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

Television microscopy was used to quantitate the responses of small arteries and veins, in the wings of unanesthetized bats, to alterations in the inspired concentrations of O2 and CO2. Mean arterial pressure, heart rate, and the diameters of small arteries (28-54 mum) and veins (50-128 mum) were measured during a 90-min protocol--30 min with an inspiratory gas mixture of 20% O2 and 80% N2 (control period); 30 min with a gas mixture containing 5% O2 (hypoxic period) or 12, 20, or 28% CO2 (hypercapnic period); and 30 min with the original control gas. The hypoxic responses were dilatation of arteries and no change in the veins in both innervated and surgically denervated wings. Hypercapnia resulted in artery dilatation in innervated wings. Hypercapnia resulted in artery dilatation in innervated wings and constriction in denervated wings. The veins constricted in both innervated and denervated wings during the hypercapnia period. In another series, topical application of Krebs solutions (pH ranging from 7.7 to 6.7) to exposed segments of small arteries and veins produced dilatation of both vessels with decreasing pH. Artery dilatation during hypoxia and vein constriction during hypercapnia involve non-neural mechanisms, while both a neural stimulus for dilatation and a non-neural stimulus for constriction are components in the response of innervated arteries to hypercapnia. The non-neural stimulus for artery and vein constriction during hypercapnia is not a local decrease in pH.
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PMID:Sensitivity of small subcutaneous vessels to altered respiratory gases and local pH. 0 91

Hypercapnic acidosis (pH 7.0) inhibits the lipolytic response of canine subcutaneous adipose tissue to i.v. infused noradrenaline (NA) by 80 per cent or more. The response to sympathetic nerve stimulation, on the other hand, is only reduced by 10-40 per cent during acidosis. The fate of intravenously infused 3H-labelled NA (0.35 ug X kg-1 X min-1 for 30 min) was not significantly altered by acidosis. The rate of disappearance of unmetabolized NA from the arterial plasma after an infusion was the same at pH 7.4 and 7.0 and the calculated increase in circulating NA during infusions was 4 ng/ml at both pH:s. I.v. infusion of Na increases adipose tissue blood flow, an effect which is attenuated by acidosis. There was a significant correlation (p less than 0.001) between adipose tissue blood flow and the lipolytic response at normal pH. Preventing the NA-induced increase in blood flow by constant flow perfusion reduced the lipolytic response at normal pH. The degree of inhibition by acidosis of the lipolytic response to i.v. NA was significantly reduced (from 79 to 56 per cent, p less than 0.05) when the adipose tissue was perfused at constant flow. These data suggest that adipose tissue blood flow is important in determining the lipolytic response to i.v. NA, probably by influencing the delivery of NA to the tissue. The marked inhibition by acidosis of lipolysis due to i.v. infused NA therefore appears to be the combined effect of a direct antilipolytic effect of acidosis and a decreased delivery of NA to the adipose tissue due to the attenuated blood flow response.
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PMID:Influence of adipose tissue blood flow on the lipolytic response to circulating noradrenaline at normal and reduced pH. 0 78

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
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PMID:Mechanisms of arrhythmias in chronic obstructive lung disease. 1 Feb 30

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

Cardiac performance was assessed in 33 lambs less than 1 to 5 days of age by means of left ventricular function curves. Performance was quantified by determining stroke volume ejected at end diastolic pressure 10 cm H2O (SV10) with constant afterload. Coronary flow, myocardial O2 consumption (MVO2), blood gas tensions and pH were determined. Measurements were obtained before and at 30 min intervals following hemorrhage to 30 mm Hg arterial pressure, and in controls (arterial pressure 75 mm Hg). Effects of metabolic acidosis, hypercapnia and beta-blockade were determined. In control lambs acidosis and hypercapnia failed to reduce SV10 after two hours. In hemorrhaged animals both factors sharply reduced SV10 and lambs with prior beta-blockade showed no greater reduction. MVO2 fell following hemorrhage but did not differ with metabolic conditions and did not relate to SV10. It is concluded that beta-adrenergic function is critically important in preserving left ventricular performance in newborn exposed to acidosis or hypercapnia. With sustained hemorrhage this mechanism fails leading to a significant depression of ventricular function. MVO2 was not a determining factor in these studies.
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PMID:Cardiac function and metabolism following hemorrhage in the newborn lamb. 1 55

Minute ventilation was measured in conscious dogs, at rest and during exercise (1 mph), over 60 min immediately following the acute inhalation of 5% carbon dioxide in air and at 2, 4, 7, and 14 days while breathing the same gas mixture in a chamber. The dogs were also studied in the immediate period of air recovery from chronic hypercapnia and 1 day later. Control studies were carried out with the dogs breathing air in the chamber under comparable conditions. A triphasic ventilation change was ovserved in dogs at rest over the 14 days of hypercapnia. After an initial marked increase in ventilation during acute hypercapnia, ventilation returned to control levels by 2 days and then appeared to be elevated above control studies from 4 to 14 days at a time when blood acid-base balance became compensated. When the same dogs were studied during exercise, ventilation was also not different from air control at 2 days of hypercapnia; however during exercise, unlike the resting studies, there was only a tendency for a secondary increase in ventilation at 7 and 14 days of hypercapnia. During the immediate recovery from chronic hypercapnia when the dogs breathed air there was no evidence of hypoventilation either at rest or exercise despite arterial alkalosis. At 24 h of recovery it appeared that dogs while at rest had a slightly reduced ventilatory response to 5% carbon dioxide relative to control studies. The findings provide suggestive evidence that other factors, in addition to acid-base balance, might contribute to the regulation of ventilation during chronic hypercapnia and the recovery from chronic hypercapnia.
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PMID:Ventilation in conscious dogs during acute and chronic hypercapnia. 1 31

During general anesthesia for bronchoscopy, hypoxemia is a major risk, especially in patients with a severe intrapulmonary shunt. With the technique of apnea in pure oxygen, after one hour denitrogentation, and with an intake of 50 liters of oxygen per minute through the bronchoscope, the PaO2 was greater than 400 mm of Hg, but hypercapnia and acidosis occurred. To compensate the latter, five minute sessions of apnea, alternating with two minutes of jet hyperventilation, nevertheless, have the disadvantage of producing a Ventrui phenomena at the proximal end of the bronchoscope, hence a fall in FiO2 which was dangerous in these high risk patients. The authors propose a method so that the Venturi phenomenon, which cannot be prevented, occurs in pure oxygen.
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PMID:[Seeking an ideal protocol for the stability of blood gases during general anesthesia for bronchosopies]. 1 91

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 oxygen affinity of hemoglobin and the factors determining the position of the oxygen dissociation curve were investigated in twenty-five patients with severe chronic obstructive lung disease. Patients have been separated into three groups: group I showed a normal or mild decrease of PaO2, group II a moderate fall in arterial oxygen pressure, and group III a severe hypoxia with balanced acid-base equilibrium and hypercapnia. Blood hemoglobin exhibited a significant increase in all groups, indicating an improved oxygen transport. In most patients a leftward shifting of the oxygen dissociation curve occurred. It is discussed that the tendency to left shifting is based upon alkalosis inside the red cells, evidently demonstrated in all groups studied. 2,3-diphosphoglycerate showed no close relation to evaluated oxygen affinity of hemoglobin. The evidence for an increased oxygen affinity may reveal a further compensatory mechanism in oxygen transport in patients with pulmonary disorders. Additionally the alkalosis inside the cells may counterbalance too great a right shifting of oxygen dissociation curve in vivo when severe hypoxia and hypercapnia occur.
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PMID:Oxygen affinity of haemoglobin and red cell acid-base status in patients with severe chronic obstructive lung disease. 1 84

In order to test the effects of hypercapnia on the acid-base status of fish, larger spotted dogfish were exposed to sudden changes of PCO2 in a closed seawater recirculation system. pH, PCO2 and PO2 were determined in arterial blood and seawater. The exchange of bicarbonate between extracellular space (ECS), intracellular space (ICS), and seawater (SW) was obtained from changes of the total bicarbonate amount in ECS and SW. After fourfold increase of PCO2 arterial pH fell markedly, but started to recover immediately towards control values. This was caused by compensatory accumulation of bicarbonate in the ECS. According to the origin of the extracellular bicarbonate increase three periods could be distinguished: 1.-- Bicarbonate transferred from ICS to both ECS and SW; 2. -- Bicarbonate transferred from both SW and ICS to ECS; 3. -- Bicarbonate transferred from SW to both ECS and ICS. After return to normocapnia similar periods occurred with opposite transfer directions and delayed period transitions. In the first period the ICS was found to be the only source for compensatory bicarbonate increases and even in the second period the ICS contributed to compensation of the extracellular pH. Thus bicarbonate exchange with the ICS appears to be an important regulatory mechanism diminishing the extracellular pH variations after changes in PCO2, before other compensatory mechanisms are initiated.
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PMID:Hypercapnia and resultant bicarbonate transfer processes in an elasmobranch fish (Scyliorhinus stellaris). 1 88


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