PubMed Health⌕ Search

Biomedical subjects

M S Scheller

Publications and source records attributed to M S Scheller.

At least 37 records · Page 2Linked to original sources
PubMed1991

Hypothermia prevents ischemia-induced increases in hippocampal glycine concentrations in rabbits.

We subjected 10 New Zealand White rabbits to 10 minutes of global cerebral ischemia under either normothermic (37 degrees C) or moderately hypothermic (29 degrees C) conditions. Hippocampal concentrations of glutamate, aspartate, and glycine were monitored using in vivo microdialysis. Outcome was assessed by both neurological and neuropathologic criteria. Hypothermia afforded nearly complete protection from ischemic injury. Ischemia-induced increases in the concentrations of glutamate, aspartate, and glycine in the normothermic group (3, 12, and 3 times baseline) were strikingly attenuated in the hypothermic group. In addition, the prolonged postischemic elevation of glycine levels seen in the normothermic group was absent in the hypothermic group. These results suggest that the neuroprotective properties of hypothermia may reside, in part, in their ability to prevent increases in the extracellular concentrations of amino acids that enhance the activity of the N-methyl-D-aspartate receptor complex.

Animals↗
PubMed1990

A comparison of the cerebral and haemodynamic effects of mannitol and hypertonic saline in an animal model of brain injury.

There has recently been an increased interest in the use of hypertonic saline solutions in the fluid resuscitation of trauma victims and to control intracranial hypertension. In this study, the cerebral and haemodynamic effects of a 3.2% hypertonic saline solution were compared with those of either a 0.9% saline or 20% solution were compared with those of either a 0.9% saline or 20% mannitol solution in a rabbit model of brain injury. Forty-five minutes following the creation of a left hemispheric cryogenic brain lesion, equal volumes of hypertonic saline, 0.9% saline, or mannitol were infused over a 5 minute period. Monitored variables over the ensuing 120 minutes included mean arterial pressure, central venous pressure, intracranial pressure, hematocrit, serum osmolality and oncotic pressure. Upon conclusion of the two hour study period, hemispheric water contents were determined by the wet/dry weight method. There were no significant differences in mean arterial pressure between the three groups at any point during the experiment. Plasma osmolality was significantly increased by 10-11 mOsm/kg in both the mannitol and hypertonic groups. The infusion of either mannitol or hypertonic saline produced a transient decrease in intracranial pressure lasting approximately 60 minutes whereas animals in the saline group demonstrated a continual increase in intracranial pressure. The lesioned hemisphere demonstrated a significantly greater water content than the non-lesioned hemisphere.

Animals↗
PubMed1990

Effects of central bolus injections of potassium chloride on arterial potassium concentration in patients undergoing cardiopulmonary bypass.

The effects of central venous bolus injections of potassium chloride (KCl) on arterial potassium concentration were studied in patients undergoing cardiopulmonary bypass. Ten subjects were studied, and each received a rapid bolus injection of KCl, 33 microEq/kg, both before and after cardiopulmonary bypass. Injections were delivered through the proximal infusion port of a 7.5F pulmonary artery catheter, which was situated in either the superior vena cava or the right atrium. Monitored variables included the electrocardiogram, mean arterial, central venous, and pulmonary artery pressures, end-tidal carbon dioxide and inspired oxygen concentrations, and temperature. Blood was sampled continuously at either the radial artery alone or both the radial artery and aortic root at 2 mL/4.3 s. The difference in magnitude between the maximal potassium concentration achieved and the prebolus baseline potassium concentration (delta K) was correlated with cardiac output, stroke volume, and prebolus baseline potassium concentration (baseline [K+]), using simple linear regression analysis. Although significant hyperkalemia (eg, 7 to 9 mEq/L) developed in both the aortic root and radial artery, this was of no electrocardiographic or hemodynamic consequence, presumably because of the transient nature of the hyperkalemic response, following bolus injection of KCl. There was no significant correlation between delta K and cardiac output or stroke volume; however, delta K did correlate significantly with the Baseline [K+] in a direct linear relationship. It is concluded that central bolus injections of KCl through the proximal infusion port of the pulmonary artery catheter at 33 microEq/kg are safe. This technique should be used cautiously in patients with extremely low cardiac outputs or where intracardiac shunting of blood may exist, as these situations could potentially result in greater hyperkalemic responses than those observed in the current study.

Adult↗
PubMed1990

Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane.

The cerebral effects of sevoflurane were compared in dogs with those of enflurane and isoflurane. Initially, the minimum alveolar concentrations (MAC) of sevoflurane and enflurane were determined and the electroencephalographic (EEG) responses to increasing doses of sevoflurane (1.5, 2.0 and 2.5 MAC) or enflurane (1.5 and 2.0 MAC) in unparalysed animals were examined. Administration of sevoflurane was not associated with seizure activity at any concentration either during normocapnia (PaCO2 5.3 kPa) or hypocapnia (PaCO2 2.7 kPa), even in the presence of intense auditory stimuli. All dogs anaesthetized with enflurane demonstrated sustained EEG and motor evidence of seizure activity induced by auditory stimuli at concentrations of enflurane greater than 1 MAC, particularly during hypocapnia. In a separate group of dogs, the effects of increasing concentrations of sevoflurane and isoflurane (0.5, 1.5 and 2.15 MAC) were compared directly on arterial pressure, cardiac output and heart rate, cerebral blood flow and the cerebral metabolic rate for oxygen (CMRO2) using the venous outflow technique. Sevoflurane, in common with isoflurane, had minimal effects on cerebral blood flow at the concentrations studied, but significantly reduced the CMRO2 at end-tidal concentrations sufficient to produce a burst suppression pattern on the EEG (approximately 2.15 MAC). Both sevoflurane and isoflurane significantly decreased arterial pressure in a dose-dependent manner, but neither drug significantly altered cardiac output.

Acoustic Stimulation↗
PubMed1990

Glucose administration before cardiac arrest worsens neurologic outcome in cats.

The effects of glucose on neurologic and neuropathologic outcome following global cerebral ischemia were examined in 20 cats subjected to 14 min of cardiac arrest, followed by closed chest resuscitation and intensive care monitoring. Beginning 30 min prior to cardiac arrest, 15 ml/kg of 5% dextrose in 0.45% saline or the same volume of 0.9% saline was administered in a blinded fashion over 15 min. Ventricular fibrillation was electrically induced and cardiac resuscitation was performed according to a standardized protocol, which included closed chest cardiac compressions, epinephrine, lidocaine, sodium bicarbonate administration, and electrical defibrillation. Animals not resuscitated within 4 min were excluded from further study. Resuscitated animals were managed in an intensive care setting for 24 h postresuscitation. Neurologic deficits were scored at 2, 4, and 7 days postresuscitation. Subsequently, the animals' brains underwent histologic examination. Nine cats were excluded from data analysis. Three did not meet protocol criteria and six could not be resuscitated within 4 min. As a result of a technical error, the brain of one glucose-treated cat was not analyzed. Six saline-treated and five glucose-treated animals met all protocol criteria and survived for 7 days postresuscitation. Plasma glucose concentration before cardiac arrest was 118 +/- 24 mg/dl (mean +/- SD) in the saline group and 269 +/- 21 mg/dl in the glucose group (P less than 0.01). Neurologic outcome rank at 2, 4, and 7 days postresuscitation was significantly worse in glucose-treated cats (P less than 0.01, P less than 0.01, and P less than 0.01, respectively). The neuropathologic score did not differ between glucose- and saline-treated groups (P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Dexmedetomidine, an alpha 2-adrenergic agonist, decreases cerebral blood flow in the isoflurane-anesthetized dog.

The purpose of this study was to examine the effects of dexmedetomidine, an alpha 2-adrenergic agonist, on cerebral blood flow and metabolic rate in dogs anesthetized with 0.64% isoflurane. After intubation and institution of mechanical ventilation, arterial, venous, pulmonary artery, and sagittal sinus catheters were inserted. Measurements of cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), mean arterial pressure, cardiac output, and blood gas tensions were made at various levels of isoflurane anesthesia (0.64%, 1.9%, and 2.8%), after the administration of 10 micrograms/kg of dexmedetomidine (a dose that has been shown to reduce anesthetic requirements in dogs by greater than 90%) and finally after 0.3 micrograms/kg of the alpha 2-adrenergic antagonist idazoxan. Despite an increase in arterial pressure, dexmedetomidine caused a marked reduction (greater than 45%, P less than 0.05) in CBF when compared with all preceding concentrations of isoflurane. The administration of dexmedetomidine had no effect on the CMRo2. The electroencephalogram showed a loss of high-frequency activity in a pattern similar to that seen with 1.90% isoflurane. Administration of dexmedetomidine was associated with a 57% decrease in cardiac output (to 0.89 L/min). Administration of idazoxan (an alpha 2-adrenergic antagonist) resulted in an increase in cardiac output and a reversal of the electroencephalogram effects. This experiment indicates that 10 micrograms/kg of dexmedetomidine in isoflurane-anesthetized dogs is associated with a profound decrease in CBF and cardiac output in the face of an unaltered CMRo2. Despite the large reduction in the CBF/CMRo2 ratio, there was no evidence of global cerebral ischemia.

Adrenergic alpha-Agonists↗
PubMed1989

The efficacy of three different methods of transtracheal ventilation.

The ability of three different techniques of transtracheal ventilation to reverse hypoxia and provide pulmonary ventilation were examined. Five swine were anaesthetized with isoflurane in oxygen, their tracheas were intubated, and their lungs mechanically ventilated to produce a PaCO2 of 35-40 mmHg. A 14-gauge catheter was inserted percutaneously into the trachea caudad to the tip of the tracheal tube. The animals were then left apnoeic until their oxygen saturation fell to 60 per cent. At this point, attempts were made to ventilate and oxygenate the animals through the tracheal catheter with one of three systems (Jet--50 psi [2585 mmHg] driving pressure controlled with a thumb operated valve, Flush-fresh gas outlet of an anaesthetic machine with flow controlled by the flush button, or Circle--standard anaesthesia circle system with pressures greater than 60 mmHg). Arterial blood gas determinations were made every minute for five minutes after beginning transtracheal ventilation. Both the Jet and Flush modes resulted in a mean PaO2 greater than 250 mmHg within one minute of their initiation whereas the PaO2 with the Circle system never exceeded 180 mmHg even at five minutes. The Flush and Jet modes produced a decrease in the PaCO2 (from 80 mmHg to 35-45 mmHg) over the five minutes. In contrast, it was not possible to provide adequate ventilation with the Circle system as evidence by an increasing PaCO2 (from 80 mmHg to less than 110 mmHg at five minutes).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Obstruction↗
PubMed1989

The noncompetitive N-methyl-D-aspartate receptor antagonist, MK-801 profoundly reduces volatile anesthetic requirements in rabbits.

Rabbits anesthetized with volatile anesthetics were given bolus doses of the n-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Following observation and recording of the hemodynamic and electroencephalographic effects of MK-801, the animals were tested for requirements of volatile anesthetic to prevent movement to a noxious stimulus. It was demonstrated that MK-801 significantly reduced anesthetic requirements in a dose-dependent manner, while also affecting hemodynamics and the electroencephalogram in a manner consistent with the production of a deeper plane of anesthesia.

Anesthesia↗
PubMed1989

The influence of fresh gas flow and inspiratory/expiratory ratio on tidal volume and arterial CO2 tension in mechanically ventilated surgical patients.

The relative importance of fresh gas flow and inspiratory/expiratory ratio in determining delivered tidal volume and PaCO2 was studied in anesthetized adult patients ventilated with a fixed ventilator bellows volume. The fresh gas flows studied were 2, 6, and 10 L/min, and inspiratory/expiratory ratio was either 1:2 or 1:4.5. Bellows volume and respiratory rate were held constant throughout the study. At the lowest fresh gas flow and smallest inspiratory/expiratory ratio, PaCO2 was 43 +/- 2 mm Hg. The PaCO2 decreased progressively and significantly with each increase in fresh gas flow during ventilation with either inspiratory/expiratory ratio setting. PaCO2 averaged 30 +/- 3 during ventilation with the highest fresh gas flow and largest inspiratory/expiratory ratio. As fresh gas flow increased, PaCO2 and tidal volume changed to a significantly greater degree in response to changes in inspiratory/expiratory ratio. These data demonstrate that altering either fresh gas flow or inspiratory/expiratory ratio can produce clinically significant perturbations in PaCO2 and tidal volume during anesthesia. These perturbations occur even if bellows volume is held constant. Furthermore, changes in inspiratory/expiratory ratio will affect these parameters to a greater degree as fresh gas flow is increased.

Adult↗
PubMed1989

A comparison of the effects of central v peripheral bolus injections of potassium chloride on aortic root potassium concentrations in swine.

Clinically relevant doses of potassium chloride (equivalent to 2 mEq/60 kg of body weight) were administered as rapid intravenous (IV) boluses to healthy halothane-anesthetized pigs. Potassium was given either peripherally through a standard IV ear catheter or centrally through the central venous port of a pulmonary artery catheter. Multiple injections were made in each pig, and cardiac output was varied by changing end-tidal halothane concentration. The aortic root potassium concentration was measured every three to six seconds for 90 seconds following potassium administration in each pig. Monitored variables included end-tidal halothane, end-tidal carbon dioxide, pulmonary artery pressure, mean arterial blood pressure, cardiac output, electrocardiogram, and temperature. Following both peripheral and central administration of potassium chloride, aortic root potassium increased significantly. However, the time required to achieve the peak aortic root potassium concentration was significantly less after central administration. In addition, the change in aortic root potassium concentration was greater following central administration compared with peripheral. The change in aortic root potassium concentration correlated inversely with cardiac output only after central, but not peripheral injection. Despite marked transient hyperkalemia in all animals, no electrocardiographic evidence of hyperkalemia could be demonstrated. It is concluded that small bolus doses of potassium chloride (2 mEq/60 kg) can be given safely either peripherally or centrally in normal, hemodynamically stable swine.

Animals↗
PubMed1989

MK-801, an excitatory amino acid antagonist, does not improve neurologic outcome following cardiac arrest in cats.

The excitatory amino antagonist MK-801 was administered to cats following resuscitation from cardiac arrest to evaluate its effect on neurologic and neuropathologic outcome in a clinically relevant model of complete cerebral ischemia. In 29 cats studied, cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was successfully performed in 21 cats. Four animals underwent a sham arrest. MK-801 or placebo was administered in a blinded, randomized manner. Beginning at 5 min post resuscitation (PR), MK-801 330 micrograms/kg over 2 min followed by 73 micrograms/kg/h for 10 h or the same volume of placebo was administered. Resuscitated animals remained paralyzed and sedated in an intensive care setting for 24-30 h PR. Neurologic examinations were performed at 2, 4, and 7 days PR by observers blinded to the treatment groups. Seventeen cats were entered into data analysis (nine MK-801-treated and eight placebo-treated). MK-801-treated animals had a significantly greater neurologic deficit score (NDS) rank (0 = normal, 100 = brain death) 2 days PR (mean rank 12.1 vs. 5.6; p = 0.008). This difference is most likely due to ongoing sedative actions of MK-801. There were no significant differences in NDS rank at 4 (10.3, MK-801 vs. 7.5, placebo) and 7 (9.6, MK-801 vs. 8.3, placebo) days PR. There were no significant differences in frontal cortex, hippocampus, occipital cortex, or cerebellar neuropathology between groups. Sham-arrested cats had normal neurologic and neuropathologic evaluations. In the circumstance of complete cerebral ischemia as employed in the current study, MK-801 had no beneficial effect upon neurologic or neuropathologic outcome.

Animals↗
PubMed1989

Electroencephalographic effects of laudanosine in an animal model of epilepsy.

We examined the effects of laudanosine, one of the principal metabolites of atracurium, on the electroencephalogram (EEG) in an animal model of induced epilepsy. Fourteen rabbits were anaesthetized with 4% halothane in oxygen, the trachea intubated and the lungs ventilated mechanically with 30% oxygen and 1% halothane in nitrogen. Animals were assigned randomly to receive either an infusion of laudanosine (laudanosine group, n = 7) at a rate calculated to produce plasma concentrations similar to those found following the clinical use of atracurium, or an equal volume of normal saline (control group, n = 7). To induce an epileptogenic focus, gelfoam sponges soaked in a pH-adjusted 4% cefazolin solution were applied bilaterally to the parietal cortical surface. This resulted in the production of spike and burst EEG activity in all animals. However, scoring the frequency of the spikes and bursts revealed no significant differences between the laudanosine and control groups. We conclude that, in this animal model of epilepsy, no increased incidence of seizure activity was produced by mean plasma laudanosine concentrations as great as 0.8 micrograms ml-1. These results suggest that the routine use of atracurium is unlikely to provoke seizures, even in the presence of an epileptogenic focus.

Animals↗
PubMed1989

Effect of a hypertonic lactated Ringer's solution on intracranial pressure and cerebral water content in a model of traumatic brain injury.

There has recently been an increased interest in the use of hypertonic solutions for fluid resuscitation of trauma victims. In this study, we examined the acute cerebral effects of a hypertonic lactated Ringer's solution (measured osmolality = 469 mOsm/kg) in an animal model of traumatic brain injury. Following the production of a cerebral cryogenic lesion, eight New Zealand white rabbits were randomized to undergo hemodilution with either lactated Ringer's (measured osmolality = 254 mOsm/kg) or hypertonic lactated Ringer's. Over the course of the experiment the lactated Ringer's group required significantly more fluid than the hypertonic group to maintain stable central venous and mean arterial pressure (245 +/- 5 ml vs. 132 +/- 20 ml; p less than 0.0001). Osmolality increased in the hypertonic group by 13.5 +/- 3.3 mOsm/kg whereas it decreased in the lactated Ringer's group by 5.5 +/- 2.6 mOsm/kg. Intracranial pressure increased in both groups over the course of the experiment but the increase in pressure was greater in the lactated Ringer's group than the hypertonic group (9.5 +/- 2.4 mm Hg vs. 1.7 +/- 1.5 mm Hg; p less than 0.001). Brain water content was significantly increased in the region of the lesion as assayed by both the wet/dry weight method and cortical specific gravity determinations, but there was no difference between the two treatment groups. Water content of the nonlesioned hemisphere was significantly less in the hypertonic group. This study suggests that hypertonic saline solutions may be useful for the resuscitation of hypovolemic patients with localized brain injury.

Animals↗
PubMed1989

Nimodipine does not improve neurologic outcome after 14 minutes of cardiac arrest in cats.

We tested the effects of nimodipine upon neurologic outcome in 31 cats subjected to 14 minutes of cardiac arrest followed by resuscitation. With the dose schedule used, nimodipine had no effect upon neurologic outcome or upon the percentage of ischemic neurons in frontal, hippocampal, occipital, or cerebellar brain sections. The electroencephalographic recovery pattern did not correlate with neurologic or pathologic findings.

Animals↗
PubMed1988

MAC of sevoflurane in humans and the New Zealand white rabbit.

The minimum alveolar concentration of sevoflurane necessary to prevent movement in 50 per cent of patients (MAC) was determined to be 2.05 per cent in 20 adult surgical patients. Because this value was higher than the only other experimentally determined human MAC value for sevoflurane (1.71 per cent), MAC was also determined in New Zealand white rabbits. Comparisons of the MAC ratios of sevoflurane to other volatile anaesthetics in both the human and the rabbit suggest that the human MAC value we obtained for sevoflurane is consistent with experimental determinations of MAC of other volatile anaesthetics in humans.

Adult↗