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

The interconnections between EEG, intermediary and energy metabolism of the brain cortex and CSF potassium level are studied during severe hypercapnia in anaesthetized, artificially ventilated cats. Hypercapnic animals were ventilated with 40 to 50% to CO2 in oxygen. During severe hypercapnia the EEG becomes isoelectric. The CSF potassium concentration is raised and the changes in metabolism suggest an acidosis-induced inhibition of phosphofructokinase and, probably, of hexokinase. The energy charge potential remains unchanged whereas the cortical ATP concentration increases slightly. It is assumed that the changes in P-creatine and creatine levels are related to the pH-dependency of creatine phosphokinase. Recovery animals were ventilated with 40% CO2 in O2 and subsequently with room air. After termination of CO2 inhalation the EEG reappears, the CSF potassium concentration normalizes, and the inhibition of the glycolytic enzymes disappears. The energy charge potential shows a small decrease. It is not possible to trace back the disappearance of the EEG to only one of the recorded parameters. Cortical P-creatine levels, CSF potassium concentration, changes in membrane permeability and cortical amino acid concentrations are considered in this context.
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PMID:Influence of severe hypercapnia upon cerebral cortical metabolism, CSF electrolyte concentrations and EEG in the cat. 13 59

This report describes a syndrome of delayed respiratory distress occurring in premature infants usually under 1,250 gm at birth. Unlike hyaline membrane disease, this syndrome occurs after four to seven days in a previously healthy infant; also unlike hyaline membrane disease, it persists for two to four weeks. Chronic pulmonary insufficiency of prematurity (CPIP) carries a 10% to 20% mortality rate. The infants are frequently apneic, require supplemental oxygen, but lack the radiologic findings of hyaline membrane disease or bronchopulmonary dysplasia. When compared with nondistressed infants of similar birthweight, infants with CPIP demonstrate slowly progressive atelectasis, hypoxemia, and hypercapnia. Recovery is usually complete by 60 days of age. The importance of CPIP is that an awareness of its existence can eliminate a false sense of security, often communicated to anxious parents, during the four-to-seven-day grace period before its appearance is clinically obvious. The physiologic similarities between CPIP and hyaline membrane disease suggest that lack of surfactant may play a role in the pathogenesis of CPIP.
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PMID:Chronic pulmonary insufficiency of prematurity (CPIP). 23 87

Tissue (gas pocket) oxygen levels and erythropoietic activity were monitored in groups of rats chronically exposed to hypoxia (70 Torr PIO2), hypercapnia (60 Torr PICO2), or a combination of the two conditions. Arterial gas tensions and pH were also measured. Overall condition of the animals was assessed by comparison of growth rates with pair-fed controls. Hypoxic-hypercapnic pocket PO2 values (24-40 Torr) were similar to normoxic-normocapnic values (28-37 Torr), but greater than in hypoxia-normocapnia, and less than in normoxia-hypercapnia. Erythropoietic activity during hypoxia-hypercapnia ceased and the rats had a growth rate significantly below that of other groups. While chronic CO2 does increase tissue (pocket) oxygenation to near normal levels, probably due to increased ventilation and subsequently PaO2, the hypoxic-hypercapnic rats evidenced greater detrimental effects than did rats in hypoxic or hypercapnic environments.
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PMID:Tissue oxygenation and splenic erythropoiesis during chronic hypoxia and hypercapnia. 23 6

Arterial blood gases and vital signs were monitored in a patient receiving electroconvulsive therapy (ECT) during the third trimester of pregnancy. Alterations in blood pressure and heart rate were similar to those noted in prior studies. Pretreating with 100 percent oxygen (02) and assisting ventilation until return of adequate spontaneous respirations, prevented hypoxemia, significant hypercarbia, and cardiovascular changes. The administration of succinylcholine prevented the systemic manifestations of the electrically-induced seizure. One fetal arrhythmia occurred, apparently unrelated to changes in maternal Pa02, and resolved spontaneously. This technic of anesthesia would appear to be acceptable for ECT in the parturient.
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PMID:Arterial blood-gas analyses during electroconvulsive therapy in a parturient. 23 61

Guinea pigs and rats exposed to 15% CO2 for 7 days showed a parallel time course of changes in pH, body temperature (TB), and oxygen consumption (VO2). Between 1 and 6 h of exposure the maximal drop in actual pH occurred in guinea pigs simultaneously with the maximal fall in TB and VO2. During the subsequent period pH TB, VO2 rose again. Skin blood content (heat loss) also exhibited a biphasic pH-dependent time course. Animals showing no partial compensation of respiratory acidosis during 3 days exposure also failed in raising their TB back to normal in this time. The behavior of TB was found to be a good indicator of the acid-base status and adaptive potential of the animals to hypercapnia. Similar results were obtained in rats. Thermo-regulatory processes in the hypothalamus were affected during exposure to 15% CO2. Both guinea pigs and rats showed a decrease in norepinephrine content of the hypothalamus during the first part of exposure reaching a maximal fall at the end of 24 h. The serotonin content increased slightly during this period. During prolonged exposure to 3% CO2 for 7 days, TB showed a transient rise, and VO2 was slightly elevated.
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PMID:Effect of chronic hypercapnia on body temperature regulation. 23 76

The respiratory responses of 21 cats were examined upon exposure to hypercapnia and isocapnic hypoxia. Animals having bilateral electrolytic lesions localized in the pontile pneumotaxic center exhibited hypercapnia-induced minute volumes which were significantly less than those of unlesioned control cats. The hypoxia-induced minute volumes of pneumotaxic lesioned animals, examined at isocapnic alveolar gas partial pressures, were likewise significantly less than control animals at end-expired oxygen partial pressures (PAO2) in excess of 65.0 mm Hg. At PAO2 levels below 65.0 mmHg. the minute volume of experimental animals rose sharply and became statistically indistinguishable from that of the unlesioned cats. The placement of control brain stem lesions typically produced no significant alterations in the respiratory responses to hypoxia or hypercapnia. It was concluded that the pneumotaxic center constitutes an integral component of the central chemoreceptor CO1-H+ CONTROLLING SUBSYSTEM. The concept of differing anatomical sites within the brain stem serving integrative functions for central chemoreceptor and peripheral chemoreceptor afferent stimuli is also supported.
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PMID:Differing responses to hypercapnia and hypoxia following pneumotaxic center ablation. 23 89

Arterial blood gases were measured during 7 hours of sleep in 15 patients with severe stable chronic obstructive pulmonary discrease (COPD); 6 awake patients with COPD studies in recumbency for an average of 5 hours served as controls. Mean maximal decrease in arterial oxygen partial pressure (PaO2) (plus or minus SD) was 13.5 plus or minus 3.9 mm Hg for sleeping patients (p less than 0.005) and 5.5 plus or minus 1.7 mm Hg for controls (p less than 0.1), respectively. Changes in pH during sleep were of the magnitude expected with acute changes in arterial carbon dioxide partial pressure (PaCO2) in patients with chronic hypercapnia. Consistent changes in heart rate, respiratory frequency or cardiac rhythm were not observed during sleep. Nocturnal worsening of hypoxemia could be explained by alveolar hypoventilation in six sleeping patients and in five controls; in nine sleeping patients, further impariment of ventilation-perfusion mismatch also contributed to worsening of hypoxemia. There was no relationship between the decrease in PaO2 during sleep and the degree of airways obstruction or the PaO2 level when awake. Because of low PaO2, when awake, a fall in PaO2 during sleep brings values into the steep part of the oxyhemoglobin dissociation curve where slight changes in PaO2 result in marked changes in oxygen content. All patients with COPD whose waking PaO2 was below 60 mm Hg had PaO2 below 50 mm Hg during sleep; nocturnal oxygen therapy should be considered in such patients, particularly in the presence of polycythemia or troublesome right-sided heart failure.
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PMID:Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease. 23 52

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.
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PMID:Effect of liver failure on the response of ventilation and cerebral criculation to carbon dioxide in man and in the goat. 23 83

In resting conscious dogs physiological dead space was calculated using the Bohr equation and measurements of arterial and mixed expired carbon dioxide tension. Whenever dogs inhaled carbon dioxide mixtures (5-10%) that had normal or low oxygen concentrations, the calculated dead space became negative. This paradox was based on the fact that the mixed expired carbon dioxide tension in resting hypercapnic dogs. Under these circumstances carbon dioxide was produced from the lung as measured by gas analyses and blood analyses. By the lung as measured by gas analyses and blood analyses. By reasoning this implies that "alveolar" carbon dioxide tension was higher than pulmonary venous carbon dioxide tension. The negative carbon dioxide gradient persisted at 14 days of chronic hypercapnia and reverted to normal within 10 min of breathing air after chronic hypercapnia. These findings suggest that the exchange of carbon dioxide in the lung cannot be explained solely on the basis of passive diffusion.
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PMID:Negative arterial-mixed expired PC02 gradient during acute and chronic hypercapnia. 23 27

1. The purpose of this investigation was to determine the effects of maternal hyperoxaemia and hypercapnia on the uterine vascular bed and foetal oxygenation in the large white sow at 80-90 days gestation. 2. When maternal hyperoxaemia was induced with 100% oxygen, there was a highly significant rise in the maternal arterial oxygen tension, but no other significant blood gas or vascular changes were observed. 3. When mild maternal hypercapnia was superimposed on maternal hyperoxaemia (oxygen plus 6% carbon dioxide), the oxygen tension and saturation of both the maternal uterine venous and foetal umbilical venous bloods were found when severe hypercapnia was induced (oxygen plus 50% carbon dioxide) but in this case all blood samples showed dramatic changes in PCO2 and pH. These changes were accompanied by an increase in the systemic blood pressure and uterine blood flow, and a decrease in uterine vascular resistance. 4. When mild hypercapnia was induced without hyperoxaemia (air plus 5% carbon dioxide) significant increases were recorded in the oxygen tension and saturation of uterine venous and foetal umbilical venous bloods. Systemic and uterine vascular resistance fell. 5. It was concluded that the increased foetal oxygen tension during maternal hypercapnia was the result of the increased uterine blood flow and greater mass delivery of oxygen to the placenta, so that once the oxygen requirements of the placental tissues themselves were exceeded there would be an increased oxygen gradient at the site of gas exchange. 6. Carbon dioxide concentration in arterial blood plays an important role in determining blood flow through the pregnant uterus in the sow.
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PMID:The effects of maternal hypercapnia on foetal oxygenation and uterine blood flow in the pig. 23 26


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