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

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.
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PMID:Effect of hyperventilation on dynamics of cerebral energy metabolism. 23 2

This article attempts correlating changes in cellular energy metabolism, acid-base alterations, and ion homeostasis in ischemia and other conditions. It is emphasized that loss of ion homeostasis, with thermodynamically downhill fluxes of K+, Ca2+, Na+, Cl-, and H+, occurs because energy production fails and (or) ion conductances are increased. In ischemia, energy failure is the leading event but, in hypoglycemia, activation of ion conductances is what precipitates energy failure. The initial event is a rise in K+ e, at least in part caused by activation of K+ conductances modulated by Ca2+ or ATP/ADP ratio. Secondarily, this leads to release of excitatory amino acids and massive activation of unspecific cation (and anion) conductances. Production of H+ occurs in states characterized by energy failure (ischemia and hypoxia) or by alkalosis (hypocapnia and ammonia accumulation). H+ equilibrates between intra- and extra-cellular fluid via nonionic diffusion of lactic acid, and transmembrane fluxes of H+ or HCO3- via ion channels. Since the relationship between lactate and either pHi or pHe is linear, there are no abrupt pH shifts explaining why hyperglycemia worsens ischemic damage. The reversible insults seem to induce a sustained stimulation of H+ extrusion from cells giving rise to intracellular alkalosis and extracellular acidosis.
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PMID:Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. 128 29

With a level of hypoglycemia (1-1.5 mM) that does not alter cerebral O2 uptake and glucose uptake in dogs, induction of hypocapnia may cause severe electroencephalographic (EEG) abnormalities. The aim of this study was to determine the effect of hypoglycemia (blood glucose = 1.1 +/- 0.1 mM) and hypocapnia (arterial PCO2 = 15 +/- 1 mmHg) on cerebral ATP, phosphocreatine, and intracellular pH (pHi; 31P magnetic resonance spectroscopy), cerebral blood flow (CBF; radiolabeled microspheres), global O2 uptake, and glucose uptake in anesthetized dogs. Neither hypoglycemia nor hypocapnia alone altered brain high-energy phosphates, pHi, O2 or glucose uptake or caused major EEG abnormalities. Hypocapnia alone decreased CBF to 62 +/- 4% of control. The combination of hypoglycemia and hypocapnia did not decrease CBF (85 +/- 6% of control), and O2 and glucose uptake were unchanged. During hypocapnic hypoglycemia, isoelectric EEG was seen in 40% of animals, ATP and phosphocreatine decreased to 38 +/- 12 and 43 +/- 12% of control, respectively, while pHi increased from 7.13 +/- 0.05 to 7.43 +/- 0.09. The increase in pHi was related reciprocally to the decrease in venous PCO2, indicating little change in intracellular bicarbonate concentration ([HCO3-]i). With normoglycemic hypocapnia, in contrast, estimated [HCO3-]i decreased 57 +/- 1%. These data suggest that active regulation of pHi during normoglycemic hypocapnia is impaired during hypoglycemic hypocapnia associated with decreased ATP.
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PMID:Hypocapnic-hypoglycemic interactions on cerebral high-energy phosphates and pH in dogs. 148 10

Hypophosphatemia revealed in patients with acute disorders of cerebral circulation was one of the causes of a decrease of the content of 2,3-DPG, ATP in red blood cells and of a reduction of Ca2(+)-ATPase activity in red blood cell membranes. In the given group of patients, hypophosphatemia was provoked by complete parenteral feeding, hypocapnia and by loss of phosphorus with urine and congestive gastrointestinal contents.
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PMID:[Causes, sequelae and possible ways of preventing hypophosphatemia in patients with cerebral ischemia]. 196 92

The first 5 days of treatment of 98 patients with acute disorders of the cerebral blood circulation revealed hypophosphatemia and related reduction of the level of 2, 3 DPG, ATP in the erythrocytes. The causes of hypophosphatemia in these patients were absence of entrance of phosphorus to the body, its loss with the urine and gastrointestinal contents and hypocapnia. The possible ways of correction of these disorders are discussed.
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PMID:[Characteristics of phosphorus metabolism in patients with acute disorders of cerebral circulation]. 262 71

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.
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PMID:Relationship between intracellular pH and energy metabolism in dog brain as measured by 31P-NMR. 359 78

The effect of a stepwise decrease in PaCO2 from 3.9-1.6 kPa on rCBF, rCMRO2, tissue PO2 and concentrations of glucose, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine in the brain cortex was studied in cats lightly anaesthetized with sodium pentobarbital. 1. Moderate lowering of PaCO2 to 2.5 kPa induced in all animals a homogeneous decrease of rCBF in corresponding areas of the right and left hemisphere. Mean rCBF fell from 129.2 to 103.1 ml X 100 g-1 X min-1, while rCMRO2 remained unchanged (12.7-12.9 ml X 100 g-1 X min-1). The tissue PO2 frequency histograms showed a shift to lower values without indicating the presence of brain tissue hypoxia. 2. Severe arterial hypocapnia (PaCO2 = 1.6 kPa) caused an inhomogeneous blood flow reaction. Both further decreased as well as increased rCBF values were measured simultaneously in the brain cortex of individual animals (mean rCBF = 97.6 ml X 100 g-1 X min-1). At the same time tissue PO2 measurements and metabolite assays indicated the presence of pronounced brain tissue hypoxia. The tissue concentrations of lactate and pyruvate and the lactate/pyruvate ratio were significantly increased, while the phosphocreatine concentration was significantly reduced. In addition, rCMRO2 decreased to 11.3 ml X 100 g-1 X min-1. The results provide conclusive evidence that severe arterial hypocapnia leads to an insufficient O2 supply of the brain cortex, which in turn seems to counteract the influence of hypocapnia on cortical blood flow regulation.
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PMID:Effects of severe arterial hypocapnia on regional blood flow regulation, tissue PO2 and metabolism in the brain cortex of cats. 681 15

Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral blood flow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induce hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paCO2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p less than 0.05). When paCO2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypocapnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.
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PMID:Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats. 681 44

To determine the effect of changes in potassium (K+) flux on airway constriction, we studied effects of lemakalim, a K+ channel opener, and glibenclamide, an ATP-sensitive K+ channel blocker. A wedged bronchoscope technique was used to measure peripheral airway resistance (Rp) in anesthetized dogs. Rp was measured before and after constriction of the airways by hypocapnic challenge, acetylcholine aerosol, or dry air hyperpnea. Lemakalim (5 micrograms/kg i.v.) was administered, and the challenge was repeated. Lemakalim attenuated responses to hypocapnia by 72 +/- 7% (n = 6, P = 0.0007) and to dry air challenge by 37 +/- 8% (n = 6, P = 0.005) but not to acetylcholine. On separate days, sublobar segments were pretreated with aerosolized glibenclamide (2 mg/ml), and responses to hypocapnic challenge were measured before and after lemakalim (5 micrograms/kg i.v.), nifedipine (20 micrograms/kg i.v.), or albuterol (1 microgram/kg i.v.). In the presence of glibenclamide, lemakalim had no significant effect on responses to hypocapnia; however, both nifedipine (n = 6, P = 0.0003) and albuterol (n = 6, P = 0.0001) attenuated responses to hypocapnic challenge. These findings suggest that lemakalim attenuated hypocapnic bronchoconstriction by promoting K+ efflux through ATP-sensitive K+ channels.
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PMID:Lemakalim attenuates hypocapnia- and dry air-induced bronchoconstriction in canine peripheral airways. 837 5

Anaerobic metabolism in the limnic annelid Hirudo medicinalis L. was investigated by direct and indirect calorimetry. During long-term severe hypoxia, the rate of heat dissipation was reduced up to 13% of the aerobic rate. At the same time, the rate of ATP turnover was reduced to about 30% of the aerobic rate, indicating that metabolic depression is an important mechanism to ensure survival of the leech during environmental anaerobiosis. Heat dissipation during hypoxia was monitored under two experimental conditions, favouring either concomitant hypocapnia (continuous N2 bubbling) or hypercapnia (self-induced hypoxia). The reduction in heat dissipation during hypocapnic hypoxia was less pronounced than during hypercapnic hypoxia, indicating that the different experimental conditions may influence anaerobic metabolism and the extent of metabolic depression. Biochemical analysis of known anaerobic substrates and endproducts provided the basis for indirect calorimetry during self-induced hypoxia. From changes in metabolites, the expected heat dissipation was calculated for initial (0-8 ,h) and long-term severe hypoxia (8-72 h). During the initial period, the calculated heat dissipation fully accounted for direct calorimetric determination. During long-term hypoxia, only 71% of the measured heat production could be explained from biochemical analysis of metabolites. Therefore, an additional unknown endproduct cannot be excluded, especially when anaerobic ammonia production and analysis of the carbohydrate balance are considered.
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PMID:Anaerobic metabolism in the leech (Hirudo medicinalis L.): direct and indirect calorimetry during severe hypoxia. 876 66


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