Biomedical subjects

D Torbati

Publications and source records attributed to D Torbati.

At least 37 records · Page 2Linked to original sources

PubMed1989

Effects of acute hyperbaric oxygenation on respiratory control in cats.

We studied ventilatory responsiveness to hypoxia and hypercapnia in anesthetized cats before and after exposure to 5 atmospheres absolute O2 for 90-135 min. The acute hyperbaric oxygenation (HBO) was terminated at the onset of slow labored breathing. Tracheal airflow, inspiratory (TI) and expiratory (TE) times, inspiratory tidal volume (VT), end-tidal PO2 and PCO2, and arterial blood pressure were recorded simultaneously before and after HBO. Steady-state ventilation (VI at three arterial PO2 (PaO2) levels of approximately 99, 67, and 47 Torr at a maintained arterial PCO2 (PaCO2, 28 Torr) was measured for the hypoxic response. Ventilation at three steady-state PaCO2 levels of approximately 27, 36, and 46 Torr during hyperoxia (PaO2 450 Torr) gave a hypercapnic response. Both chemical stimuli significantly stimulated VT, breathing frequency, and VI before and after HBO. VT, TI, and TE at a given stimulus were significantly greater after HBO without a significant change in VT/TI. The breathing pattern, however, was abnormal after HBO, often showing inspiratory apneusis. Bilateral vagotomy diminished apneusis and further prolonged TI and TE and increased VT. Thus a part of the respiratory effects of HBO is due to pulmonary mechanoreflex changes.

Animals↗

PubMed1988

Effect of prolonged normobaric hyperoxia on regional cerebral metabolic rate for glucose in conscious rats.

The CNS tolerance to prolonged normobaric hyperoxia (NH) was investigated using alterations in regional cerebral metabolic rate for glucose (rCMRgl) as a sensitive measure of brain oxygen poisoning. Conscious rats were continuously exposed either to air or to oxygen for 24 h at atmospheric pressure inside a closed and ventilated environmental chamber. The rCMRgl was measured during ongoing air or oxygen exposures by [14C]2-deoxyglucose (2-DG) autoradiographic technique. No significant difference in the rCMRgl of 29 neuroanatomical structures investigated was found between two groups of air- and oxygen-exposed rats. At the same time however, a significant reduction in the respiratory frequency (f) was observed only in the oxygen-exposed rats. It is suggested that brain energy metabolism is not affected at least up to 24 h NH in conscious rats. The NH-induced reduction in f on the other hand, may be due to alterations in afferent inputs from peripheral and central chemoreceptors or lung stretch receptors. Furthermore, since slight changes in rCMRgl of small neuroanatomical structures are not detectable by limited resolution power of [14C]2-DG autoradiographic technique, a subtle NH-induced damage to central respiratory control mechanisms cannot yet be ruled out.

Animals↗

PubMed1986

Regional cerebral glucose metabolic rate during thirty minutes hypoxia of 7% oxygen in adult conscious rats.

The effect of hypoxia on the regional cerebral metabolic rate for glucose (rCMRgl) was measured in 28 neuroanatomical structures of adult, conscious, unrestrained rats by the 2-[14C]deoxyglucose autoradiographic technique. Rats were cannulated in one femoral artery and vein 3 days before the experiments. The rCMRgl was measured in 15 rats during 30 min air breathing and in 13 rats during 30 min hypoxia of 7% O2 in N2. Statistically significant increases in rCMRgl in the order of 39-95% were observed in 25 of the 28 neuroanatomical structures examined. The highest increases in rCMRgl were observed in cerebral and cerebellar white matter (95% and 60%, respectively), as well as in limbic structures ranging from a 91% increase in the septal nuclei to a 55% increase in the hypothalamus. The superior olivary nucleus and inferior colliculus (auditory structures) were the only structures which did not show changes in glucose utilization. The present data are compared with previous studies during hypoxia in conscious or anesthetized animals. It is concluded that the degree of rCMRgl response to hypoxia is affected by anesthesia, age and species.

Animals↗

PubMed1986

Central nervous system glucose utilization rate during oxygen-induced respiratory changes at 2 atmospheres oxygen in the rat.

Hyperbaric oxygenation (HBO) at pressures higher than 3 atmospheres absolute (ATA) primarily affects the CNS, while at lower pressures, the respiratory functions are predominantly changed. Due to the outstanding respiratory manifestations of HBO at pressures lower than 3 ATA O2, the possible overlapping neurological effects of oxygen toxicity may not be easily identified. However, rats exposed for 1 and 4 h to 2 ATA O2 have shown increases in the regional cerebral metabolic rate for glucose (rCMRgl) when neither visible signs of respiratory nor nervous distress were observed. The purpose of the present study was to differentiate between the CNS and the respiratory effects of HBO at 2 ATA during development of the early signs of the respiratory distress. Changes in the rCMRgl measured by [14C]-2-deoxyglucose (2-DG) autoradiographic technique and respiratory frequency (Rf) were used as criteria for determination of CNS and respiratory effects of HBO, respectively. The results demonstrate no differences in the rCMRgl (28 major structures examined) among 3 groups of conscious rats exposed to 2 ATA O2 and normoxia at 1 and 2 ATA. At the same time a significant reduction was found in the Rf of the oxygen-exposed rats. In conclusion the respiratory system at 2 ATA O2 is apparently affected earlier than, and independent from the CNS. However, due to limited resolution power of the [14C]2-DG technique, the effect of HBO on certain undetected central respiratory control centers cannot yet be ruled out.

Animals↗

PubMed1986

Effect of propranolol on cortical electrical activity in conscious and anesthetized rats.

The effect of propranolol on electrocorticographic (ECoG) activity was studied in conscious and anesthetized rats. Cortical electrodes and femoral venous cannulae were implanted 5 days before the experiments. The ECoG was recorded continuously and analyzed to different frequency bands, 2 hr before and 4 hr after the administration of propranolol. After a single infusion of 2 and 5 mg/kg or 5 consecutive daily doses of 2 mg/kg propranolol, frequent bursts of large amplitude 6-7 c/sec wave in the ECoG were observed. This ECoG phenomenon lasted between 60-100 min after the infusion of propranolol and was entirely abolished by pentobarbital anesthesia. Frequency analysis of the ECoG showed an immediate shift from predominantly delta (delta 0.5-4 c/sec) activity to overwhelmingly theta (theta 4-8 c/sec) activity following the infusion of propranolol. It is suggested that these changes in ECoG induced by propranolol are related to the sleep-enhancing and tranquilizing effects of propranolol.

Anesthesia, General↗

PubMed1986

Blood glucose as a predictive measure for central nervous system oxygen toxicity in conscious rats.

Blood glucose concentration was measured during continuous electrocorticographic (ECoG) recording in conscious rats exposed to 3 and 5 atmosphere absolute oxygen (ATA O2). The preconvulsive oxygen-induced ECoG changes included increased slow wave activity in delta range, followed by the appearance of successive paroxysmal electrical discharges. A correlation between increases in blood glucose concentration and ECoG changes was observed at both 3 and 5 ATA O2. No significant changes in blood glucose concentration were found in the absence of the ECoG changes. Equivalent periods of exposure to N2-O2 normoxic pressures of 1, 3, and 5 ATA did not produce changes either in ECoG or blood glucose concentration. It is therefore considered possible that an increase in blood glucose concentration may be a useful predictive measure of the ECoG manifestations of oxygen toxicity in conscious unrestrained rats. The possible mechanisms for increase in blood glucose concentration during development of brain oxygen toxicity are discussed.

Animals↗

PubMed1985

The relationship between cortical electrical activity and regional cerebral glucose metabolic rate in rats exposed to 3 atmospheres absolute oxygen.

The regional cerebral metabolic rate for glucose (rCMRgl) was autoradiographically measured in conscious rats during 180-210 min of exposure to 3 atmospheres absolute oxygen (ATA O2), 3 ATA N2-O2 normoxia and air at 1 ATA. The exposure time and oxygen pressure in the present study were purposely matched to a parallel project in human subjects. The electrocorticogram (ECoG) was continuously recorded throughout the exposure. According to the ECoG responses, the oxygen-exposed rats fell into two categories: 'resistant' ones, those without changes in ECoG throughout the exposure; and 'sensitive' rats, those with changes in EcoG before or during the rCMRgl measurements. The observed ECoG changes were increased slow wave activity in the delta range, which was in some cases followed by paroxysmal electrical discharges. No changes in rCMRgl were observed in oxygen-exposed 'resistant' rats as compared to air breathing or N2-O2 normoxic rats at 3 ATA. However, in the 'sensitive' rats there were increases in rCMRgl in 8 of the 28 neuroanatomical structures examined as compared to the air breathing and 3 ATA normoxic controls. It is concluded that the increase in rCMRgl are related to the onset of the oxygen-induced preconvulsive changes in ECoG.

Animals↗

PubMed1985

Effect of pentobarbital anesthesia on regional cerebral metabolic rate for glucose during hyperbaric oxygenation in rat.

Hyperbaric oxygenation (HBO) at different pressures and durations of exposure produces an increase in regional cerebral metabolic rate for glucose (rCMRgl) in conscious rats. Pentobarbital anesthesia is known to significantly reduce rCMRgl in rats during air breathing. To test if pentobarbital anesthesia is also effective in reducing HBO-induced increases in rCMRgl, the combined effect of pentobarbital anesthesia and HBO on rCMRgl was autoradiographically measured in 28 neuroanatomical structures. Two groups of rats (11 each) were chronically cannulated in one femoral artery and vein 3 days prior to the experiments. Thirty minutes before the rCMRgl measurements the rats were anesthetized with intravenous injection of 50 mg/kg pentobarbital and exposed to either 1-h air breathing at atmospheric pressure or oxygen at 2 atm absolute. No differences in rCMRgl between oxygen-exposed and air-exposed anesthetized rats were observed in 27 of the 28 neuroanatomical structures examined. The superior olivary nucleus was the only one of the 28 structures showing a significant reduction in rCMRgl following anesthesia and HBO. The possible factors involved in the elimination by anesthesia of the previously observed increases in rCMRgl in conscious rats exposed to HBO are discussed.

Anesthesia↗

PubMed1985

Regional cerebral metabolic rate for glucose immediately following exposure to two atmospheres absolute oxygen in conscious rats.

Hyperbaric oxygenation (HBO) at different pressures produces significant increases in the regional cerebral metabolic rate for glucose (rCMRgl) of various neuroanatomical structures in conscious rats. These increases in rCMRgl precede the neurological signs of oxygen toxicity. In previous studies 1- and 4-h exposures to 2 atmospheres absolute oxygen (ATA O2) produced significant increases in rCMRgl of several neuroanatomical structures. These observations are now extended to include the rCMRgl changes produced during a brief 30-min exposure to 2 ATA O2. The purpose of the present study was to investigate whether HBO has an immediate effect on rCMRgl and to determine the neuroanatomical basis of changes in brain energy metabolism during an early stage of HBO. The rCMRgl was autoradiographically measured by 2-[14C]deoxyglucose technique in conscious unrestrained rats exposed either to air at atmospheric pressure or oxygen at 2 ATA O2 for 30 min. Statistically, no significant changes in rCMRgl were observed between air-exposed and oxygen-exposed groups in the 28 neuroanatomical structures examined. It is concluded that HBO requires a certain amount of time to elicit its effect on rCMRgl in a given pressure. However, the neuroanatomical origins of the previously observed increases in rCMRgl during prolonged HBO could not be detected in this early period of exposure to 2 ATA O2.

Animals↗

PubMed1985

Heparin effects during hyperbaric oxygenation in rats.

The effects of heparin were studied concurrently with development of neurological and respiratory signs of oxygen toxicity in awake unrestrained rats exposed to 3 atmosphere absolute (ATA) oxygen. The modification of the early electrophysiological manifestations of CNS oxygen toxicity by heparin in the absence of obvious signs of pulmonary oxygen toxicity was also determined at 5 ATA oxygen by electrocorticographic recording. The femoral artery of all rats was cannulated two days before the exposures to hyperbaric oxygenation (HBO), and the effect of intraarterial injection of 10 U/100g/3h heparin or an equivalent volume of saline was studied in experimental and control rats, respectively. In rats exposed to 3 ATA oxygen, the latency of the onset of the first oxygen-induced convulsions, the time interval between the first convulsion and death, and the survival time were measured. Exposure to 5 ATA oxygen was continued until the onset of the first preconvulsive paroxysmal electrical discharges (FED), considered to be an early electrophysiological indicator of CNS oxygen toxicity. The onset of convulsions was slightly delayed in heparin-treated rats exposed to 3 ATA oxygen, and the time interval between the first convulsions and death was significantly reduced in heparinized rats. No difference in survival time between heparin- and saline-treated rats was observed. Heparin significantly delayed the time of onset of the FED during exposure to 5 ATA oxygen. Gross postmortem examination of the lungs and internal organs revealed only a bloody froth in the trachea of the heparin-treated rats exposed to 3 ATA oxygen. It is concluded that the heparin-hyperoxic interaction during development of pulmonary and CNS oxygen toxicity may be related to the anticoagulant effect of heparin and hyperoxic-induced pulmonary lesions.

Animals↗

PubMed1985

Effect of propranolol on brain electrical activity during hyperbaric oxygenation in the rat.

The effect of 1, 2, and 5 mg/kg propranolol on the neuroelectrophysiological manifestations of CNS oxygen toxicity was studied in conscious rats. Cortical electrodes for electrocorticographic (ECoG) recording and femoral venous cannula for i.v. infusion were implanted 7 and 3 d, respectively, before the experiment. The rats were divided into 5 groups. Groups I to III were treated with 1, 2, and 5 mg/kg propranolol, respectively, and Group IV with saline. Groups I-IV were exposed to 5 ATA O2 until the appearance of the first cortical paroxysmal electrical discharges (FED), considered to be a preconvulsive electrophysiological manifestation of CNS oxygen toxicity. Rats in Group V were exposed to 5 ATA N2-O2 normoxia and treated with 5 mg/kg propranolol. After the hyperbaric exposures and the i.v. administration of propranolol a typical ECoG pattern consisting of frequent bursts of high amplitude spindle-like waves of 6-7 c/s activity was observed. In hyperbaric oxygen-exposed rats, the paroxysmal electrical discharges were always preceded by the propranolol-induced spindle wave activity (in theta range) and oxygen-induced slow wave activity (in delta range) in ECoG. Infusion of 2 and 5 mg/kg propranolol significantly delayed the time of onset of the oxygen-induced slow wave activity and the FED. It is suggested that the protective effect of propranolol against the neurological manifestations of oxygen toxicity, may be related to its multiple effects on physiological systems rather than beta adrenergic blocking action alone.

Animals↗

PubMed1984

Local cerebral glucose utilization rate following intermittent exposures to 2 atmosphere absolute oxygen.

Previous studies have shown significant increases in regional cerebral metabolic rate for glucose (rCMRgl) in 14 of 28 investigated brain structures in rats exposed to 1-h oxygen at 2 atmosphere absolute (ATA O2). Continuous 4-h exposure to 2 ATA O2 resulted in significant increases only in superior olivary nucleus and inferior colliculus. In the present study, the rCMRgl was autoradiographically measured by the [14C]2-deoxyglucose technique during the last 30 min of 4 intermittent 1-h exposures to either 2 ATA O2 or air at atmospheric pressure, with 3 h of breathing air outside the pressure chamber between each oxygen or air exposure. Statistically significant reductions in rCMRgl of the oxygen-exposed rats were observed in superior olivary nucleus and inferior colliculus, while no changes were observed in 26 other investigated structures. The previously observed increases in rCMRgl in a single 1- or 4-h exposure at 2 ATA O2 were reduced or reversed during the intermittent hyperbaric oxygen exposure. The relation of the observed changes in rCMRgl during single and intermittent hyperbaric oxygen exposures to the extension of tolerance to hyperbaric oxygenation is discussed.

Animals↗

PubMed1984

Correlation of age and body weight with local cerebral glucose utilization in 8-14 week-old rats.

The regional cerebral metabolic rate for glucose (rCMRgl) in 8-14 week-old, male, albino, Wistar rats, weighing 200-385 g was autoradiographically measured using the [14C]2-deoxyglucose (2-DG) technique. Three age-weight groups of rats were tested: (I) 8-9 weeks old (200-250 g, average 227 +/- 14); (II) 10-11 weeks old (255-300 g, average 280 +/- 15 g); (III) 12-14 weeks old (305-385 g; average 331 +/- 25 g). A gradual reduction in rCMRgl was observed in the older and heavier groups. The reductions were statistically significant in 18/28 investigated structures in group III as compared to group I. Since such significant variation in the investigated age-weight range may affect rCMRgl values obtained in different experiments, it is suggested to use narrow and uniform age-weight groups for experimentation concerning brain metabolic functions.

Aging↗

PubMed1984

Regional cerebral glucose utilization rates in rats during asymptomatic period of exposure to 1, 2 and 3 atmospheres absolute of oxygen.

A previous study has shown an increase in regional cerebral metabolic rate for glucose prior to the onset of central nervous system oxygen toxicity in rats exposed to 5 atmospheres absolute of oxygen. The present study was designed to measure regional cerebral glucose utilization rates at pressures used for oxygen therapy and prolonged exposures during which rats are known to be asymptomatic. The regional metabolic rate for glucose in 26 brain structures and in gray and white matter of the thoracic and lumbar spinal cord was autoradiographically measured in awake unrestrained rats using the autoradiographic [14C]2-deoxyglucose technique. Femoral artery and vein cannulae were inserted 3 days before the experiment. Rats were divided into four groups of 15: (a) air control; (b) 6 h at 1 atmosphere absolute oxygen; (c) 4 h at 2 atmospheres oxygen; and (d) 2 h at 3 atmospheres oxygen. Statistically significant increases in glucose utilization (p less than 0.05) are seen only in lateral thalamus at 3 atmospheres oxygen, in superior olivary nucleus and inferior colliculus at 2 atmospheres oxygen and in superior olivary nucleus at 1 atmosphere oxygen. The combination of our previous data at 5 atmospheres oxygen and the present results at prolonged and safe exposures to lower pressures indicated that increased glucose utilization in some neuronal structures precedes the onset of the central nervous system manifestations of oxygen toxicity.

Animals↗

PubMed1983

Regional cerebral metabolic rate for glucose during hyperbaric oxygen-induced convulsions.

Hyperbaric oxygen-induced convulsions in awake unrestrained rats are preceded by electrocorticographic changes including paroxysmal electrical discharges (PED). During oxygen induced convulsions, alterations in regional cerebral metabolic rate for glucose (rCMRgl) were autoradiographically measured and compared with rCMRgl results obtained during pre-convulsive periods in an earlier study. Statistically elevated rCMRgl during oxygen-induced convulsions were found in globus pallidus, substantia nigra, limbic structures, and cerebellar cortex. Significant reductions were found largely in auditory structures and cerebral cortex. This pattern of changes in rCMRgl resembles the pattern of changes during successive PED in the absence of overt convulsions. This similarity may indicate that a common sequence of biochemical changes leads to both oxygen-induced pre-convulsive as well as convulsive electrical discharges.

Animals↗

PubMed1983

Correlation of brain glucose utilization and cortical electrical activity during development of brain oxygen toxicity.

Central nervous system (CNS) oxygen toxicity in rats is characterized by the appearance of alterations in electrical cortical activity (ECoG), followed by the appearance of paroxysmal electrical discharges and finally the onset of clinical convulsions. The correlation between the changes in ECoG and the regional cerebral metabolic rate for glucose (rCMRgl) during progressive oxygen toxicity was studied. Cortical electrodes for ECoG recording and venal arterial cannula for autoradiographic measurement of rCMRgl were chronically implanted. Using [14C]2-deoxyglucose (2-DG), the rCMRgl was measured in conscious unrestrained rats during different periods of exposure to 5 atmospheres absolute oxygen as well as an equivalent normoxic high pressure, while ECoG was continuously recorded and analyzed. A statistically significant increase in rCMRgl in 13 out of 24 investigated brain structures was found during the pre-paroxysmal electrical discharge period. This increase was accompanied by an elevation in slow and a reduction in fast ECoG frequency bands. The largest increase in rCMRgl was found in cerebellar and cerebral cortices, limbic, auditory and visual structures. Following the appearance of the first paroxysmal electrical discharge (FED) some limbic structures and cerebellar cortex showed further increases in rCMRgl, while several auditory and visual structures exhibited a significant decrease. Five atmospheres normoxic pressure had no effect on rCMRgl in any of the brain structures examined. It is concluded that pre-paroxysmal electrical discharge ECoG changes and the onset of the FED during progressive oxygen toxicity are not due to inhibition of brain energy metabolism. The possible mechanisms leading to alterations in rCMRgl during hyperbaric oxygenation are discussed.

Animals↗

PubMed1982

Effects of hyperbaric oxygen on heart, brain, and lung functions in rat.

Electrocardiogram (ECG), electrocorticogram (ECoG), and respiratory rate (RR) were monitored in awake, unrestrained rats during continuous exposure to 1, 3, and 5 ATA O2 until death. The RR showed a consistent pattern at 1 and 3 ATA O2, while no pattern at 5 ATA O2 was observed. A characteristic pattern in heart rate (HR) was demonstrated at 3 ATA O2. At 5 ATA O2 a continuous reduction in HR occurred, while at 1 ATA O2 no significant change was found. The ECG at 3 ATA O2 showed various arrhythmias prior to convulsions, which were severely intensified concurrently with and following convulsions and respiratory distress. The ECG arrhythmias at 1 ATA O2 occurred after the first day of exposure and were intensified during respiratory distress and increased RR. The ECG arrhythmias at 5 ATA O2 usually occurred following the appearance of the first paroxysmal cortical electrical discharges (FED), and were extremely intensified following the onset of the first generalized clinical convulsions. Increased slow-wave activity in ECoG preceded the onset of the FED at 3 and 5 ATA O2. During days 2 and 3 at 1 ATA O2 the ECoG mostly contained slow and low-amplitude waves. The different levels of oxygen in this study often showed different effects on a particular physiological parameter. It is concluded that alterations in ECG, ECoG, HR, and RR at some pressures signal the appearance of severe pathophysiological changes during prolonged hyperbaric oxygen exposure in rats, and that the relations of these effects are not uniform at all oxygen pressures.

Animals↗

PubMed1981

Frequency analysis of EEG in rats during the preconvulsive period of O2 poisoning.

The EEG of rats exposed to hyperbaric oxygenation (HBO) displays electrical discharges prior to the onset of generalized clinical convulsions (GCC). The characteristics of preconvulsive electrocorticogram (ECoG) in awake, unrestrained rats exposed to 3, 4, and 5 ATA O2 were determined. The ECoG was continuously monitored and analyzed by a hybrid analog-digital system until GCC developed. The time integral of rectified voltage of the individual delta (0.5-4 c/s), theta (4-8 c/s), alpha (8-13 c/s) beta 1 (13-20 c/s), and beta 2 (20-30 c/s) bands were plotted vs. time. An elevation in delta and a temporary reduction in alpha activity before the onset of the first electrical discharge (FED) was observed. There was a continuous reduction in beta 1 and beta 2 frequency bands during the entire pre-electrical discharge period. The activity of theta, and alpha frequency bands was significantly elevated only about 1 min before the onset of the FED, and of beta 1 and beta 2 during appearance of the FED. The possible relationship between the occurrence of preconvulsive EEG changes and pathological effects of hyperbaric oxygenation is discussed.

Animals↗