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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocapnia is known to have an antiphosphaturic effect that overcomes the phosphaturic effect of hypoxia. The objective of this study was to examine whether conscious rats exposed to acute hypoxia show a decrease in phosphate excretion due to the concomitant hypocapnia. Wistar rats weighing 200 g were exposed to hypoxia (inspired oxygen fraction = 0.10) or normoxia (inspired oxygen fraction = 0.21) for 6 h; and rats were alternately exposed to hypoxia or normoxia every 12 h for a total 36 h. Renal clearance and hormone studies were performed. Rats exposed to 6 h of hypoxia (n = 11) showed significant hypophosphaturia and decreases in absolute and fractional excretion of phosphate (0.38 +/- 0.10 microgram min-1, mean +/- SE, P < 0.0001 and 0.59 +/- 0.15%, P < 0.0001) as compared with normoxic rats (n = 11, 3.91 +/- 0.68 micrograms min-1 and 5.62 +/- 0.85%). In addition, nephrogenous adenosine 3',5'-cyclic monophosphate level per glomerular filtrate was significantly decreased (-0.87 +/- 0.64 nmol dL GF-1, P < 0.05) and plasma parathyroid hormone level was unchanged (45.2 +/- 9.5 pg mL-1) after 6 h of hypoxia as compared with normoxic rats (4.03 +/- 1.83 nmol dL GF-1 and 54.3 +/- 10.4 pg mL-1). A parallel increase in urinary noradrenaline and a decrease in dopamine excretion was observed in rats after 6 h of hypoxia. The decreased phosphate and adenosine 3',5'-cyclic monophosphate excretion during acute hypoxia were restored to normoxic levels by reoxygenation with 21% oxygen in the study of 12-h intermittent hypoxia. In summary, (1) hypoxia produced by inhalation of 10% oxygen for 12 h or less causes reduced phosphate and adenosine 3',5'-cyclic monophosphate (cAMP) excretion by spontaneously breathing rats; (2) these effects are reversed by reoxygenation and (3) hypoxia elicits a parallel increase in noradrenaline excretion and a decrease in dopamine excretion. These data suggest that renal adrenergic and dopaminergic systems play important roles in hypophosphaturia during acute hypoxia in conscious rats.
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PMID:Phosphate and cyclic AMP excretion decreases during less than 12 hours of hypoxia in conscious rats. 897 Dec 52

1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)-treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia. 2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n = 8) or saline vehicle (n = 9). Thirty-minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx- (n = 7) and saline-treated (n = 8) rats. 3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3', 5'-cyclic mono-phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late-phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH-mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline and constant dopamine excretion were observed in endotoxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle. 4. To test whether renal tubular sensitivity to parathyroid hormone related-protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx- (n = 7) and saline-treated rats (n = 7) was examined. Parathyroid hormone related-protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx-than in saline-treated rats. 5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH-mediated phosphaturia after PTH infusion.
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PMID:Renal regulation of phosphate excretion in endotoxaemic rats. 914 87

We previously have demonstrated that hypocapnia aggravates and hypercapnia protects the immature rat from hypoxic-ischemic brain damage. To ascertain cerebral blood flow (CBF) and metabolic correlates, 7-d postnatal rats were subjected to hypoxia-ischemia during which they were rendered either hypo-(3.5 kPa), normo- (5.1 kPa), or hypercapnic (7.3 kPa) by the inhalation of either 0, 3, or 6% CO2, 8% O2, balance N2. CBF during hypoxia-ischemia was better preserved in the normo- and hypercapnic rat pups; these animals also exhibited a stimulation of cerebral glucose utilization. Brain glucose concentrations were higher and lactate lower in the normo- and hypercapnic animals, indicating that glucose was consumed oxidatively in these groups rather than by anaerobic glycolysis, as apparently occurred in the hypocapnic animals. ATP and phosphocreatine were better preserved in the normo- and hypercapnic rats compared with the hypocapnic animals. Cerebrospinal fluid glutamate, as a reflection of the brain extracellular fluid concentration, was lowest in the hypercapnic rats at 2 h of hypoxia-ischemia. The data indicate that during hypoxia-ischemia in the immature rat, CBF is better preserved during normo- and hypercapnia; the greater oxygen delivery promotes cerebral glucose utilization and oxidative metabolism for optimal maintenance of tissue high energy phosphate reserves. An inhibition of glutamate secretion into the synaptic cleft and its attenuation of N-methyl-D-aspartate receptor activation would further protect the hypercapnic animal from hypoxic-ischemic brain damage.
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PMID:Effect of carbon dioxide on cerebral metabolism during hypoxia-ischemia in the immature rat. 921 33

A unique method for simultaneously measuring interstitial (pHe) as well as intracellular (pHi) pH in the brains of lightly anesthetized rats is described. A 4-mm microdialysis probe was inserted acutely into the right frontal lobe in the center of the area sampled by a surface coil tuned for the collection of 31P-NMR spectra. 2-Deoxyglucose 6-phosphate (2-DG-6-P) was microdialyzed into the rat until a single NMR peak was detected in the phosphomonoester region of the 31P spectrum. pHe and pHi values were calculated from the chemical shift of 2-DG-6-P and inorganic phosphate, respectively, relative to the phosphocreatine peak. The average in vivo pHe was 7.24+/-0.01, whereas the average pHi was 7.05+/-0.01 (n = 7). The average pHe value and the average CSF bicarbonate value (23.5+/-0.1 mEq/L) were used to calculate an interstitial Pco2 of 55 mm Hg. Rats were then subjected to a 15-min period of either hypercapnia, by addition of CO2 (2.5, 5, or 10%) to the ventilator gases, or hypocapnia (PCO2 < 30 mm Hg), by increasing the ventilation rate and volume. pHe responded inversely to arterial Pco2 and was well described (r2 = 0.91) by the Henderson-Hasselbalch equation, assuming a pKa for the bicarbonate buffer system of 6.1 and a solubility coefficient for CO2 of 0.031. This confirms the view that the bicarbonate buffer system is dominant in the interstitial space. pHi responded inversely and linearly to arterial PCO2. The intracellular effect was muted as compared with pHe (slope = -0.0025, r2 = 0.60). pHe and pHi values were also monitored during the first 12 min of ischemia produced by cardiac arrest. pHe decreases more rapidly than pHi during the first 5 min of ischemia. After 12 min of ischemia, pHe and pHi values were not significantly different (6.44+/-0.02 and 6.44+/-0.03, respectively). The limitations, advantages, and future uses of the combined microdialysis/31P-NMR method for measurement of pHe and pHi are discussed.
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PMID:In vivo microdialysis of 2-deoxyglucose 6-phosphate into brain: a novel method for the measurement of interstitial pH using 31P-NMR. 988 94

The aim of the paper was to describe an unusual case of non lactic metabolic acidosis connected to hypophosphatemia and refractory to infusion of bicarbonate. A 37 year old man was admitted to Intensive Care Unit with a severe metabolic acidosis. On admission the arterial gas analysis showed non lactic metabolic acidosis (pH 7.17; base excess [BE] -20.3; lactic acid 0.8 mMol/L), with hypoxemia and critical hypocapnia. Despite therapy with bicarbonate the acidosis persisted. After 4 hours glucose phosphate was administered, although the phosphoremia was unknown. After phosphate supplementation an improvement of acidosis was observed. Our hypothesis is that in the kidney phosphate depletion caused impaired tubular reabsorption of bicarbonate, which led to a non lactic metabolic acidosis.
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PMID:Hypophosphatemia and metabolic acidosis. 1583 52

Substantial controversy persists in the literature concerning the physiologic consequences hypocapnia, or low partial pressure of carbon dioxide (PaCO(2)). Invasive animal studies have demonstrated large pH increases (>0.25 U), phosphocreatine (PCr) decreases (>30%), and adenosine triphosphate (ATP) decreases (>10%) after hyperventilation (HV) (20 mm Hg PaCO(2)). However, using magnetic resonance spectroscopy, HV studies in awake humans have demonstrated only small pH changes ( approximately 0.05 U) and no changes in PCr or ATP. It remains important to ascertain whether this failure to detect PCr changes in human studies reflects a true absence of changes, or a limitation in data fidelity. The present study used a rapidly interleaved phosphorus-proton spectroscopy acquisition from large samples at high magnetic field (4 T), to measure pH, PCr, inorganic phosphate, beta-ATP, and lactate changes with high temporal and signal sensitivity. Five of six subjects had usable data. During 20 mins HV, PaCO(2) reached a minimum at 16 mins (17 mm Hg); however, the maximum pH change (+0.047) peaked earlier (14 mins). Maximal lactate increases were measured at 15 mins. By 10 mins, maximum changes were observed for PCr (-3.4%) and inorganic phosphate (+6.4%). No changes in beta-ATP were observed. The peak in pH, despite continued decreases in PaCO(2), suggests active buffering during HV. These data, and the small magnitude of early PCr and inorganic phosphate changes, do not support substantial energy compromise during HV. Other mitigating factors, such as anesthesia-induced deregulation of the cerebrovasculature, might have contributed to the exaggerated metabolic changes observed in previous animal investigations.
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PMID:Brain changes to hypocapnia using rapidly interleaved phosphorus-proton magnetic resonance spectroscopy at 4 T. 1689 47


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