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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multivariate analysis of P50 changes in hypoxia, hypercapnia and polycythaemia was performed in an heterogeneous group of forty three patients: hypoxic subjects with or without hypercapnia, with or without polycythaemia and polycythaemic subjects without hypoxia. A statistical analysis was undertaken using comparison of the means, study of the correlations, principal component analysis, multiple regression and correspondence analysis. In the patients studied, P50 changes were not wholly explained by those of 2-3 DPG and pH; PaCO2, per se, did not play an important part. Haemoglobin concentration and P50 value would represent an adaptative mechanism to hypoxia: when hypoxia is moderate (80 greater than PaO2 greater than or equal to 65 torr) and isolated, oxygen haemoglobin affinity decreases (P50 increases); when hypoxia is severe (PaO2 less than 65 torr) and combined with hypercapnia and disturbed acid-base equilibrium, P50 comes back to normal range but haemoglobin increases, restoring thus, the normal blood oxygen content.
Biomedicine 1977 Dec
PMID:Changes of P50 in hypoxaemia, hypercapnia and polycythaemia: multivariate analysis. 60 4

Experiments were designed to determine the contribution of increased extracellular HCO3- concentration, [HCO-3e], to the net extracellular-to-intracellular HCO3- flux observed in hearts during hypercapnia. Isolated rabbit hearts were perfused by recirculating for 15-min periods a small volume of Ringer solution in which [HCO-3e] and carbon dioxide tension (PCO2) could be independently altered. A net HCO-3 flux was evidenced by a decrease in [HCO-3e] during recirculation. [HCO-3e] was randomly increased from 19 mM over a range of 19-42 mM at a constant PCO2 of 38.7 Torr. The resulting flux increased linearly with the [HCO-3e] existing at the start of recirculation. The same relationship was observed at 95.8 Torr PCO2. The disappearance of HCO-3 from the perfusate could not be explained by dilution in the interstitium or by lactate accumulation. When PCO2 was increased from 40 Torr over a range of 40-160 Torr at a constant [HCO-3e] of 20 or 30 mM, a small flux was observed only at the highest PCO2 levels. Essentially the same results were obtained when recirculation time was prolonged to 30 min. These results suggest that the major determinant of the HCO-3 flux is a change in extracellular HCO-3 concentration.
J Appl Physiol Respir Environ Exerc Physiol 1977 Dec
PMID:Determinants of transmembrane bicarbonate flux during acid-base changes. 60 97

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (VE), end-tidal carbon dioxide tension (PETCO2), venous bicarbonate concentration [HCO3-], oxygen consumption (VO2), hypercapnic ventilatory response (deltaVE/deltaPCO2), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 +/- 2.0 mg/dl. VE increased (P less than 0.05, PETCO2 decreased (P less than 0.05), and [HCO3-] did not change significantly during drug ingestion. deltaVE/deltaPCO2 increased gradually to a value 37% greater than control by day 3 and remained constant (P less 0.01). A increased by 251% and VO2 by 18% within 2 h and remained constant for the remainder of the ASA period (P less than 0.01). All values returned to base line within 24 h following cessation of ASA. We conclude that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanically linked to changes in metabolic rate.
J Appl Physiol Respir Environ Exerc Physiol 1977 Dec
PMID:Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion. 60 1

Changes in acid-base equilibrium and blood lactate and pyruvate concentrations were studied during recovery (breathing room air) after three days hypercapnia (FICO2 = 0.10) in awake dogs. Fast return to FICO2 = 0 produced a slight alkalosis in arterial blood and an increase in lactate and pyruvate concentrations which seemed to be maximum at the 15th minute. These changes were inhibited by previous injection of acetazolamide (50 mg/kg body weight). During progressive return to FICO2 = 0, over 1 hour, the peak value of blood lactate and pyruvate was delayed until the end of that hour, at the same time as a slight blood alkalosis appeared. These phenomen are most probably explained by a stimulation, due to alkalosis, of glycolysis at the level of phosphofructokinase.
Respir Physiol 1977 Dec
PMID:Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis. 60 52

Cholinergic involvement in the regulation of the hypothalamic-pituitary-adrenocortical (HPA) system of male rats was evaluated using muscarinic (atropine and methacholine) and nicotine (mecamylamine and nicotine) agents, which were selected for their specificity on cholinergic receptors (ChR). They were administered either intracerebroventricularly (icv) to produce central effects, or ip to produce both central and peripheral effects, prior to subjecting the animals to either auditory or hypercapnic stress for 1 h. Plasma corticosterone was used as an index of HPA activity. The results suggest that central muscarinic ChR are involved in inhibiting HPA activity in both non-stressed and stressed animals, whereas central nicotinic ChR are excitatory during stress but inactive in the non-stressed state. Stimulation of peripheral nicotinic ChR appeared to potentiate the HPA response to hypercapnia, and to inhibit the central excitatory nicotinic ChR when the latter were activated in non-stressed and auditory stress rats. These data suggest that during auditory stress the HPA system is more dependent upon the cholinergic system for its activation than during non-stressed and hypercapnic states.
Acta Endocrinol (Copenh) 1978 Dec
PMID:Cholinergic influences on hypothalamic-pituitary-adrenocortical activity of stressed rats: an approach utilizing agonists and antagonists. 71 78

Controlled oxygen therapy may aggravate carbon dioxide retention during acute exacerbations of chronic obstructive pulmonary disease (COPD). Of 50 consecutive patients with COPD and acute respiratory failure, 13 required intubation because of carbon dioxide narcosis. With discriminant analysis of their arterial oxygen tension (PaO2) and pH on admission, a diagram separated patients into those at high risk and those at low risk for carbon dioxide narcosis. This diagram was then used to predict carbon dioxide narcosis in 73 patients with COPD and acute respiratory failure who were treated with controlled oxygen. In 16 of these patients carbon dioxide narcosis developed. Thirteen (81 per cent) were predicted by the diagram to be at high risk for this complication. Only two (4 per cent) patients judged by the diagram to be at low risk for carbon dioxide narcosis required mechanical ventilation. Utilizing an oxygen tension (PO2), carbon dioxide tension (PCO2) diagram a patient's ventilatory response was compared to that of ambulatory patients with COPD. These data suggest that hypoxemia and acidosis are more discriminatory for "carbon dioxide narcosis" than hypercapnia.
Am J Med 1978 Dec
PMID:Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: a reappraisal. 74 28

A consecutive series of ten patients with chronic bronchitis and hypercapnia were studied. All seven patients with chronic hypercapnia and one patient with intermittent hypercapnia showed evidence on skull radiographs of raised intracranial pressure. In five male and three female chronic bronchitics matched for age and ventilatory impairment, but without hypercapnia, no such radiological abnormalities were shown. The clinical significance and pathophysiology of this hitherto unreported finding is discussed. It would appear that in some cases the chronicity of hypercapnia may be diagnosed from a radiograph of the pituitary fossa.
Thorax 1978 Dec
PMID:Chronic hypercapnia and radiological changes in the pituitary fossa. 74 95

Seventeen male patients with chronic obstructive airways disease in remission were separated into two groups according to arterial carbon dioxide tensions. Hypercapnia was associated significantly with hypoxia and increased red cell volume whereas normocapnia was not. Normocapnic patients were significantly lighter than those with hypercapnia. Total body potassium (TBK) measured by the whole body monitor was significantly low in two of the patients studied (P less than 0.005). The mean value for TBK for the normocapnic group as a whole was significantly low (P less than 0.005), but the mean value for the hypercapnic group was not. Serum potassium and erythrocyte potassium concentrations were normal even when TBK was low, and diuretics had no apparent influence on these potassium values. Of four patients (two in the series and two others) who had TBK measured after a recent episode of cor pulmonale, three had significantly low values. The only previous studies using a whole body monitor to measure TBK in chronic obstructive airways disease found no such low values, though other workers estimating exchangeable potassium by isotope dilution techniques had found evidence of gross potassium depletion. It is concluded that low TBK does indeed occur in patients with chronic obstructive airways disease and that gross depletion is more likely to follow an episode of cor pulmonale.
Thorax 1978 Dec
PMID:Potassium studies in chronic obstructive airways disease. 74 98

Report on a female patient aged 29 with gramnegative bacterial peritonitis due to perforation of a postpyloric ulcer. A reduction of lung volume was observed, followed after 24 h by non cardiogenic interstitial and alveolar edema resulting in severe hypoxemia and hypercapnia with metabolic acidosis for 4 days. Return of gas exchange to physiological values was established prior to the restoration of normal lung volume. The pathophysiological mechanism of these phenomena is discussed.
Schweiz Med Wochenschr 1975 Dec 06
PMID:[Initial reduction of the lung volume and capillary escape syndrome in gram negative peritonitis]. 76 77

The influence of continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP) on mortality and complication rates in severe hyaline membrane disease (HMD) was evaluated in a randomized, prospective study. Patients were admitted to the study if the Po2 was less than 50 mm Hg with FiO2 greater than 0.6. Twenty-four patients in each of three weight groups were equally divided between treatment and control groups. The treatment regimen included CPAP (6 to 14 cm H2O) for spontaneously breathing patients and PEEP for patients requiring mechanical ventilation for apnea or hypercapnia (Pco2 greater than 65 mm Hg). Control patients received oxygen and were mechanically ventilated if they had apnea, hypercapnia, or Po2 less than 50 mm Hg with FiO2 greater than 0.8. Oxygenation improved after the start of CPAP or PEEP; however, Pco2 rose after CPAP was initiated. There was no significant difference between treatment and control groups in mortality, requirement for mechanical ventilation, or incidence of pulmonary sequelae. The incidence of pulmonary air-leak was increased with Peep. the findings suggest that CPAP and PEEP have not significantly altered the outcome of HMD.
Pediatrics 1976 Dec
PMID:Is continuous transpulmonary pressure better than conventional respiratory management of hyaline membrane disease? A controlled study. 79 89


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