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

The authors showed that 2,3-DPG red cell concentration (2,3-DPG) WAS SIGNIFICANTLY HIGHER DURING THE LAST WEEK Of the menstrual cycle of five women (1.08+/-0.09 mol-,p;Hb-1) (M +/- 1 SE) THAN DURING THE First part and the last but one week of the cycle (0.86+/-0.04 mol-molHb-1, p less than 0.01). PACO2 was significantly lower during the last week of the cycle (36.3+/-1.3 torr) than during the first part and the last but one week of the cycle(40.1+/-0.8 torr, p less than 0.001). This hypocapnia was due to transient hyperventilation in the second part of the menstrual cycle. 5 men were studied during 4 weeks to determinate control values. No change was observed. The 2,3-DGP mean value (1.10+/-0.01 mol-molGb-1) was not significantly different of the values observed in the women during the last week of the cycle. These results suggest that the 2,3-DPG increase during the last week of the menstrual cylce is problably due to a respiratory alkalosis induced by progesterone secretion.
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PMID:2,3-Diphosphoglycerate red cell concentration changes during the menstrual cycle in woman. 95 48

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.
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PMID:Effects of high altitude and hypophagia on mineral metabolism of rats. 105 80

This study examined the hypothesis that prevention of hypocapnia and alkalosis would ameliorate the symptoms of acute mountain sickness (AMS). Five subjects were exposed to simulated high altitude for 4 d with 3.8% CO2 added to the chamber to maintain normocapnia. Four other subjects were exposed for 4 d to hypobaric hypoxia without CO2 supplementation, and became hypocapnic. Barometric pressure was lower in the group with added CO2 so that alveolar oxygen tensions (55-60 mm Hg) would not be different. The severity of symptoms was clearly greater in normocapnic than in hypocapnic subjects. Thus, prevention of hypocapnia did not alleviate AMS symptoms. The efficacy of CO2 addition in reducing symptoms, as reported by earlier workers, was probably the result of induced hyperventilation and partial relief of hypoxia. Indeed, in the present study with two comparably hypoxic groups, CO2 addition augmented the sysptoms, possibly by causing increased cerebral vasodiladation and spinal fluid pressure.
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PMID:Acute mountain sickness: increased severity in eucapnic hypoxia. 115 91

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.
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PMID:Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2. 126 78

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

The analysis of both clinical findings and diagnostic procedures results were performed in 26 patients with thromboembolic pulmonary disease in order to determine the incidence of signs indicating pulmonary thromboembolism. Sudden dyspnea, hemoptysis and chest pains are the most common symptoms of the disease. These symptoms associated with radiographically confirmed pulmonary infiltrations with the elevation of hemidiaphragm and pleural effusion, particularly if they are bilateral, are the main clues for the diagnosis of pulmonary embolism. Perfusion defect on the pulmonary scintigraphy makes this diagnosis almost certain. Hypoxemia and hypocapnia and respiratory alkalosis are frequent findings in thromboembolic pulmonary disease, as well. Fever, increases RBC sedimentation rate and leukocytosis are present in a great deal of patients. In addition, the presence of risk factors related to the development of thrombosis of the lower limbs deep veins, and particularly those related to the long term immobilization as well as diagnostically confirmed venous thrombus are basic guidelines for the diagnostic of pulmonary thromboembolism.
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PMID:[Personal experience in the diagnosis and therapy of pulmonary thromboembolism]. 130 9

The oxygen-binding properties of Hb molecule are unchanged in the third trimester of normal pregnancy and in pregnancy complicated by slight iron-deficiency anemia. Hb affinity to oxygen in whole blood is formed under the effect of the three main ligands H+, CO2, and 2,3-DPH. The development of hypocapnia in pregnant women results in elevation of pH values, reduction of pCO2, increase of intraerythrocytic 2,3-DPH concentration by 15-18%. Variously directed effects of H+, CO2, and 2,3-DPH on Hb affinity to O2 result in normal P50 values and therefore the Hb-O2 dissociation curve is not shifted to the right. Thus, in pregnant women with alkalosis 2,3-DPH effect on Hb affinity to oxygen completely eliminates H+ and CO2 effects but not compensates for Hb deficiency in the blood.
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PMID:[Status of the oxygen transport system of hemoglobin in physiological pregnancy and pregnancy complicated by iron deficiency anemia]. 147 17

Very low arterial CO2 tension (PaCO2) experienced by birds during high-altitude flight may result in cerebral vasoconstriction and reduced cerebral O2 delivery. To examine this possibility, we measured regional cerebral blood flow (CBF) and tissue PO2 in pentobarbital-anesthetized geese (Anser domesticus). Twenty-five-micrometer Teflon-coated platinum electrodes for H2-clearance measurements of local blood flow or tissue PO2 were implanted in the cerebral cortex in 11 geese. Tissue H2 and O2 were measured by voltage clamping the electrodes at +0.30 and -0.5 V, respectively. Washout kinetics of H2 gas administered via unidirectional lung ventilation was used to calculate local blood flow for those electrodes exhibiting one- or two-compartment washout kinetics of H2 (128 of 296 washouts in 31 electrodes). PaCO2 was controlled between 8 and 55 mmHg by altering pulmonary gas flow or by adjusting inspired PCO2. CBF decreased as PaCO2 fell from 50 to 20 mmHg but did not decrease further as PaCO2 was reduced below 20 mmHg. CBF was uniformly distributed in different regions of the cortex. Despite the plateau in CBF during severe hypocapnia, tissue PO2 continued to decline as PaCO2 fell below 20 mmHg. Severe alkalosis may limit cerebral O2 delivery in birds during high-altitude flight.
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PMID:Regional cerebral blood flow and tissue oxygenation during hypocarbia in geese. 151 Jan 62

The effects of hypocapnic alkalosis on the vasodilating action of nicardipine were studied in 6 patients after cerebral arterial aneurysm surgery. Each patient served as his/her own control during the 6 steps of the study. T0: baseline; T1: hypocapnic alkalosis alone (PaCO2: 3.5 kPa); T2: hypocapnic alkalosis and bolus injection of nicardipine (30 micrograms.kg-1 i.v.); T3: hypocapnic alkalosis and continuous 60 min infusion of nicardipine (0.5 microgram.kg-1.min-1), T4: determination of the infusion rate required to neutralize the effect of hypocapnic alkalosis; T5: same continuous dose of nicardipine as in T4 but reversal of hypocapnic alkalosis. Hypocapnic alkalosis alone caused a significant increase in the systemic vascular resistance index by 20% (T1). The bolus injection of nicardipine reversed this first effect (T2). The continuous infusion of nicardipine in T3 was insufficient to cancel the haemodynamic effect of hypocapnic alkalosis. During T4 the plasma levels required to neutralize completely the effect of hypocapnic alkalosis were twice those at T3. Normalization of the PaCO2 in step T5 induced a significant fall in the systemic vascular resistance index by 27.5% as compared with T0. In this study hypocapnic alkalosis modified the relationship between plasma levels of nicardipine and its expected vasoactive effects. This interaction was reversible.
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PMID:Systemic vasomotor interaction between nicardipine and hypocapnic alkalosis in man. 161 4

1. During hyperthermia-induced thermal panting, there was a progressive development of alkalosis, hypocapnia, hypocalcemia and plasma lactate accumulation in both mature and immature domestic fowl. 2. The results of this study further demonstrate that hypocalcemia is a general consequence of respiratory alkalosis in animals. 3. The significant (P less than 0.05) regression analysis of plasma lactate vs arterial blood pH, suggest a relationship between these two variables. 4. Plasma lactate accumulation may therefore play an important role as an extrarenal buffering component in the normal defense against severe alkalosis.
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PMID:The time course in development of hypocalcemia and plasma lactate accumulation in mature and immature hyperthermic domestic fowl (Gallus domesticus). 167 87


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