Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic tolerance of low intracellular pH (pH(i)) was studied in well-oxygenated, perfused, neonatal, rat cerebrocortical brain slices (350 microns thick) by inducing severe hypercapnia. In each of 17 separate experiments 80 brain slices (approximately 3.2 g wet weight) were suspended in an NMR tube, perfused with artificial CSF (ACSF), and studied at 4.7 T with 31P and 1H NMR spectroscopy. Spectra obtained every 5 min monitored relative concentrations of lactate or high-energy phosphate metabolites, from which pH(i) and extracellular pH were determined. Unperturbed slice preparations were metabolically stable for > 10 h, with no significant changes occurring in pHi, ATP, phosphocreatine (PCr), inorganic phosphate, or lactate. Different levels of hypercapnia were produced by sequentially perfusing slices with the following different ACSF batches, each having previously been equilibrated with a specific mixture of CO2 in oxygen: (a) 10% CO2, 15 min of perfusion; (b) 30% CO2, 15 min of perfusion; (c) 50% CO2, 15 min of perfusion; (d) 70% CO2, 30 min of perfusion; (e) 50% CO2, 15 min of perfusion; (f) 30% CO2, 15 min of perfusion; and (g) 10% CO2, 15 min of perfusion. At the completion of this protocol slices were again perfused with fresh ACSF that was equilibrated with a 95% O2/5% CO2 gas mixture. In each of five separate 1H and 31P experiments, brain slices were recovered within 2 h after termination of exposure to high CO2. The pHi was determined from measurements of the chemical shift difference between phosphoethanolamine and PCr, using a calibration curve obtained for our preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Tolerance of low intracellular pH during hypercapnia by rat cortical brain slices: A 31P/1H NMR study. 140 24

NMR in vivo spectroscopy is one of the few methods available for non-invasive investigations of cerebral metabolism in animals and humans. 31P and 1H spectroscopy are particularly suitable for monitoring the cerebral energy metabolism by determining the cerebral levels of ATP, ADP, phosphocreatine (PCr), inorganic phosphate (Pi), lactate and intracellular pH (pHi). These techniques also seem to be suitable for studying the effects of anesthetics by directly comparing the anesthetized and unanesthetized states in the same subject. The effects of halothane and isoflurane on the changes elicited in the cerebral energy metabolism by experimental hypercapnia were investigated by in vivo NMR spectroscopy. Halothane was found to aggravate the decrease in PCr attributed to the shift in creatine kinase equilibrium induced by the cerebral acidosis associated to hypercapnia, while the level of cerebral ADP was decreased to a lesser extent than in unanesthetized animals. In contrast isoflurane did not modify the changes in cerebral energy metabolism elicited by hypercapnia except that the decrease in PCr was significantly slowed, suggesting a lower creatine kinase activity. These data indicate that isoflurane and halothane act by two different mechanisms to produce a decrease in oxygen consumption. Halothane could interfere with oxidative metabolism by disturbing ATP metabolism, while isoflurane could decrease oxygen consumption by a general sedative action, slowing both cerebral functional activity and cerebral energy homeostasis.
 ...
PMID:[Value of in vivo NMR spectroscopy in the study of cerebral metabolism under inhalation anesthesia]. 184 37

Phosphocreatine (PCr) and intracellular pH changes were monitored by 31P-NMR spectroscopy in isolated, arterially perfused cat biceps and soleus muscles, while the pH of the CO2-bicarbonate buffered perfusate was decreased from 7.1-7.4 to 6.4-6.7 by increasing the CO2 in the equilibrating gas from 5 to up to 70%. In biceps (fast twitch) muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force decreased by 8%, but the rise and relaxation times of tetanic were not significantly changed. In soleus muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force was unchanged, but the rise and relaxation times of tetani were increased by 27 and 112%, respectively. In both muscles greater decreases in tetanic force were observed during repetitive or ischemic stimulation, which resulted in intracellular pH similar to that produced by hypercapnia. Contrary to previous reports, there was no significant decrease in PCr level in either muscle type with decreased intracellular pH. In the soleus at 30 degrees C there was a significant increase in PCr level with decreased pH.
 ...
PMID:Effect of decreased pH on force and phosphocreatine in mammalian skeletal muscle. 190 90

In vivo measurement of cerebral physiology by dynamic contrast-enhanced NMR is demonstrated. Time-resolved images of the cerebral transit of paramagnetic contrast agent were acquired using a new ultrafast NMR imaging technique and a novel mechanism of image contrast based on microscopic changes in tissue magnetic susceptibility. Global hypercapnia in dogs was used to establish the relationship between susceptibility-induced signal change and brain blood volume, and the response of gray and white matter to this microvascular stimulus was measured.
 ...
PMID:Functional cerebral imaging by susceptibility-contrast NMR. 235 35

The energy metabolism and the brain intracellular pH regulation under arterial CO2 tensions of 25-90 mm Hg were investigated in unanesthetized spontaneously breathing rats by in vivo phosphorus nuclear magnetic resonance spectroscopy (31P NMR). The 31P brain spectra, recorded with a high resolution spectrometer (AM 400 Brucker), allowed repeated non-invasive measurements of cerebral pH (pHi), phosphocreatine (PCr), inorganic phosphate (Pi) and adenosine triphosphate (ATP) levels in 15 rats breathing a gas mixture containing 21% O2, N2, and a varied percentage of CO2. The pHi decreased significantly when the paCO2 was increased by hypercapnia. The percentage of pH regulation, estimated from the linear regression analysis of pHi versus the logarithm of the paCO2 was 78%. This result indicates that spontaneously breathing unanesthetized animals have better pHi regulation under hypercapnia investigated than that estimated for higher levels of hypercapnia in previous studies on unanesthetized animals, suggesting that there is a threshold for this highly efficient regulation. Furthermore, there were no significant correlations between the PCr, ATP and Pi levels and the paCO2 levels during hypercapnia. This indicates that physiological variations of the CO2 tension in the blood, and consequently in the brain parenchyma, have little effect on cerebral energy metabolism in unanesthetized spontaneously breathing animals.
 ...
PMID:Cerebral intracellular pH regulation during hypercapnia in unanesthetized rats: a 31P nuclear magnetic resonance spectroscopy study. 236 88

The build-up and clearance of halothane in rat brain have been measured non-invasively by 19F NMR spectroscopy using a surface coil placed on the intact scalp. When the halothane supply (3% in O2/N2O, 33/66%) was turned off, the 19F signal decreased exponentially to approximately 50% of the initial value, with a time constant, in normal rats, of 8.6 +/- 0.7 min (mean +/- SEM, n = 16), followed by a decay slower by at least one order of magnitude. The time constant of the rapid decay (tau), which was found to be specific for brain, was reduced in hypoxic/hypercapnic (5% O2/5% CO2) rats to 2.9 +/- 0.2 min (p = 0.001, n = 4), in rats infused with physostigmine (20 micrograms/kg/min i.v.) to 5.7 +/- 0.3 min (p = 0.005, n = 6) and increased in rats injected with pentothal (40 mg/kg i.p.) to 10.7 +/- 1.6 min (p = 0.2, n = 5). Based on the theory of exchange of inert gas at the lungs and tissues developed by Kety, the rapid exponential decay of the 19F signal was used to calculate relative cerebral blood flow (CBF). Assuming the cortical CBF in a normal rat to be about 130 mL min-1 100 g-1, the following CBF values (means +/- SEM) were obtained: controls 130 +/- 10, hypoxia/hypercapnia 390 +/- 59, hypercapnia 220 +/- 25, physostigmine 195 +/- 26, pentothal 105 +/- 23 mL min-1 100 g-1. These values are in good agreement with published values obtained with established methods.(ABSTRACT TRUNCATED AT 250 WORDS)
NMR Biomed 1989 Sep
PMID:Non-invasive determination of cerebral blood flow changes by 19F NMR spectroscopy. 251 56

The activity of electroencephalogram (EEG) and cortical somatosensory evoked potential (SEP) was suppressed during cerebral ischemia in rats subjected to the 4-vessel occlusion. Considerable variations were demonstrated in the decrease of phosphocreatine and ATP concentration during ischemia among the rats measured with 31P-NMR, accompanied with cerebral acidification. Hypercapnia, induced in the rats studied by the inhalation of a gas mixture of 30-40% CO2, suppressed the activity of EEG and cortical SEP. The cerebral acidification observed during the ischemia was more severe than that under the hypercapnia, implying that cerebral acidification is one of the possible causes for the decrease in the electrical activity of the brain during ischemia.
 ...
PMID:Effect of cerebral ischemia and hypercapnia on cerebral pH studied with 31P-NMR and electrical activity in rat brain. 272 63

31P NMR brain spectra were obtained from piglets over a range of mild hypocarbia to severe hypercarbia (PaCO225 to 198 mm Hg). The chemical shifts of the phosphoethanolamine and inorganic phosphate were used to calculate intracellular brain pH (pHet and pHpi, respectively). Both pHpi and pHet underwent parallel significant decreases during hypercarbia, corresponding to 51 and 53% pHregulation, respectively. We conclude that the chemical shift of the phosphomonoester peak in vivo can be used to measure decreases in intracellular pH in neonatal brain.
 ...
PMID:Quantitation of acidosis in neonatal brain tissue using the 31P NMR resonance peak of phosphoethanolamine. 312 49

When exposed to hypercapnia, several muscles deteriorate with respect to their mechanical performance. Exposure to metabolic acidosis and, perhaps surprisingly, to compensated metabolic acidosis has the same effect on the diaphragm. The mechanisms involved in these effects remain unclear. If the diaphragmatic intracellular pH (pHi) is assumed to decrease with hypercapnia, to remain unchanged during metabolic acidosis, and to increase during compensated metabolic acidosis, it would appear that different mechanisms must be responsible for the depreciation in the diaphragm's mechanical performance. The present experiments using 31P nuclear magnetic resonance (31P-NMR) spectroscopy were undertaken to determine the effect of metabolic acidosis and compensated metabolic acidosis on pHi and on high-energy phosphate metabolites in the resting rat diaphragm. A whole diaphragm was slightly stretched while being stitched onto a fiberglass mesh. The area approximated that at functional residual capacity. It was superfused in the NMR sample tube with a phosphate-free Krebs-Ringer bicarbonate solution [( HCO3-] = 6 meqO equilibrated with either 95% O2-5% CO2 or 98.75% O2-1.25% CO2). Spectra were acquired during 15-min intervals for control (30 min of normal Krebs-Ringer bicarbonate superfusate, equilibrated with 95% O2-5% CO2), for 120 min of exposure to either form of acidosis and for 60 min of recovery with normal superfusate. The pHi decreased rapidly during metabolic acidosis but did not change significantly during compensated metabolic acidosis. In both forms of acidosis, phosphocreatine declined gradually but not significantly, whereas ATP and inorganic phosphate did not change at all. The results suggest that HCO3- passes freely through the diaphragmatic sarcolemma, very much like the cardiac sarcolemma.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:NMR study of rat diaphragm exposed to metabolic and compensated metabolic acidosis. 320 72

We used the transmembrane distribution of 5,5-[2-14C]dimethyloxazolidine-2,4-dione ([14C]DMO) and 31P magnetic resonance spectroscopy (NMR) to investigate the effects of hypercapnia on intracellular pH (pHi) in brain and skeletal muscle of two lizard species: Anolis equestris and Dipsosaurus dorsalis. In control animals (normocapnic), plasma PCO2 (3.3 +/- 0.1 kPa) and plasma pH (7.52 +/- 0.01) for D. dorsalis were not significantly different from the values for A. equestris (2.8 +/- 0.2 kPa and 7.59 +/- 0.02, respectively). Furthermore 60 min of 5% CO2 increased plasma PCO2 and decreased plasma pH by the same amounts in both species. Brain pHi values determined with the DMO method were not significantly different from values determined with NMR. Control values of brain pHi (DMO, 7.16 +/- 0.01; NMR, 7.11 +/- 0.02) and muscle pHi were significantly higher for D. dorsalis (DMO, 7.15 +/- 0.03) than for A. equestris (DMO, 6.99 +/- 0.03; NMR, 7.02 +/- 0.02 for brain; DMO, 6.97 +/- 0.03 for muscle). In addition, changes in tissue pHi after 60 min of 5% CO2 were significantly different for the two species. In D. dorsalis muscle and brain pHi decreased significantly after hypercapnia, whereas in A. equestris muscle pHi decreased significantly but brain pHi was unchanged. Our findings were independent of the methods used to determine pHi. The smaller change in brain and muscle pHi than in plasma pH for A. equestris is consistent with the view that pHi regulation involves active processes such as transmembrane ion transport.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Intracellular pH in lizards after hypercapnia. 773 98


1 2 3 4 5 Next >>