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A Mayevsky

Publications and source records attributed to A Mayevsky.

At least 109 records · Page 6Linked to original sources

Pyridine nucleotide oxidation-reduction state of the cerebral cortex in the awake gerbil.

A new approach to study the effect of ischemia on the brain of the awake gerbil is described. The measurement of NADH fluorescence from the surface of the cortex is done by a time-sharing fluorometer/reflectometer connected to the brain via a flexible light guide and an implanted cannula. The response of the gerbil brain to anoxia and spreading depression is described. By unilateral occlusion of the carotid artery an increase in NADH was measured in the ipsilateral hemisphere.

Animals↗

Heterogeneity of oxygen delivery in normoxic and hypoxic states: a fluorometer study.

An on-line, real-time histogram display of heterogeneity of oxygen delivery to perfused and in situ organs is afforded by a flying-spot fluorometer that provides excitation for either oxidized flavoprotein of the mitochondrial space or reduced pyridine nucleotide of mitochondrial and cytosolic spaces. Emission from the two fluorochromes is acquired at 10(4) to 10(5) data points/s and histograms of the fluorescence intensity versus the number of occurrences of that intensity are displayed at 1--10 times per second. The histograms show alterations of the intensity and of the degree of heterogeneity of the redox states of perfused heart with model coronary occlusion, of perfused and in situ rat liver, and of rat and gerbil models of stroke. The percentage change of oxygen delivery to the intracellular space can be calculated from the areas under the histogram.

Brain↗

The dynamics of K+ leakage and recovery in cerebral ischemia.

A combination of K+/DC surface electrode and a fiberoptic fluorometric probe are applied to measurements in brain during cerebral ischemia. The kinetics of the responses of extracellular K+ activity and intracellular NADH fluorescence in the gerbil cerebrum following reversible carotid ligation are measured. K+e shows a two-phase response to carotid occlusion and an extended recovery phase following recirculation. The length of the recovery phase is dependent on the duration and severity of the ischemic period. In the gerbil model the degree of communication in the anterior circulation is variable, whereas a bilateral carotid occlusion is presumed to give complete cerebral ischemia. Pyridine nucleotide fluorescence serves as an indicator of the degree of ischemia. Bilateral carotid occlusions of up to 35 minutes in duration were performed. K+e reaches 30--50 mEq/liter in the extracellular space within the first two minutes. This represents cell depolarization and equilibration of K+ activity levels. Recovery appears to be complete in terms of the ability of the system to clear raised levels of K+e from the extracellular space.

Animals↗

Application of a solid membrane ion-selective electrode to in vivo measurements.

A solid membrane electrode containing a highly selective ion-complexing agent immobilized in a polymer membrane is applied to measurements in vivo from the surface of an organ. For the measurements reported here, an ion-complexing agent selective for potassium is incorporated in a silicone rubber membrane and applied to measure ion changes in the brain. Comparison is made to the measurements recorded with an ion-selective microelectrode in the cortical tissue. The surface electrode compares favorably with the microelectrode in terms of amplitude of response and response time for the changes seen in the phenomenon of cortical spreading depression of Leao. The methods reported here are amenable to a selection of ion measurements by incorporation of a suitable ion exchanger in a polymer membrane. Extracellular ion activity is monitored in the anesthetized animal by holding the electrode in a balanced suspension which provides a light, flexible contact to the organ of interest. In the unanesthetized animal, when recording from the brain, the electrode is fixed in a skull-implanted cannula.

Animals↗

Brain energy metabolism of the conscious rat exposed to various physiological and pathological situations.

Using a time-sharing fluorometer-reflectometer, pyridine nucleotide (NADH) and flavoprotein (Fp) fluorescence, as well as reflected light at the excitation wavelength, were measured and correlated with the electrical activity of an awake cerebral cortex. Exposure of the rat to a nitrogen atmosphere (anoxia) led to an increase in signals representing the reduction of pyridine nucleotides and flavins, with very similar kinetics. Inducement of partial ischemia by bilateral carotid artery ligation led to an increase in NADH, accompanied by a very small effect on the electrical activity (ECoG). In most animals, 2-3h after ligation, the ECoG became flat or depressed. Exposure of this ischemic cerebral cortex to KC1 solution caused depression of the electrical activity without metabolic response probably due to the limitation of oxygen supply. The metabolic state of an awake cerebral cortex was identified by exposing the brain to various levels of oxygen, epileptoform activity, spreading depression, hyperbaric pressure of oxygen and an uncoupler. From our results we conclude that the awake cerebral cortex is close to the resting state, state 4, rather than to the active state, state 3.

Animals↗

Metabolic responses of the awake cerebral cortex to anoxia hypoxia spreading depression and epileptiform activity.

Using the time sharing fluorometer/reflectometer the measurement of NADH fluorescence as well as the reflected light was obtained from the surface of the awake rat brain cortex. The light was transferred to and from the brain via a flexible light pipe (made of quartz fibers) connected to a cannula implanted permanently above the brain. Exposing the rat to pure nitrogen atmosphere increased the fluorescence (reduction of NADH) by 32.3 +/- 6.1% in comparison to the normoxic fluorescence level. During cortical spreading depression (SD) the NADH fluorescence decreased (oxidation of NADH) by 17.3 +/- 2.8%. Exposing the rat to nitrogen after SD was elicited blocked the oxidation cycle observed during SD. Exposing the awake ras to 10, 7.5 or 5% O2 did not block the response of the brain to spreading depression or to Metrazol applied locally to the cortex. Under hypoxic conditions the brain showed a typical response to SD, namely, an oxidation cycle of NADH except that the duration of the cycle was longer and the decrease in the NADH level was smaller. The EEG activity recovered to normal even under 5%. The same effect of hypoxia was found when Metrazol was applied and epileptic activity was developed.

Animals↗

The effect of trimethadione on brain energy metabolism and EEG activity of the conscious rat exposed to HPO.

The use of trimethadione (TMO) as a protector in hyperbaric oxygen toxicity in the conscious rat has been examined in detail. The oxidation-reduction state of pyridine nucleotides was measured simultaneously with the EEG activity from the surface of the brain cortex. From the data obtained, a few parameters were calculated. The results show that in TMO-treated animals the time to the onset of convulsions, the time to the onset of NADH oxidation-reduction cycles, and the survival time were significantly longer than in the control group. The effect of TMO on the EEG shows that the tonic phase of the convulsive activity was almost completely abolished.

Animals↗

In vivo measurement of 32P in the brain of a freely moving rat.

A new method for measuring the uptake of materials labeled with radioactive phosphorus (32P) in the brain of a freely moving rat is described. The rate of uptake in the brain of a single animal of 32P-labeled phosphate was compared to the uptake rate in the animal's blood or liver. A comparison was made between the uptake following an intravenous (IV) or an intraperitoneal (IP) injection. The effect of convulsions caused by injections of metrazol on the kinetics of 32P uptake in the brain is described.

Animals↗

In vivo measurement of variations in the oxygen 18 content of water in rat brain.

A method of analysis for oxygen 18 is described, based on the anodic oxidation of specially prepared tantalum wires implanted through cannulas into the tissue of living animals. The thin anodic oxide layer formed on these wires is then analyzed by the 18O(p,alpha)15N reaction. The isotopic oxygen concentration of water in the brain obtained by this method compares very well with the values obtained by conventional analysis using mass spectrometry. This in vivo method of nuclear microanalysis has been used in both metabolic and equilibration experiments involving oxygen 18. The half-life for the turnover of 18O in body water was found to be about 3 days. A simple three-pool model is presented which can account for the experimental results obtained from the dilution by body water of interperitoneally injected water highly enriched in 18O.

Animals↗