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Biomedical subjects

W L Lanier

Publications and source records attributed to W L Lanier.

At least 37 records · Page 2Linked to original sources
PubMed1999

Retinopathy associated with enterococcus enteropathy in the neonatal rat.

PURPOSE: Preretinal neovascularization has been previously observed in neonatal rats with spontaneously occurring diarrhea. This neovascularization appears analogous to retinopathy of prematurity (ROP), which occurs in human neonates. A new enterococcus species, designated Enterococcus rattus, has been isolated from the duodenum of these rats. In the present controlled study, the effect of the enteropathy induced by this organism on the retinal vasculature in the neonatal rat was further investigated. METHODS: One hundred fifty newborn Sprague-Dawley rats were randomly assigned to 6 expanded litters (n = 25). On the second day of life, animals were gavaged with either 100 microl of E. rattus suspension (1.0 X 10(7) colony forming units, inoculated group, n = 100 rats) or 100 microl saline (control group, n = 50 rats). All rats were raised in room air and were killed on day 13 of life. Duodenal and blood samples were cultured. The retinal vasculature was assessed using fluorescent microscopy and ADPase staining in a masked manner. Two additional inoculated litters and one control litter were studied for evaluation of arterial blood gases and validation of the grading method for preretinal neovascularization. RESULTS: One hundred percent of rats in the inoculated group developed severe diarrhea and had duodenal cultures positive for E. rattus compared with 0% in the control group. Preretinal neovascularization similar to ROP occurred in 55% of rats in the inoculated group compared with 2% in the control group (P = 0.001). Retinal vascular areas were reduced in the inoculated group (mean +/- SD, 89% +/- 5% versus 96% +/- 2%; P < 0.001). Rats in the inoculated group demonstrated severe growth retardation (final weight, 9.7 +/- 2.2 versus 16.7 +/- 2.7 g, P < 0.001). Inoculated animals also experienced acidosis (pH 7.31 +/- 0.06 versus 7.39 +/- 0.06 control, P = 0.04). CONCLUSIONS: A previously undescribed enterococcal enteropathy was associated with preretinal neovascularization similar to ROP in the neonatal rat. This supports an independent role for factors other than inspired oxygen in the development of ROP.

Animals↗
PubMed1998

Anesthetic technique influences brain temperature during cardiopulmonary bypass in dogs.

BACKGROUND: Because different anesthetics have different effects on cerebral blood flow and cerebral metabolism, we hypothesized that they also may have different effects on brain temperature during hypothermic cardiopulmonary bypass (CPB) and subsequent rewarming. METHODS: Sixteen dogs were anesthetized either with inhaled halothane, 1.0 minimum alveolar concentration (ie, an anesthetic that should increase cerebral blood flow and minimally affect cerebral metabolism; n = 8), or with intravenous high-dose pentobarbital (ie, an anesthetic that should reduce cerebral blood flow and cerebral metabolism by approximately one half; n = 8). Normocapnia (alpha-stat technique) and a blood pressure near 90 mm Hg were maintained. Thermistors were placed in the esophagus (ie, the body core), in the parietal epidural space, and in the parietal brain parenchyma at depths of 1 and 2 cm. Initially, all temperatures were controlled at 38.0 degrees +/- 0.2 degrees C (mean +/- standard deviation). Thereafter, atrial-femoral artery CPB was initiated, and after 15 minutes at 38 degrees C, the core temperature was decreased to 28 degrees C over approximately 21 minutes. After 30 minutes at 28 degrees C, the core temperature was returned to 38 degrees C over approximately 21 minutes and was maintained at 38 degrees C for the next 30 minutes. RESULTS: In halothane-anesthetized dogs, the mean brain-to-core temperature gradient always was 1.0 degrees C or less for all brain sites during all phases of CPB. In contrast, in pentobarbital-anesthetized dogs, the mean brain temperature during active cooling typically exceeded the core temperature by 1.7 degrees to 2.2 degrees C. This brain-to-core temperature gradient persisted into the period of stable hypothermia. During the rewarming phase of CPB, the mean brain temperature was 2.9 degrees to 3.4 degrees C cooler than the core temperature. This trend of relative cerebral hypothermia persisted well into the period in which the core temperature was 38 degrees C. CONCLUSIONS: Deep barbiturate anesthesia resulted in a brain-to-core temperature gradient during CPB that was of a magnitude greater than the 1 degrees C previously reported to modulate ischemic neurologic injury. We speculate that the timely administration of barbiturates (eg, during the latter stages of CPB) may be useful as part of a cerebroprotective regimen in humans undergoing CPB, in part because the barbiturates influence brain temperature.

Anesthesia↗
PubMed1998

Selective convective brain cooling during hypothermic cardiopulmonary bypass in dogs.

BACKGROUND: Neurologic complications, primarily resulting from ischemic insults, represent the leading cause of morbidity and disability, and the second most common source of death, after cardiac operations. Previous studies have reported that increases (as occur during the rewarming phase of cardiopulmonary bypass [CPB]) or decreases in brain temperature of a mere 0.5 degrees to 2 degrees C can significantly worsen or improve, respectively, postischemic neurologic outcome. The purpose of the present study was to evaluate a novel approach of selectively cooling the brain during hypothermic CPB and subsequent rewarming. METHODS: Sixteen dogs were anesthetized with either intravenous pentobarbital or inhaled halothane (n = 8 per group). Normocapnia (alpha stat technique) and a blood pressure near 75 mm Hg were maintained. Temperatures were monitored by placing thermistors in the esophagus (i.e., core), parietal epidural space, and brain parenchyma at depths of 1 and 2 cm beneath the dura. During CPB, core temperature was actively cycled from 38 degrees C to 28 degrees C, and then returned to 38 degrees C. Forced air pericranial cooling (air temperature of approximately 13 degrees C) was initiated simultaneous with the onset of CPB, and maintained throughout the bypass period. Brain-to-core temperature gradients were calculated by subtracting the core temperature from regional brain temperatures. RESULTS: In halothane-anesthetized dogs, brain temperatures at all monitoring sites were significantly less than core during all phases of CPB, with one exception (2 cm during systemic cooling). Brain cooling was most prominent during and after systemic rewarming. For example, during systemic rewarming, average temperatures in the parietal epidural space, and 1 and 2 cm beneath the dura, were 3.3 degrees +/- 1.3 degrees C (mean +/- standard deviation), 3.2+/-1.4 degrees C, and 1.6 degrees +/-1.0 degrees C, cooler than the core, respectively. Similar trends, but of a greater magnitude, were noted in pentobarbital-anesthetized dogs. For example, during systemic rewarming, corresponding brain temperatures were 6.5 degrees +/-1.7 degrees C, 6.3 degrees +/-1.6 degrees C, and 4.2+/-1.3 degrees C cooler than the core, respectively. CONCLUSIONS: The magnitude of selective brain cooling observed in both study groups typically exceeded the 0.5 degrees to 2.0 degrees C change previously reported to modulate ischemic injury, and was most prominent during the latter phases of CPB. When compared with previous research from our laboratory, application of cold forced air to the cranial surface resulted in brain temperatures that were cooler than those observed during hypothermic CPB without pericranial cooling. On the basis of the assumption that similar beneficial brain temperature changes can be induced in humans, we speculate that selective convective brain cooling may enable clinicians to improve neurologic outcome after hypothermic CPB.

Animals↗
PubMed1998

Selective convective brain cooling during normothermic cardiopulmonary bypass in dogs.

OBJECTIVE: Although normothermic cardiopulmonary bypass results in improved cardiac outcome, patients do not benefit from hypothermia-mediated brain protection and thus may be at high risk for ischemic brain injury. The present study evaluated the efficacy of selective forced-air cerebral cooling. METHODS: Sixteen dogs were anesthetized with either intravenous pentobarbital or inhaled halothane (n = 8 for each group). Temperatures were monitored in the esophagus (i.e., core), parietal epidural space, and brain parenchyma. Normothermic atrial-femoral cardiopulmonary bypass and forced-air pericranial cooling (to approximately 13 degrees C) were maintained for 150 minutes. Data between groups were compared by means of repeated-measures analysis of variance and two-sample t test. Within each group, brain-to-core temperature gradients were compared to zero by means of the one-sample t test. RESULTS: In pentobarbital-anesthetized dogs, after 30 minutes of cerebral cooling, temperatures in the parietal epidural space and 1 cm and 2 cm beneath the dura were 3.3 degrees +/- 1.4 degrees C (mean +/- standard deviation), 2.6 degrees +/- 1.3 degrees C, and 1.1 degrees +/- 0.6 degrees C cooler than the core temperature, respectively. At the conclusion of the study (i.e., 150 minutes), these temperatures were 4.5 degrees +/- 1.8 degrees C, 3.9 degrees +/- 1.6 degrees C, and 2.0 degrees +/- 0.9 degrees C cooler than the core temperature, respectively. Similar changes were observed in halothane-anesthetized dogs. CONCLUSIONS: Regardless of the background anesthetic, the magnitude of selective cerebral cooling observed in our study was larger than the 1 degree to 2 degrees C changes previously reported to modulate ischemic brain injury.

Analysis of Variance↗
PubMed1998

Occurrence of potentially detrimental temperature alterations in hospitalized patients at risk for brain injury.

OBJECTIVE: To ascertain the incidence and timing of fever in patients at risk for temperature modulation of brain injury resulting from ischemia or trauma. DESIGN: We retrospectively reviewed the medical records of patients admitted between January 1991 and December 1994. MATERIAL AND METHODS: We investigated three groups of hospitalized patients considered at risk for ongoing brain injury resulting from a prior cerebral insult: successful resuscitation from out-of-hospital cardiac arrest (CA), subarachnoid hemorrhage (SAH), or traumatic closed-head injury (CHI). Forty patients per condition were randomly selected from those who survived for more than 24 hours after hospital admission. RESULTS: During the initial 72 hours of hospitalization, temperature increases to 38 degrees C or more (that is, temperatures previously reported to worsen neurologic outcome after brain injury) were noted in 83% of patients with CA, 70% of those with SAH, and 68% of those with CHI. Within the cohort of febrile patients, 18 to 44% of all temperature measurements were 38 degrees C or higher, and the febrile episodes occurred randomly throughout the study interval. Fewer than one-eighth of the febrile patients received drugs possessing antipyretic properties (such as aspirin or acetaminophen) in a dose appropriate to treat fever. No other method of temperature control (for example, physical means) was used in any patient. The fractions of patients who were dismissed from the hospital with permanent neurologic injury were as follows: CA, 20%; SAH, 45%; and CHI, 43%. CONCLUSION: In these hospitalized patients at risk for ongoing brain injury, the incidence of temperature increases within the range reported to worsen neurologic outcome (elevations of 1.0 degree C or more) was very high. The characterization of these potentially injurious, randomly occurring, and traditionally undertreated temperature increases may have implications for the design of future protocols aimed at providing cerebral protection.

Adult↗
PubMed1998

Failure to attain electrocardiogram-facilitated positioning of right atrial catheters when using the Arrow Antecubital Central Venous Catheterization Kit.

When right atrial catheters are used to diagnose and treat venous air emboli in sitting neurosurgical patients, it is possible to position the catheter tip near the junction of the superior vena cava and right atrium using electrocardiogram (ECG)-based methodologies. This report describes three patients in whom this technique could not be accomplished when using the Arrow Antecubital Central Venous Catheterization Kit (Product #AK04250). The problem resulted from an imperfection in the kit's catheter-to-ECG adapter which, in turn, produced an electrical resistance that was 2.5 times greater than normal. Replacement of the adapters with the Arrow-Johans ECG Adapter (Product #EG04900) reduced the electrical resistance and permitted positioning of the catheter using the ECG.

Cardiac Catheterization↗
PubMed1998

Carbon dioxide-induced retinopathy in the neonatal rat.

PURPOSE: Hypercarbia has been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of hypercarbia on the retinal vasculature of the neonatal rat to determine whether hypercarbia alone could induce preretinal neovascularization analogous to ROP. METHODS: In a preliminary blood gas study, 8-11-day-old rats were exposed to specific levels of inspired O2 and either 0.2% CO2 or 10% CO2. Arterial blood gases were obtained, and a level of inspired O2 was determined that, when combined with inspired 10% CO2, would produce a PaO2 equivalent to room air (pure hypercarbia). In the formal retinopathy study, 300 newborn rats raised in 12 expanded litters (n = 25 each) were exposed for 7 days to either room air, 10% CO2 in 21% O2 and nitrogen (high-inspired CO2 group) or 10% CO2 in 12.5% O2 and nitrogen (pure-hypercarbia group). Each type of exposure was followed by recovery in room air for 5 days. Animals were sacrificed on day 13 and retinae were analyzed, using fluorescein perfusion and ADPase staining techniques. RESULTS: Neovascularization occurred in 19% of rats in the high-inspired CO2 group, and 14% of rats in the pure-hypercarbia group, compared to 0% of rats exposed to room air alone (p = 0.001, Chi square). CONCLUSIONS: In the neonatal rat model, exposure to hypercarbia alone, followed by room air recovery, results in preretinal neovascularization similar to that seen in oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.

Animals↗
PubMed1997

The effect of carbon dioxide on oxygen-induced retinopathy in the neonatal rat.

PURPOSE: Hypercarbia has been suggested as a risk factor for retinopathy of prematurity. We investigated the effect of raised inspired carbon dioxide on oxygen-induced retinopathy in the neonatal rat. METHODS: Newborn rats raised in expanded litters (n = 25 each) were exposed to cycles of hyperoxia (80% O2) and hypoxia (10% O2 for 7 days, followed by room air recovery for 5 days. During cyclic oxygen exposure, 3 litters (n = 75) were exposed to 10% CO2 (PaCO2 78 mm Hg +/- 6; mean +/- SD) and 3 litters (n = 75) were exposed to 0.2% CO2 (PaCO2 45 mm Hg +/- 7). Animals were sacrificed on day 13 and retinae were analyzed using fluorescein perfusion and ADPase staining techniques. RESULTS: Neovascularization occurred in 85% of rats exposed to high CO2 compared to 52% of rats exposed to low CO2 (p = 0.001). The severity of neovascularization, in clock hours, was also greater in the rats exposed to high CO2 (p < 0.001). CONCLUSIONS: Exposure to high CO2 results in an increased incidence and severity of neovascularization in a rat model for oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.

Administration, Inhalation↗
PubMed1996

Glucose modulation of ischemic brain injury: review and clinical recommendations.

Ischemic brain injury is the third-leading cause of death among Americans and the leading cause of serious disability. Based on studies of animal models, a substantial amount of experimental evidence shows that hyperglycemia at the onset of brain ischemia worsens postischemic neurologic outcome. Consistent with these observations, hyperglycemia also is associated with a worsening of postischemic brain injury in humans. In humans, however, data are often difficult to interpret because of problems in determining the timing of hyperglycemia relative to a critical ischemic event and in elucidating the effect of coexisting pathophysiologic processes (for example, a stress response) on outcome. Glucose modulation of neurologic injury is observed when ischemia is either global (for example, that accompanying cardiac arrest or severe systemic hypotension) or focal (for example, that accompanying thrombotic or embolic stroke). Toxicity is probably the result of an intracellular lactic acidosis. Specifically, the associated hydrogen ions are injurious to neurons and glia. On the basis of these factors, we recommend diligent monitoring of blood glucose concentrations in patients who are at increased risk for new-onset, ongoing, or recurring cerebral ischemia. In such patients, the use of fluid infusions, corticosteroid drugs, and insulin, as well as stress management, should be tailored to treat preexisting hyperglycemia and prevent new-onset hyperglycemia. Maintenance of normoglycemia is recommended. When one attempts to treat preexisting hyperglycemia, care should be taken to avoid rapid fluid shifts, electrolyte abnormalities, and hypoglycemia, all of which can be detrimental to the brain.

Adrenal Cortex Hormones↗
PubMed1996

Divergence of intracranial and central venous pressures in lightly anesthetized, tracheally intubated dogs that move in response to a noxious stimulus.

BACKGROUND: Intracranial pressure (ICP) may increase in tracheally intubated subjects during periods of movement (e.g, "bucking" and coughing). Recent research has suggested that factors other than passive congestion of the cerebral vessels, resulting from increases in central venous pressure, may contribute to the ICP response. The current study evaluated this issue in a canine model of intracranial hypertension and additionally evaluated the relationship between ICP and static increases in superior vena caval pressure. METHODS: Six dogs were lightly anesthetized with 0.65% end-expired halothane in oxygen and nitrogen, and ventilation was mechanically controlled. Intracranial pressure was increased to a stable baseline of 15-20 mmHg using a subarachnoid infusion of warm 0.9% saline solution. The following variables were quantified before, and for 6 min after, initiating a 1-min noxious stimulus to the trachea and skin: ICP, central venous pressure, electromyograms (masseter, deltoid, and intercostal muscles), intrathoracic pressure, and cerebral perfusion pressure (defined as mean arterial pressure -- ICP). Later, the protocol was repeated in the presence of neuromuscular block with pancuronium. Finally, in the same dogs, occlusion of the superior vena cava at its junction with the right atrium was used to increase superior vena caval pressure in 5-mmHg increments, from 5 to 30 mmHG, so that the resulting increases in ICP could be quantified. RESULTS: In unparalyzed dogs whose heads were maintained at the level of the right atrium, there was a 22-mmHg increase in ICP at 1 min after initiating the noxious stimulus (P<0.05). The ICP increase was related to electromyogram activation and a 6-mmHg increase in central venous pressure; however, it was not associated with significant increases in intrathoracic pressure or cerebral perfusion pressure. Treatment with pancuronium abolished the electromyographic, ICP, and central venous pressure responses to noxious stimulus. When superior vena caval pressure was statically manipulated, the resulting ICP increase was only one half the magnitude of the superior vena caval pressure increase. After elevating the head 14 cm, the ratio of ICP to superior vena pressure increases was reduced to one third. CONCLUSIONS: If these results apply to humans, it was concluded that increases in ICP that accompany movement in tracheally intubated patients may arise from two complementary factors: (1) cerebrovascular dilation that correlates with electromyographic activity and is mediated by ascending neural pathways that transmit proprioreceptive information, and (2) passive venous congestion that results from any increase in central venous pressure. The influence of the latter factor can be reduced by elevating the head. (Key words: Blood pressure, venous pressure; mean arterial pressure. Muscle: afferent activity; electromyograms, skeletal. Neuromuscular relaxants: pancuronium.)

Anesthesia↗
PubMed1996

Insulin treatment of corticosteroid-associated hyperglycemia and its effect on outcome after forebrain ischemia in rats.

BACKGROUND: Recent studies have reported that dexamethasone worsens neuronal injury after brain ischemia. This effect is assumed to be secondary to drug-induced hyperglycemia. The current study used a rat model to test the hypotheses that insulin treatment of dexamethasone-induced hyperglycemia would result in a postischemic neurologic outcome that is: (1) better than that of hyperglycemic, dexamethasone-treated subjects; and (2) better than, or equal to, that of saline-treated control subjects. METHODS: Twenty-four halothane-anesthetized (1.0% inspired) rats were randomly assigned to one of three treatment groups (N = 8 in each group): (1) normoglycemic, placebo-treated rats (group P) received an intravenous saline infusion; (2) hyperglycemic, dexamethasone-treated rats (group D) received 2 mg/kg intraperitoneal dexamethasone at days, 1 day, and h before ischemia plus an intravenous saline infusion; and (3) normoglycemic, dexamethasone- and insulin-treated rats (group DI) received the same treatment as group D, plus an intravenous insulin infusion shortly before ischemia. Blood gases and acid-base status were maintained within normal physiologic ranges. Pericranial and rectal temperatures were maintained at normothermia. Forebrain ischemia of 10 min duration was produced using an established model. Neurologic function was assessed by a blinded observer at 24 and 48 h postischemia. Brain histopathology was assessed at the time of ischemia-related death or after the examination at 48 h. All 24 rats were included in the analysis of neurologic function; however, only 21 rats that survived for > or = 24h post-ischemia were included in the histologic analysis. RESULTS: Rats were well matched for systemic physiologic variables, with the exception of glucose concentrations. Plasma glucose concentration immediately before ischemia was as follows: group P = 129 +/- 8 mg/dl (mean +/- SD), group D= 344 +/- 29 mg/dl, and group DI = 123 +/- 17 mg/dl. At 48h postischemia, groups P and DI were minimally injured and had similar functional scores. In contrast, all group D rats died of cerebral ischemia. Histologic injury was significantly worse in group D than in either group P or DI, but did not differ significantly between groups P and DI. When all groups were combined, there was a significant correlation between neurologic function and total histopathology score ranks. CONCLUSIONS: In the current study, dexamethasone administration before brain ischemia resulted in a worsening of postischemic outcome that was relate to drug-induced hyperglycemia. Restoration of normoglycemia, using insulin, resulted in a functional outcome similar to that in group P, and an attenuation of dexamethasone-associated histologic injury.

Animals↗
PubMed1996

Metabolism of glucose, glycogen, and high-energy phosphates during transient forebrain ischemia in diabetic rats: effect of insulin treatment.

BACKGROUND: Hyperglycemia associated with diabetes mellitus will exacerbate neurologic injury after global brain ischemia. Studies in a rat model of forebrain ischemia (bilateral carotid occlusion plus hypotension for 10 min) discovered that acute restoration of normoglycemia in diabetics, using an insulin infusion, resulted in a neurologic outcome that was similar to normoglycemic rats without diabetes. The current study evaluated cerebral glucose, glycogen, lactate, and high-energy phosphate concentrations to identify metabolic correlates that might account for an alteration in postischemic outcome. METHODS: Fifty-four pentobarbital-anesthetized Sprague-Dawley rats were assigned to three groups: chronically hyperglycemic diabetic rats (D; N = 18); insulin-treated, acutely normoglycemic diabetic rats (ID; N = 18); and nondiabetic rats (ND; N = 18). These groups were further divided into groups of six rats each that received either no ischemia, forebrain ischemia of 10 min duration without reperfusion, or ischemia plus 15 min of reperfusion. Brains were excised after in situ freezing, and metabolites were measured using enzymatic fluorometric techniques. RESULTS: Before ischemia, D rats had greater concentrations of brain glucose (12.18 +/- 2.67 micromol/g) than did either ID (5.10 +/- 1.33) or ND (3.20 +/- 0.27) rats (P < 0.05). Preischemic brain glycogen was similar in all groups. At the completion of ischemia, brain lactate concentrations in D were 86% greater than in ID and 61% greater than in ND (P < 0.05), reflecting a higher intraischemic consumption of glucose plus glycogen in D (P < 0.05). High-energy phosphate concentrations, as assessed by the energy charge of the adenylate pool, were better preserved in D (energy charge = 0.60 +/- 0.28) than in either ID (0.29 +/- 0.09) or ND (0.36 +/- 0.07; P < 0.05) rats. After 15 min of reperfusion, the energy charge returned to preischemic values (i.e., 0.91-0.92) in all groups. CONCLUSIONS: These studies demonstrated greater intraischemic carbohydrate consumption and lactate production in D than in ID or ND rats. Under these conditions, intraischemic-but not postischemic-energy status was better in D rats. Acute insulin therapy in ID rats resulted in a metabolic profile that was similar to that of ND rats. These results suggest that, in this model, primary energy failure during ischemia is not the origin of greater injury in hyperglycemic diabetics, nor is energy enhancement the origin of improved outcome after acute insulin treatment.

Adenosine Triphosphate↗
PubMed1996

Hypothermia-associated protection from ischemic brain injury: implications for patient management.

There is a large amount of experimental evidence that mild hypothermia in laboratory animals will protect the brain from ischemic injury. Conversely, mild hyperthermia will exacerbate injury. Supporting data in humans are limited. However, cerebral protection has consistently been demonstrated in humans subjected to complete circulatory arrest during profound hypothermia. Induced and passive mild hypothermia have become common in the management of patients at risk for ischemic neurological injury. Currently, brain temperature is managed largely by altering core temperature. Limitations of this approach are that gradients can develop between brain and core temperatures as a result of the surgical intervention, anesthetic interventions, or the patient's pathology. Further, large reductions in systemic temperature may place an undue burden on systemic physiology and, in extreme examples, systemic factors may adversely affect neurological well-being. Obviously, proper temperature management in humans at high risk for neurological injury will benefit from the following factors: First, greater evidence is needed that small changes in temperature modulate outcome in humans, commensurate with demonstrations of benefit in animals. Second, better methods are needed to monitor brain temperature during periods of risk for ischemic injury. And third, management techniques should be identified that will use brain-to-core temperature gradients to the patient's advantage, thus producing optimal alterations in brain temperature while minimally affecting systemic temperature and physiology. Before these goals can be accomplished, more research is needed, both in laboratory animals and in humans.

Animals↗
PubMed1996

Long-term follow-up of patients treated surgically for medically intractable epilepsy: results in 291 patients treated at Mayo Clinic Rochester between July 1972 and March 1985.

To assess the long-term outcome in patients who underwent surgical treatment of intractable epilepsy, we retrospectively reviewed the medical records of 291 consecutive Mayo patients treated between July 1972 and March 1985. We also evaluated the responses to a follow-up mailed questionnaire or telephone interview completed in 1992. Of the 291 patients, 245 (94% of the 261 patients known to be alive at the time of the survey) responded to the follow-up questioning. Information on the patients' neurologic status (including frequency of seizures, use of antiepileptic drugs, and self-reported assessment of functional capacity) and their overall satisfaction with the operative procedure and postoperative outcome were evaluated. Two hundred ninety patients survived the operation and were dismissed from the hospital. Of the 245 patients who responded to the follow-up survey, 41% and 58% had been free of seizures since surgical treatment and for 3 years preceding the follow-up survey, respectively. In addition, of the respondent cohort, 36% were successfully weaned off all antiepileptic drugs. Patients reported improvement in their daily functional capacity and quality of life after surgical treatment. For example, in comparison with the preoperative assessment, the patients' ability to obtain a driver's license was significantly increased, and seizure-related driving accidents, falls, and bodily injury significantly decreased. Furthermore, on the basis of current knowledge of the operation and its outcome, 85% reported that they would repeat the operative procedure. Thus, surgical treatment of intractable epilepsy is an effective option that is met with patient satisfaction.

Activities of Daily Living↗
PubMed1995

The temporal relationship between intraocular pressure and extraocular muscle activation in cats.

The temporal relationship between intraocular pressure and extraocular muscle activation was studied in cats in response to the administration of the depolarizing muscle relaxant, succinylcholine (i.e. bolus doses of 0.1 and 1.0 mg/kg). Simultaneous changes in intraocular pressure, extraocular muscle force, extraocular electromyograms (EMGs), limb muscle EMGs and hindlimb muscle afferent activity were recorded. Increases in intraocular pressure were associated with extraocular muscle activation and had two components: (1) an initial abrupt increase (lasting seconds) which correlated with fasciculations within the extraocular and hindlimb muscles; and (2) a latter more sustained component (minutes) presumably due to tonic muscle activation which correlated with increases in hindlimb muscle afferent activity (e.g. due to sustained activation of bag 1 intrafusal fibers by succinylcholine). In a separate group of animals, in which the extraocular muscles were detached from the right eye bilateral intraocular pressures were measured: depolarization by succinylcholine caused a significant increase in intraocular pressure only for the eye with intact muscles. Thus, increases in intraocular pressure following the administration of succinylcholine are directly related to the changes in extraocular muscle tension which is dependent on both tonic and phasic muscle fiber responses.

Animals↗
PubMed1995

Temperature changes of > or = 1 degree C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia.

BACKGROUND: Changes in basal temperature of > or = 1 degree C (e.g., fever-induced hyperthermia or anesthesia-related hypothermia) are a common occurrence in neurologically impaired patients. The current study tested the hypothesis that temperature changes as small as 1 degree C or 2 degrees C would significantly alter post-ischemic functional neurologic outcome and cerebral histopathology. The hypothesis was tested in a canine model of transient, complete cerebral ischemia. METHODS: After institutional approval, 21 dogs were randomly assigned to one of three temperature-specific groups: (1) a reference group maintained at 37.0 +/- 0.3 degree C (target temperature +/- range); (2) a 38.0 +/- 0.3 degree C group; or (3) a 39.0 +/- 0.3 degree C group (n = 7 per group). Complete cerebral ischemia 12.5 min in duration was produced using an established model of arterial hypotension plus intracranial hypertension. Right atrial and cranial (beneath the temporalis muscles) temperatures were maintained at the target value, beginning 20 min before ischemia and ceasing 1 h postischemia. Thereafter, temperatures were returned to 37.0 +/- 0.3 degree C in all dogs. After discharge from the intensive care environment, all dogs were placed in a temperature-controlled recovery area. Neurologic assessment was performed by a blinded observer at 24, 48, and 72 h postischemia using a 100-point scoring scale. After the 72 h examination (with the dogs anesthetized) or at the time of ischemia-related death, the brains were excised and preserved. The brains subsequently were histologically scored by a neuropathologist who was unaware of the treatment groups. All 21 dogs were included in the analysis of neurologic function; however, only dogs that survived for > or = 24 h postischemia were included in the histopathology analysis. RESULTS: Dogs were well matched for systemic physiologic variables throughout the study, with the exception of temperature. During the 72 h postischemic examination, dogs maintained at 37 degrees C were either normal or near normal. In contrast, dogs maintained at 39 degrees C were either comatose or died from ischemia-related causes. Dogs maintained at 38 degrees C were intermediate between 37 degrees C and 39 degrees C dogs. When compared with the reference group, both 38 degrees C and 39 degrees C dogs had significantly worse neurologic function scores (P < 0.01 and < 0.001, respectively) and histopathology scores (P < 0.01 for both). There also was a significant correlation between neurologic function and histopathology rank scores (rs = 0.96; P < 0.001). CONCLUSIONS: Small, clinically relevant changes in temperature (1 degree C or 2 degrees C) resulted in significant alterations in both postischemic neurologic function and cerebral histopathology. Assuming that our results are transferable to humans, the results suggest that, in patients at imminent risk for ischemic neurologic injury, body temperature should be closely monitored. Further, the clinician should aggressively treat all episodes of hyperthermia until the patient is no longer at risk for ischemic neurologic injury.

Animals↗
PubMed1995

Cerebral metabolic rate and hypothermia: their relationship with ischemic neurologic injury.

Hypothermia results in a progressive depression of cerebral electrical activity and metabolism. In the setting of cerebral ischemia, large reductions in temperature are associated with a better preservation of high-energy phosphates, a reduced accumulation of toxic metabolites, and an improvement in post-ischemic outcome. With temperature reductions of < or = 6 degrees C, the brain is also partially protected from ischemic neurologic injury; however, this protection does not correlate with measurable alterations in high-energy phosphate depletion or lactate accumulation. Thus, cerebral protection by hypothermia may be due to a variety of factors, including alterations in basal metabolism, ion homeostasis, agonist-specific receptor activity, and cellular structure. Further, the relative influence of these factors may change with progressive reductions in temperature.

Brain↗