. Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means +/- SD. RESULTS: During ischemia, PO2 brain decreased from 56 +/- 3 to 33 +/- 2 mmHg at 38 degrees C, from 58 +/- 3 to 32 +/- 3 mmHg at 34.4 degrees C, and from 51 +/- 2 to 32 +/- 2 mmHg at 29.4 degrees C (p = NS). PCO2 brain increased by 6.7 +/- 2 mmHg at 38 degrees C, by 5.1 +/- 1.4 mmHg at 34.4 degrees C, and by 2.3 +/- 0.8 mmHg at 29.4 degrees C. pHbrain inversely followed the trend of PCO2 brain. CONCLUSIONS: The attenuated increase in PCO2 brain during hypothermic ischemia results from the reduced CMRO2. The similar decrease in PO2 brain at all temperature levels indicates that despite the reduction in CMRO2, PO2 brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.

Analysis of Variance↗
PubMed1998

Serial determinations of cerebral water content by magnetic resonance imaging after an infusion of hypertonic saline.

OBJECTIVE: To determine regional cerebral water content in vivo by magnetic resonance imaging (MRI) after the administration of 7.5% saline in brain-lesioned rabbits. DESIGN: Randomized, controlled, intervention trial. SETTING: University animal laboratory. SUBJECTS: Eighteen male New Zealand white rabbits, randomly assigned to one of three groups. INTERVENTIONS: The animals were anesthetized (1% halothane), intubated, and mechanically ventilated to maintain end-tidal CO2 tension between 30 and 35 mm Hg (4 and 4.7 kPa). Arterial and central venous catheters were inserted and arterial blood samples were serially obtained during the experiment. Serum osmolality was measured. A cryogenic cerebral lesion was produced by pouring liquid nitrogen for 1 min into a funnel placed on the intact skull over the right hemisphere. One group of animals received 20 mL of 7.5% saline intravenously 150 mins after the cerebral lesion was generated (7.5% saline group, n = 7). A second group of animals received the same volume of 0.9% saline intravenously (0.9% saline group, n = 7). In a third group of animals (control group, n = 4) no lesion was created and no fluid administered. MEASUREMENTS AND MAIN RESULTS: Five spin-echo T2-weighted MRIs of the brain were acquired at 90 mins (Baseline 1), 120 mins (Baseline 2), 150 mins (Infusion), 180 mins (Infusion + 30 mins), and 210 mins (Infusion + 60 mins) after the generation of the cerebral lesion. In the control group, two scans separated by a time interval of 120 mins were performed. The percent changes in signal intensity between the first and the four following scans of a coronal slice of the central region were determined. Analysis of variance and the Mann-Whitney U test were used for statistical analysis. Data are presented as mean +/- SD; p < .05 was considered significant. Serum osmolality increased significantly from 308 +/- 13 mosm/L to 349 +/- 19 mosm/L after the infusion of 20 mL of 7.5% saline, but did not change after the administration of 0.9% saline. Signal intensity in the area between the caudal edge of the core of the lesion and the basal ganglia was 9 +/- 8% higher on the injured side than in the corresponding area on the contralateral side (p < .05). Compared with Baseline 1, signal intensity at Infusion + 60 mins decreased by 26.3 +/- 13.7% in the 7.5% saline group, whereas it decreased by 10.4 +/- 8.6% in the 0.9% saline group (p < .05 between groups). Signal intensity decreased only slightly and nonsignificantly by 0.6 +/- 4.4% between the two scans in the control group. CONCLUSIONS: The administration of a 7.5% saline solution causes a prompt and substantial decrease in cerebral water content as assessed by spin-echo T2-weighted MRI. Magnetic resonance imaging offers the opportunity for repeated, noninvasive in vivo determinations of cerebral water content.

Animals↗