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

Changes in the total CO2 content of tissues were determined in order to characterize variations in intracellular acid-base parameters during the onset of hypercapnia. Within two minutes after an increasement in the CO2 tension of the inspired air of rats, there were large increases in the intracellular bicarbonate concentrations of both cardiac and skeletal muscles. Greater changes occurred in the heart, and its intracellular pH remained near normal during the first hour of hypercapnia; whereas there was an intracellular acidosis in skeletal muscle. This greater capacity of the heart to buffer excess CO2 has been linked to an increased movement of bicarbonate ions into and/or hydrogen ions out of cardiac cells during hypercapnia (Lai et al., 1973c). Yet, the buffer capacity of the heart was not compromised by metabolic acidosis during which there was a greatly reduced extracellular bicarbonate ion concentration and a greatly increased extracellular hydrogen ion concentration. The intracellular pH of the cardiac ventricle was stable following the imposition of a noncarbonic acid load on normocapnic rats.
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PMID:Intracellular buffering of heart and skeletal muscles during the onset of hypercapnia. 1 Jun 16

We have studied arterial PO2, PCO2, and hydrogen ion and electroencephalogram during sleep in 10 patients with stable severe chronic respiratory failure. As a group the patients slept badly. Sleep was associated with a worsening of hypoxia and no significant change in PCO2 and H+. Two patients were restudied, receiving oxygen therapy overnight. Both had improved sleep but one, who had an intact hypoxic drive to breathing, developed marked hypercapnia and acidosis when his PO2 was restored to normal during sleep; the other, who had no hypoxic drive to breathing, developed no more hypercapnia or acidosis during sleep when breathing oxygen than when breathing air. Oxygen therapy may improve sleep disturbance in these patients, but its effect on the drive to breathing during sleep should be considered if severe hypercapnia and acidosis are to be avoided.
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PMID:Arterial blood gas tensions, hydrogen ion, and electroencephalogram during sleep in patients with chronic ventilatory failure. 1 11

The acid-base values of 13 patients with stable carbon dioxide tensions under controlled ventilation have been used to define the response to chronic hypocapnia in man. These patients had a respiratory paralysis and no apparent complicating disorders. Over a range of carbon dioxide tensions from 24 to 40 millimetres of mercury, the arterial blood hydrogen ion concentration decreased linearly by 0.32 nanomole per litre per millimetre of mercury decrement in carbon dioxide tension. Of primary interest was the finding that the slope of the regression line in chronic hypocapnia is close to that already reported for chronic hypercapnia. The physiological response to chronic hypocapnia in man is defined by a band that is approximately 10 nanomoles per litre (0.09 pH unit) wide for hydrogen ion concentration and 6 millimoles per litre wide for bicarbonate concentration. These significance bands may be used to differentiate additional acid-base disorders in patients with chronic hypocapnia over a clinically useful range of carbon dioxide tensions.
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PMID:Acid-base response to chronic hypocapnia in man. 2 Jan 87

The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
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PMID:Mechanisms of hypercapneic pulmonary hypertension. 2 1

To test the hypothesis that birth asphyxia has a role in the etiology of intraventricular hemorrhage (IVH), blood was collected from the umbilical artery (UA) at birth in 28 premature infants of 26 to 29 weeks gestation and analyzed for hydrogen ion concentration [H+], PCO2, standard bicarbonate level, and lactic acid level. The infants were followed up throughout their nursery stay until a diagnosis of IVH could be made or excluded, either by autopsy or clinical findings. Infants with IVH had lower Apgar scores. There were no differences in UA [H+] or bicarbonate or lactic acid levels. However, infants with IVH had a significantly higher UA PCO2. Although the difference appeared relatively small, the increase in PCO2 during labor may have been relatively large. It is concluded that hypercarbia, possibly by increasing cerebral blood flow, may be one important factor in the genesis of IVH.
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PMID:Hypercarbia at birth: a possible role in the pathogenesis of intraventricular hemorrhage. 3 Sep 36

The carotid bodies appear to be the only peripheral chemoreceptors mediating ventilatory control during exercise in man. While little is known about the mechanism of stimulation, much is known about the effects of carotid body stimulation upon pulmonary ventilation (VE). These effects have been produced by hypercapnia, hypoxia, metabolic acidosis, arterial blood pressure, temperature, and catecholamines. A signal from CO2 flow is attractive because of the strong correlation between CO2 output and VE during exercise. The carotid body's role in the hyperpnea depends on the intensity of exercise. During heavy exercise, pH falls and hyperventilation ensues. The carotid bodies appear to be the exclusive mediators of the ventilatory compensation for the acidosis at this exercise intensity. For moderate exercise, mean arterial PCO2 does not change. Therefore, how is the CO2 signal transmitted to the respiratory center? Two current theories are: (1) since arterial PCO2 and pH oscillate with each breath, the amplitude and period of these oscillations may change during exercise and may be of sufficient magnitude to stimulate the carotid bodies, and (2) there exists a disequilibrium between hydrogen ion activity within the red blood cell and in the plasma because carbonic anhydrase is found in the former but not the latter. This theory assumes that the enzyme is not accessible to the plasma.
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PMID:Peripheral chemoreceptors and exercise hyperpnea. 4 92

1. Mongrel dogs were anaesthetized with chloralose, paralysed, ventilated and vagotomized and given a beta-blocking drug, sotalol, in sufficient doses to block the effects of 5 microgram of adrenaline. 2. Changes in inspired CO2 concentration were produced, causing increases of arterial PCO2 up to 120 mmHg. The effects on myocardial blood flow were measured with radioactive microspheres. Coronary sinus and arterial blood was sampled. 3. In the absence of beta-blockade, an increase in arterial PCO2 produced variable effects. In some dogs coronary blood flow increased, while in others there was no change. There was a mean increase in coronary blood flow at arterial PCO2 values above 85 mmHg which was abolished by beta-blockade. 4. In the presence of beta-blockade, an increase of arterial PCO2 produced depression of left ventricular performance, i.e. a fall of maximum rate of rise of left ventricular pressure and a rise of left ventricular end-diastolic pressure. 5. In the presence of beta-blockade, there were no consistent changes in myocardial blood flow, left ventricular pressure or cardiac output. 6. In the absence of beta-blockade, coronary arterial minus venous ocygen content was reduced by hypercapnia. In the presence of beta-blockade, the changes were small and not statistically significant. The direct coronary vasodilator effect was therfore negligible. 7. It is concluded that the previously reported hypercapnic vasodilatation was mainly an effect of sympatho-adrenergic stimulation by hypercapnia. 8. In the presence of beta-blockade, coronary sinus PO2 increased markedly, with little change in coronary sinus oxygen content; this was consistent with a shift to the right of the oxy-haemoglobin dissociation curve. Under circumstances of hypercapnia, a rise in coronary sinus (and presumably tissue) PO2 failed to produce vasoconstriction. 9. It is argued that the vasodilator effect of hydrogen ions and the vasoconstrictor effect of oxygen probably cancel one another when the arterial PCO2 is raised.
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PMID:The effect of carbon dioxide upon myocardial contractile performance, blood flow and oxygen consumption. 43 Mar 87

Changes in cerebral blood flow in response to three states of acute acidosis, posthypoxic, lactic acid, and respiratory, were estimated by the microsphere technique. In all three states, the fraction of the systemic blood flow reaching the brain and the rate (ml/min) of blood flow to it increased. The increase in flow was linearly related both to the PaCO2 and to H+. Others have shown the flow rate to increase with hypercapnia, but the increase associated with an increase in hydrogen ion concentration while the PaCO2 was maintained at control levels does not appear to have been observed in mature animals.
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PMID:Cerebral blood flow during acute acidosis in perinatal goats. 47 72

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

This investigation was undertaken to determine the nature of acute alterations in renal function following the production of hypoxemia, hypercarbia, and acidosis in newborn piglets 6-96 hr of age. After completion of the surgical procedure piglets were allowed to recover from the effects of anesthesia. When respiratory dead space was increased arterial oxygen tension decreased whereas arterial carbon dioxide tension and hydrogen ion concentration increased. There was little change in glomerular filtration rate. Total renal blood flow decreased and renal vascular resistance increased significantly (504 +/- 78 mm Hg/liter/mm/m2 to 1422 +/- 504). There was no change in distribution of intrarenal blood flow. Sodium excretion and urinary flow rate demonstrated significant parallel increases following the increase in dead space. Plasma renin concentration increased from 67 to 110 ng/ml.
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PMID:Effects of asphyxia on renal function in the newborn piglet. 58 Apr 50


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