Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.
 ...
PMID:The effect of hyperventilation on distal nephron hydrogen ion secretion. 0 92

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.
 ...
PMID:Effect of hyperventilation on dynamics of cerebral energy metabolism. 23 2

Electrolyte excretion and balance were compared in meal-eating, adlibitum-fed rats maintained in Denver (1,600 m) and on Pikes Peak (4,300 m) and in meal-eating rats maintained in Denver but pair-fed to the Pikes Peak animals. Most of the changes in excretion and balance at Pikes Peak were attributable to hypophagia. At both elevations, equivalent decrements in mineral intake led to nearly equivalent decrements in mineral excretion. Comparisons of the Pikes Peak and Denver pair-fed animals, however, revealed certain changes that were unique to high altitude. These included a marked and sustained reduction in ammonia excretion over the 13-day period of exposure. The higher elevation also produced an enhanced sodium excretion on day 1 of exposure and a reduced sodium balance over the first 6 days. Potassium balance showed no changes unique to high altitude during the first 6 days on Pikes Peak but was significantly reduced during week 2 of exposure. The urinary sodium:potassium ratio was elevated during the first 4 days at 4,300 m, but this effect was attributable to altitude on day 1 only. Enhanced calcium and magnesium excretions, relative to those observed in the pair-fed rats, were observed over the middle and latter portions of the exposure period. The balance of these two minerals showed no altitude-dependent effects. Chloride and phosphate excretions showed an altitude-dependent reduction during day 1 and week 1 of exposure, respectively. These changes were associated with more positive balances. It is concluded that the altitude-dependent effects on mineral metabolism are largely, if not entirely, attributable to hypocapnia and associated alkalosis.
 ...
PMID:Effects of high altitude and hypophagia on mineral metabolism of rats. 105 80

Previous studies suggested that renal H+ retention during adaptation to hypocapnia might be critically dependent upon concomitant Na and/or K excretion. To test this hypothesis, seven dogs were allowed to recover from hypocapnia while receiving a low electrolyte diet. Despite negligible changes in Na and K excretion, cum delta net acid excretion was --33 meq during adaptation and +44 meq during recovery. Consequently, plasma [HCO3] fell from 19.2 to 14.2 meq/liter in the former and rose from 13.8 to 19.7 meq/liter in the latter groups; these changes were virtually identical to those observed previously in animals maintained on normal electrolyte intakes. These adaptive changes in renal H+ output appeared to be balanced by parallel changes in phosphate excretion. When phosphate retention was prevented during adaptation with Na remaining available for excretion, retention of H+ was still clearly evident. When both phosphate retention and augmented cation excretion were prevented during adaptation, however, H+ retention was abolished. Nevertheless, plasma [HCO3] still fell from 20.9 to 16.2 meq/liter, a level far beyond that attributable to tissue buffering.
 ...
PMID:Renal adaptation to chronic hypocapnia: dietary constraints in achieving H+ retention. 120 Jan 51

Hyperventilation/hypocapnia increases renal phosphate reabsorption and decreases the phosphaturic effect of parathyroid hormone (PTH). Recent studies suggest that the blunted phosphaturic effect of PTH in hyperventilated/hypocapnic rats may be mediated by the stimulation of renal beta-adrenoreceptors. In the present study, no differences in plasma catecholamine levels were detected in hyperventilated/hypocapnic rats as compared to hyperventilated/normocapnic rats. Therefore, studies were performed to determine the role of the renal nerves in the blunted phosphaturic effect of PTH in hyperventilated/hypocapnic rats. In clearance experiments in acutely thyroparathyroidectomized male Sprague-Dawley rats, PTH infusion increased the fractional excretion of phosphate (FEPi) in the denervated left kidney of hyperventilated/hypocapnic rats (n = 8), from 2.4 +/- 1.1 to 18.6 +/- 2.7%, as compared to 1.0 +/- 0.3 to 9.1 +/- 2.1% in the contralateral innervated kidney. Denervation of the left kidney in hyperventilated/normocapnic rats (n = 8) also significantly increased the phosphaturic response to PTH by 2.5 +/- 1.5 to 26.9 +/- 3.0% as compared to 0.9 +/- 0.5 to 18.6 +/- 2.6% in the contralateral innervated kidney. The phosphaturic responses to PTH were similar when comparing the denervated kidney in hyperventilated/hypocapnic rats with the innervated kidney of hyperventilated/normocapnic rats. Thus, renal denervation enhanced the phosphaturic effect of PTH in both hyperventilated/hypocapnic and hyperventilated/normocapnic rats. These results suggest that renal nerves play a role in the modulation of the phosphaturic effect of PTH.
 ...
PMID:Renal denervation enhances the phosphaturic effect of parathyroid hormone. 177 Sep 12

The similar localization of intracranial calcification in hypoparathyroidism and in Fahr disease without parathyroid gland disorder suggests that in these two disorders the pathomechanism of calcium phosphate deposition in the brain may be similar. It may be that in Fahr disease some factors, such as chronic respiratory alkalosis, could lead to hypoparathyroidism-like changes in the brain tissue. Abolition of the phosphaturic response to parathormone (PTH) was recently demonstrated in acute experimental hypocapnia. In three adult patients with Fahr disease, a tendency towards compensatory respiratory alkalosis and arterial hypocapnia was found. The parathormone test revealed a marked decrease in phosphaturia response to PTH, but normal cAMP response. In one patient, the parathormone test was repeated during propranolol administration and showed a considerable improvement in the phosphaturic response to parathormone. It is postulated that chronic hyperventilation and hypocapnia as well as phosphaturic resistance to PTH, intracellular increase of phosphate concentration and development of hypoparathyroidism-like intracranial calcification in patients with Fahr disease could all be caused by disturbance of adrenergic receptors and their relationship to PTH receptors.
 ...
PMID:Abolished phosphaturic response to parathormone in adult patients with Fahr disease and its restoration after propranolol administration. 283 40

Alkalosis is prominent among the many physiologic and biochemical effects of sodium lactate infusion. Though this is partially due to the conversion of lactate to bicarbonate, the metabolic component, it may also be secondary to hyperventilation before and during the infusion, the respiratory component. We analyzed pH, carbon dioxide pressure, bicarbonate, and inorganic phosphate from patients with panic disorder and agoraphobia with panic attacks and from normal controls both before and during lactate infusion. Our findings extend earlier work demonstrating that many such patients are chronic hyperventilators. Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls. Finally, low inorganic phosphate levels at baseline appear associated with patients who will panic during the subsequent lactate infusion. This last unexpected finding may reflect hyperventilation or an abnormality in intracellular glycolysis.
 ...
PMID:Blood gas changes and hypophosphatemia in lactate-induced panic. 309 75

The effects of hypoxic hypoxia on physiological variables, cerebral circulation, cerebral metabolism, and blood-brain barrier were investigated in conscious, spontaneously breathing rats by exposing them to an atmosphere containing 7% O2. Hypoxia affected a marked hypotension, hypocapnia, and alkalosis. Cortical tissue high-energy phosphates and glucose content were not affected by hypoxia, glucose 6-phosphate, lactate, and pyruvate levels were significantly increased. Blood-brain barrier permeability, regional brain glucose content and lumped constant were not changed by hypoxia. Local cerebral glucose utilization (LCGU) rose by 40-70% of control values in gray matter and by 80-90% in white matter. Under hypoxia, columns of increased and decreased LCGU were detectable in cortical gray matter. Local cerebral blood flow (LCBF) increased by 50-90% in gray matter and by up to 180% in white matter. Coupling between LCGU and LCBF in hypoxia remained unchanged. The data suggest a stimulation of glycolysis, increased glucose transport into the cell, and increased hexokinase activity. The physiological response of gray and white matter to hypoxia obviously differs. Uncoupling of the relation between LCGU and LCBF does not occur.
 ...
PMID:Cerebral circulation, metabolism, and blood-brain barrier of rats in hypocapnic hypoxia. 310 71

1. The effects of hypercapnia and hypocapnia on brain intracellular pH (pHi) and metabolism were investigated in new-born lambs under barbiturate anaesthesia. 2. 31P nuclear magnetic resonance (n.m.r.) spectroscopy was used to determine brain pHi and the relative concentrations of compounds containing mobile phosphorus nuclei including phosphocreatine (PCr), nucleoside triphosphates (NTP) and inorganic phosphate (Pi). Simultaneous measurements were made of the molar ratio of glucose to oxygen uptake by the brain. 3. During normocapnia (arterial partial pressure of CO2 Pa, CO2, 39 +/- 1 mmHg mean +/- S.E. of mean, n = 9) brain pHi was 7.13 +/- 0.02. Hypercapnia (Pa, CO2, 98 +/- 3 mmHg) was associated with a fall in brain pHi to 6.94 +/- 0.03 (n = 19, P less than 0.001), whereas no significant change in brain pHi occurred during hypocapnia (Pa, CO2, 16 +/- 1 mmHg; brain pHi 7.15 +/- 0.01). 4. During hypercapnia there was an increase in the ratio of Pi to NTP from 1.09 +/- 0.08 to 1.47 +/- 0.06 (P less than 0.001) and a decrease in the ratio PCr/Pi from 1.60 +/- 0.08 to 0.93 +/- 0.04 (P less than 0.001). There was a linear correlation between Pi/NTP and brain pHi. 5. Alterations in arterial PCO2 had no significant effect on the molar ratio of glucose to oxygen uptake by the brain, which remained close to unity. 6. The change in brain pHi observed during hypercapnia can be accounted for by the known physico-chemical buffering capacity of brain tissue. Homoeostasis of brain pHi during hypocapnia provides further evidence that additional regulatory mechanisms operate in these circumstances. 7. The observed changes in PCr and Pi can be accounted for in part by the [H+] dependence of the creatine kinase reaction.
 ...
PMID:Brain intracellular pH and metabolism during hypercapnia and hypocapnia in the new-born lamb. 311 75

The relationships between pHi (intracellular pH) and phosphate compounds were evaluated by nuclear magnetic resonance (NMR) in normo-, hypo-, and hypercapnia, obtained by changing fractional inspired concentration of CO2 in dogs anesthetized with 0.75% isoflurane and 66% N2O. Phosphocreatine (PCr) fell by 2.02 mM and Pi (inorganic phosphate) rose by 1.92 mM due to pHi shift from 7.10 to 6.83 during hypercapnia. The stoichiometric coefficient was 1.05 (r2 = 0.78) on log PCr/Cr against pHi, showing minimum change of ADP/ATP and equilibrium of creatine kinase in the pH range of 6.7 to 7.25. [ADP] varied from 21.6 +/- 4.1 microM in control (pHi = 7.10) to 26.8 +/- 6.3 microM in hypercapnia (pHi = 6.83) and 24.0 +/- 6.8 microM in hypocapnia (pHi = 7.17). ATP/ADP X Pi decreased from 66.4 +/- 17.1 mM-1 during normocapnia to 25.8 +/- 6.3 mM-1 in hypercapnia. The ADP values are near the in vitro Km; thus ADP is the main controller. The velocity of oxidative metabolism (V) in relation to its maximum (Vmax) as calculated by a steady-state Michaelis-Menten formulation is approximately 50% in normocapnia. In acidosis (pH 6.7) and alkalosis (pH 7.25), V/Vmax is 10% higher than the normocapnic brain. This increase of V/Vmax is required to maintain cellular homeostasis of energy metabolism in the face of either inhibition at extremes of pH or higher ATPase activity.
 ...
PMID:Relationship between intracellular pH and energy metabolism in dog brain as measured by 31P-NMR. 359 78


1 2 3 Next >>