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11.
Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period. 相似文献
12.
Austin K. Mircheff Dennis J. Ahnen Anisul Islam Nilda A. Santiago Gary M. Gray 《The Journal of membrane biology》1985,83(1-2):95-107
Summary Current procedures for isolating intestinal epithelial cell surface and intracellular membranes are based on the assumption that each organelle is marked by some unique constitutent. This assumption seemed inconsistent with the dynamic picture of subcellular organization emerging from studies of membrane turnover and recycling. Therefore, we have designed an alternative fractionation which is independent ofa priori marker assignments. We subjected mucosal homogenates to a sequence of separations based on sedimentation coefficient, equilibrium density, and partitioning in aqueous polymer twophase systems. The resulting distributions of protein and enzymatic markers define a total of 17 physically and biochemically distinct membrane populations. Among these are: basal-lateral membranes, with Na,K-ATPase enriched 21-fold; brush-border membranes, with alkaline phosphatase enriched as much as 38-fold; two populations apparently derived from the endoplasmic reticulum; a series of five populations believed to have been derived from the Golgi complex; and a series of five acid phosphatase-rich populations which we cannot identify unequivocally. Each of the five enzymatic markers we have followed is associated with a multiplicity of membrane populations. Basallateral, endoplasmic reticulum, and Golgi membranes contain alkaline phosphatase at the same specific activity as the initial homogenate. Similarly, Na,K-ATPase appears to be associated branes at specific activities two-to seven-fold that of the initial homogenate. 相似文献
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In the present study, we have applied the brain microdialysis technique to investigate the effect of the stimulation of adenylate cyclase on the extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the striatum of freely moving rats. Infusion of 8-bromo-adenosine 3',5'-cyclic monophosphate (8-Br-cAMP), 3-isobutyl-1-methylxanthine, or forskolin produced a significant increase in the release of DA. The effect of 8-Br-cAMP was tetrodotoxin, Ca2+, and dose dependent and was saturable. 8-Br-cAMP also caused an increase in the output of DOPAC and HVA. No effects were seen on the output of 5-HIAA, except at the highest 8-Br-cAMP concentration studied. Infusion of 8-Br-cAMP (25 microM, 1.0 mM, and 3.3 mM) together with infusion of (-)-sulpiride (1 microM) or systemic administration of (+/-)-sulpiride (55 mumol/kg i.p.) produced an additive effect on the release of DA. Infusion or peripheral administration of (-)-N-0437 (1 microM or 1 mumol/kg) both decreased the 8-Br-cAMP-induced increase in the release of DA. These results demonstrate that cyclic AMP may stimulate the release of DA, but it is unlikely that this second messenger is linked to presynaptic D2 receptors controlling the release of DA. 相似文献
15.
Rats were fed a diet containing ammonium for up to 6 months. High ammonia levels were attained in brain. The amount of polymerized tubulin in microtubules increased, while the amount of free tubulin remained unchanged. Polymerization of tubulin from brain of ammonium fed rats (30 min, 37°C) was approximately 60% of control. Depolymerization of the microtubules was also affected and took approximately 3 times longer than in controls. These results indicate that both assembly and disassembly of tubulin in brain are impaired by high ammonia levels. Interestingly, the amount of microtubule-associated proteins was not affected. 相似文献
16.
Synaptosomes were isolated from cerebrums of rats fed standard (20% protein) or protein-free diets for 30 days. Arrhenius plots of their (Na+/K+)ATPase activities revealed a transition temperature of 25.5°C for control rats and 23.4°C for rats on protein-free diet, indicating that the latter increases synaptosomal membrane fluidity. The only change observed in the composition of the synaptosomal membranes was a 26% decrease of sialic acid. In synaptosomes from rats on protein-free diet the uptake of tyrosine was slightly reduced while that of glutamate was not affected. However, the exit of glutamate was reduced. 相似文献
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Effect of naloxone on spectral shifts of the diaphragm EMG during inspiratory loading 总被引:10,自引:0,他引:10
J J Petrozzino A T Scardella J K Li N Krawciw N H Edelman T V Santiago 《Journal of applied physiology》1990,68(4):1376-1385
Shifts in the power spectrum of the diaphragm EMG to lower frequencies may occur in the presence of fatiguing inspiratory flow-resistive loads (IRL). However, such a shift of the centroid frequency (fc) could follow a reduction in central output through a differential reduction in end-inspiratory high-frequency power (HFP). In unanesthetized goats, we tested the hypothesis that activation of the endogenous opioid system by IRL would differentially reduce central respiratory output, causing a reduction in fc. IRL was imposed for 180 min after which naloxone (0.1 mg/kg, NLX) was given. fc was computed from the power spectral density estimated by the Welch method. IRL reduced fc from 148.0 +/- 9.8 (SE) Hz at base line to 141.1 +/- 8.9 Hz or to 95.5 +/- 1.3% of base line by 180 min (both P less than 0.05). NLX increased fc to 148.9 +/- 9.9 Hz or to 100.6 +/- 1.1% of base line (both P less than 0.05). The decline in fc during IRL was found to be the result of a reduction in HFP, predominantly toward the end of inspiration. The reversibility of this fc shift with NLX suggests a central mechanism consequent to elaboration of endogenous opioids and not a peripheral (muscular) event consequent to muscle fatigue. 相似文献
19.
A T Scardella J J Petrozzino M Mandel N H Edelman T V Santiago 《Journal of applied physiology》1990,69(3):1104-1109
In a previous study in unanesthetized goats, we demonstrated that continuous naloxone (NLX) administration during inspiratory flow-resistive loading (IRL) significantly increased tidal volume (VT) but not diaphragm electromyogram (EMGdi). End-expiratory gastric pressure did increase with NLX, implying that increased abdominal muscle activity may have accounted for the NLX effect. In the current study we directly tested the hypothesis that endogenous opioid elaboration depresses the abdominal muscle response to a continuous inspiratory flow-resistive load. In seven unanesthetized goats, VT, arterial blood gases, EMGdi, and EMG activity of external oblique (EMGeo), transversus abdominis (EMGta), and external intercostal (EMGei) muscles were monitored. IRL (50 cmH2O.l-1.s) was continued for 3 h, after which NLX (0.1 mg/kg) or saline was given. Our results showed that VT decreased from 323 +/- 32 (SE) ml at baseline to 260 +/- 16 ml 5 min after the load was imposed (P less than 0.05) and further decreased to 229 +/- 18 and 217 +/- 15 ml by 120 and 180 min, respectively (180 vs. 5 min, P less than 0.05). EMGdi increased from 62 +/- 5 to 83 +/- 4% max at 5 min (P less than 0.05) but was unchanged thereafter. In contrast, for this same time period EMGeo increased from 35 +/- 5 to 58 +/- 11% max but decreased from 67 +/- 11% max at 120 min to 37 +/- 5% max at 180 min (P less than 0.05). NLX administration resulted in significant increases in EMGeo (91% above 180-min value). In contrast, EMGdi increased minimally after NLX (15% above 180-min value).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
20.
Carlos Hermenegildo Goizane Marcaida Carmina Montoliu Santiago Grisolía María-Dolores Miñana Vicente Felipo 《Neurochemical research》1996,21(10):1237-1244
We proposed that acute ammonia toxicity is mediated by activation of NMDA receptors. To confirm this hypothesis we have tested
whether different NMDA receptor antagonists, acting on different sites of NMDA receptors, prevent death of mice induced by
injection of 14 mmol/Kg of ammonium acetate, a dose that induces death of 95% of mice. MK-801, phencyclidine and ketamine,
which block the ion channel of NMDA receptors, prevent death of at least 75% of mice. CPP, AP-5, CGS 19755, and CGP 40116,
competitive antagonists acting on the binding site for NMDA, also prevent death of at least 75% of mice. Butanol, ethanol
and methanol which block NMDA receptors, also prevent death of mice. There is an excellent correlation between the EC50 for preventing ammonia-induced death and the IC50 for inhibiting NMDA-induced currents. Acute ammonia toxicity is not prevented by antagonists of kainate/AMPA receptors, of
muscarinic or nicotinic acetylcholine receptors or of GABA receptors. Inhibitors of nitric oxide synthase afford partial protection
against ammonia toxicity while inhibitors of calcineurin, of glutamine synthetase or antioxidants did not prevent ammonia-induced
death of mice. These results strongly support the idea that acute ammonia toxicity is mediated by activation of NMDA receptors. 相似文献