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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial levels of ammonia, glutamate, and glutamine and the release of glutamate and glutamine were studied in the isolated perfused rat heart during perfusion with ammonium chloride, epinephrine, and conditions of anoxia or ischaemia. Perfusion for 15 min with effective ammonium chloride concentrations of 0.53, 0.71, and 2.06 mmol/l resulted in glutamine production of 1.34, 0.95, and 4.41 mmol with 15 min-1/200 dry weight compatible with the presence of glutamine synthetase in rat myocardium. Myocardial ammonium content was unchanged by perfusion with 0.53 and 0.71 mmol/l ammonium chloride, but was increased by 1.36 mumol with 15 min-1/200 mg dry weight by perfusion with 2.06 mmol/l ammonium chloride. Increased myocardial contents of ammonia and glutamine were not accompanied by depression of left ventricular pressure. Perfusion with epinephrine (0.20 mug/ml) resulted in an increased myocardial content of glutamine. Anoxia or ischaemia resulted in no changes in ammonia content, and no changes in glutamine or glutamate production. The net release of glutamine into the perfusate was about 10 times the net release of glutamate.
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PMID:Glutamine production by the isolated perfused rat heart during ammonium chloride perfusion. 24 May 5

The effects of anoxia and metabolic inhibitors on inactivation and reactivation of the fast Na system of dog ventricular muscle fibers were studied by examining (dV/dt)max of the action potential upstroke. Anoxia for 60 min, dinitrophenol (DNP) (2.0 mM), and sodium azide (2.0 mM) depressed markedly steady-state (dV/dt)max at each membrane potential produced by changing [K]o. Anoxia tended to prolong recovery slightly, but DNP and azide changed little the time course of recovery of the (dV/dt)max, which was studied by applying double pulses to elicit action potential at different intervals. It is concluded that anoxia, DNP, and azide caused prominent depression of the maximum Na conductance but had less influence on its recovery kinetics.
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PMID:Effects of anoxia and metabolic inhibitors on reaction of the fast sodium system. 103 65

Reverberation of cortical spreading depression (CSD) around a circular obstacle (thermocoagulation lesion) in the frontal cortex of anesthetized rats was elicited by appropriately timed and spaced applications of KCl. The probability of continued reverberation was increased by a pyrrolopyrimidine drug BW 58-271 (10 mg/kg) from 0.93 to 0.98. Three methods of reverberation arrest were tested: a) CSD propagation was blocked by an interfering CSD wave which was initiated in the rear of the reverberating wave, passing through a narrow segment of the circular pathway, and collided with the reverberating wave on the opposite side of the obstacle; b) CSD propagation through a part of the circular pathway was blocked by a 10-min application of 10% MgCl2 on the exposed cortical surface; c) 1-min asphyxia stopped RCSD by increasing the overall refractoriness of cortical tissue. Least reliable was the interference method which stopped reverberation, even with optimum timing, only in 42% of the trials. The magnesium blockade was reliable but slow, the reverberation stopping only 30 min after MgCl2 application. Asphyxia evoked in any phase of the reverberation cycle stopped RCSD reliably and immediately. The results obtained with the interference method confirm the predictions of the mathematical model of impulse reverberation in sheets of excitable tissue. Anoxia seems best suited for practical control of CSD reverberation in functional decortication studies.
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PMID:Techniques for termination of reverberating spreading depression in rats. 111 Mar 77

Canine vein strips were mounted for isometric tension recording. Anoxia did not affect basal tension of saphenous and pulmonary strips mounted in standard Krebs-Ringer solution or after 30 min of incubation in glucose-free solution. Anoxia depressed the strength of spontaneous contractions of mesenteric veins; in glucose-free solution (30 min), anoxia relaxed the strips. Veins placed in glucose-free solution for more than 60 min contracted with anoxia; this contraction was not inhibited by iproveratril. When the vein strips were contracted by norepinephrine or KCl, anoxia depressed the contractions, most in mesenteric and least in saphenous preparations; this depression was greater in the absence of glucose. When oxygen was present, the absence of glucose had little effect on the response to vasoactive agents. Contractions with acetylcholine were depressed by anoxia in mesenteric and pulmonary strips but were augmented in saphenous veins; the latter potentiation was inhibited by iproveratril and by incubation in glucose-free solution. Thus, especially in the saphenous vein, anaerobic glycolysis can provide most of the energy requirements, and intracellular substrates are available for oxidative metabolism.
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PMID:Effects of anoxia and glucose depletion on isolated veins of the dog. 127 67

Electrical depression in the turtle brain during anoxia has been suggested as a strategy for sparing energy and promoting the extraordinary survival capacity of this tissue. The present study was aimed toward defining the changes in membrane properties during anoxia that may underlie such electrical depression. Studies were conducted in isolated cerebellum from turtle brain. Anoxia caused transmembrane potentials (TMP) to become relatively less polarized in most Purkinje cells. In no cell, however, was TMP depolarized to levels associated with the complete loss of transmembrane ion gradients produced by tissue superfusion with iodoacetate during anoxia. Sodium (and likely calcium) spike thresholds were increased, postsynaptic responses from the major afferent input pathways to Purkinje cells were depressed, and input resistance decreased significantly during anoxia. These changes likely contribute to the sparing of energy needed for ion transport and perhaps other functions that may be directly related to cell survival.
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PMID:Membrane and synaptic activity during anoxia in the isolated turtle cerebellum. 144 23

A new in vivo model for studying brain metabolic and haemodynamic oscillatory phenomena during ischaemia is described. In this model acute or chronic occlusion of one or two carotid arteries in the rat is performed. Due to the partial ischaemia developed, oscillations in the level of intramitochondrial pyridine nucleotides (NADH) as well as flavoproteins (Fp) were recorded from the brain by monitoring the fluorescence of these respiratory chain components. The two fluorescent signals (NADH and Fp) were measured by using the time sharing or DC fluorometer/reflectometer. The changes in the reflected light at the excitation wavelengths (366 and 450 nm) were recorded simultaneously. Bilateral carotid artery occlusion induced immediate oscillations (6-9 waves per min) in the mitochondrial redox state as well as in tissue blood volume in both hemispheres. To verify the accuracy of the NADH monitoring system, including the correction technique for haemodynamic and other artifacts, we used the intracarotid artery saline bolus injection approach. The results could be summarized as follows: (1) unilateral carotid artery occlusion resulted in delayed development of oscillations, particularly in the ipsilateral hemisphere; (2) the oscillation phenomenon was reversible if recirculation restarted within 5 min. Occlusion for more than 30 min resulted in irreversible oscillations; (3) the oscillation appearances and intensities were affected by various physiological conditions. Vasoconstriction, induced by hyperoxia, stimulated the oscillations while vasodilation, induced by hypercapnia, depressed them. Anoxia, hypoxia and spreading depression (SD) abolished the oscillations. Glucose injection was not effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oscillations of cortical oxidative metabolism and microcirculation in the ischaemic brain. 167 46

1. The carotid body chemoreceptors are stimulated in situ by hypoxia. We have studied type I cells freshly dissociated from the carotid body of the rabbit. We have used microfluorimetric and patch clamp techniques to examine the responses to hypoxia, to anoxia, and to metabolic inhibition. 2. NADH autofluorescence measured at both 400 and 500 nm increased rapidly and reversibly in response to anoxia or to cyanide (CN-), reflecting a change in mitochondrial metabolism. 3. Indo-1 was used to measure changes in intracellular calcium, [Ca2+]i. Anoxia reversibly increased [Ca2+]i from approximately 50-100 to approximately 200-450 nM in all cells tested. The response showed a striking temperature sensitivity. Responses to hypoxic stimuli were barely detectable at 17-20 degrees C, and were dramatically increased on warming to 36 degrees C. In contrast, responses to K(+)-induced depolarization were only slightly increased in rate of onset and recovery by warming. 4. The rise in [Ca2+]i originated largely from an intracellular store which was slowly depleted by exposure to nominally Ca2(+)-free solutions. Responses were unaffected by blockade of Ca2+ channels with organic (D600, verapamil) or inorganic (Co2+) blockers, by blockade of Na+ channels with tetrodotoxin (TTX), or by increasing action potential duration with tetraethylammonium (TEA). Responses to anoxia were increased by the increased [Ca2+]i loading that follows prior exposure to Ca2(+)-free solutions. 5. Responses to anoxia, to blockade of electron transport by CN-, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP), were equivalent in amplitude. The response to anoxia was occluded by concurrent application of FCCP, suggesting that the Ca2+ originates from the same pool in each case. 6. At 35-36 degrees C, responses to graded levels of PO2 were also graded. Thresholds varied between cells, but were typically 30-50 mmHg. Stimulus-responses curves were essentially hyperbolic, increasing dramatically as the PO2 approached 0 mmHg. 7. The sensitivity of cells to hypoxic solutions was increased by acidification of the superfusate over the pH range from 7.3 to 6.85. 8. Cell-attached patch clamp recordings showed depression of spontaneous action potentials associated with a rise in [Ca2+]i during exposure to anoxic solutions. Whole-cell recordings showed that anoxia increased a voltage-gated gK as described previously for CN-, while producing no change in resting conductance. 9. These data suggest that the rise in [Ca2+]i originates largely from Ca2+ efflux from a mitochondrial pool.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Responses of type I cells dissociated from the rabbit carotid body to hypoxia. 223 19

To evaluate the contribution of extracellular H+ activity toward depression of brain electrical activity during anoxia, extracellular pH (pHe) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectrodes. This study tests the hypothesis that unique regulation of pHe contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO2 ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pHe. Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pHe during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.
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PMID:Extracellular pH and suppression of electrical activity during anoxia in turtle and rat brain. 230 33

1. The effects of brief anoxia (2-4 min) on membrane currents--especially the tetrodotoxin (TTX)-insensitive, Cd2+-sensitive slow inward currents, presumed to be Ca2+ currents--were studied by single-electrode voltage clamp in CA1 and CA3 neurons in submerged hippocampal slices from adult and newborn Wistar rats (PN1-13). 2. In mature neurons, anoxia had no effect on Q-type inward relaxations, but slowly activating C-type outward currents were depressed. The most striking change was the suppression of Ca inward currents (especially the slowly inactivating L-type, by greater than 95%). This effect of anoxia was not sensitive to the N-methyl-D-aspartate (NMDA) receptor blocker, D-aminophosphonovalerate. Anoxia also reversibly abolished the NMDA-evoked inward current. 3. In neurons from newborn animals (PN1-6), Q-type inward relaxations and postanoxic outward currents were very small or undetectable. The slow inward (Ca) currents were smaller than in mature cells, but they showed a clearer separation between low-threshold, fast-inactivating and high-threshold, slowly inactivating currents. Both types of current were more resistant to anoxia (mean depression of L-type was by only 53.3 +/- 5.6%, mean +/- SE). 4. In such immature neurons, the NMDA-evoked inward currents were also more resistant to anoxia. 5. By PN7-13, increasing maturation was reflected in 1) larger voltage-dependent inward currents, 2) increasingly evident Q-type relaxations and postanoxic outward currents, and 3) near-complete blockade of inward currents by anoxia (at PN11-13, mean depression of L-type currents was by 98.5 +/- 1.5%).
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PMID:Anoxia on slow inward currents of immature hippocampal neurons. 255 81

The relation between PO2 and vessel tone was studied in isolated porcine left descending coronary artery rings. Porcine left descending coronary artery mounted isometrically and equilibrated in Krebs-bicarbonate solution (37 degrees C, pH 7.4, when gassed with 95% oxygen + 5% carbon dioxide) exhibited spontaneous basal tone. Decreasing bath PO2 to 40%, 20%, and 12% elicited sustained increases in basal tension which were reversible, ranging between 10% and 20% of the contraction induced by 40 mM potassium chloride. Further decreases in PO2 to near zero (anoxia) resulted in relaxation to baseline. Cyclooxygenase inhibitors indomethacin (5.5 X 10(-6) M), aspirin (5 X 10(-5) M), and meclofenamate (10(-5) M) decreased vascular tone and totally prevented coronary vasoconstriction induced by lowering bath PO2 to 12% or 40% but did not affect anoxic vasorelaxation. Neither basal tone nor the vasoconstriction induced by decreases in bath PO2 were influenced by the antihistaminergic drug pyribenzamine (10(5) M) or by the alpha-adrenergic blocker phentolamine (10(-6]. Isoproterenol (10(-9) to 10(-8) M) or an elevation of the bath potassium concentration from 5.9 to 11 mM significantly augmented coronary vasoconstriction induced by lowering bath PO2 from 95% to 40%. Elevation of the bath potassium chloride concentration to 40 mM further increased isometric force but inhibited the vasoconstriction in response to decreasing PO2 from 95% to 40%. Anoxia relaxed contractions induced by 40 mM potassium chloride, histamine, or ouabain. The data suggest the existence of two distinct oxygen-sensitive mechanisms in porcine coronary arteries, both of which regulate vascular tone. One is activated at relative high PO2 values (10-40%), and the vasoconstriction induced by this mechanism is mediated by vascular prostaglandin synthesis. The other is expressed at low PO2 values (near zero), and the depression of mechanical activity by this mechanism may be related to limitation of oxidative energy metabolism. The first mechanism can be augmented by beta-adrenoceptor stimulation indicative of an interaction between vascular prostaglandin synthesis and beta-adrenergic mechanisms in the coronary artery wall.
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PMID:Two distinct effects of oxygen on vascular tone in isolated porcine coronary arteries. 298 44


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