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

1. The ventilatory responses to transient and steady-state hypoxia were measured in ten patients with hepatic cirrhosis and in ten healthy control subjects. Successive measurements of these responses were also obtained in six goats before and after the experimental production of liver failure. Changes in the effect of steady-state hypoxia on the ventilatory response to hypercapnia were evaluated by successive studies in another goat. 2. In spite of a respiratory alkalosis during liver failure, the response to transient hypoxia was greater in the patients than in the control subjects. This response was increased after the onset of liver failure in all the goats. 3. In healthy humans and goats the responses to transient and steady-state hypoxia were similar in magnitude. During liver failure there was a disparity between the size of these responses, since the ventilatory increment evoked by steady-state hypoxia was unchanged in spite of the increase in response to transient hypoxia. Steady-state hypoxia consistently enhanced the ventilatory response to hypercapnia in a healthy goat, but frequently depressed the response to hypercapnia during liver failure. 4. The findings suggest that liver failure heightens the sensitivity of the peripheral chemoreceptors to the hypoxic stimulus, but may increase the tendency of the medullary centres to become depressed in hypoxia.
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PMID:Effect of liver failure on the ventilatory response to hypoxia in man and the goat. 0 6

1. Techniques for the measurement of unidirectional flux rates in fish which require no anaesthesia or surgery are described. 2. Resting values for Cl- uptake at 10 and 17 degrees C were 8-03 +/- 1-11 and 13-52 +/- 0-95 mu-equiv. 200 g-1 h-1 (+/- S.E.), respectively; and for Na+ the rates were 15-49 +/- 0-40 and 26-30 +/- 0-36, respectively. 3. Hypercapnic acidosis caused an increase in Na+ uptake, presumably through Na+/H+ (or NH+4) exchange. It is suggested that this is a compensation mechanism leading to the increase in blood buffering observed in response to hypercapnia. 4. Alkalosis was observed following acute temperature increase and was accompanied by an increase in the rate of Cl-/HCO-3 exchange and also by an increase in Na+/H+ exchange. 5. The role of these branchial ion exchange mechanisms in overall acidbase regulation is discussed.
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PMID:Branchial ion uptake in arctic grayling: resting values and effects of acid-base disturbance. 0 14

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

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

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.
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PMID:Local mechanism of CO2 action of cat pial arterioles. 1 34

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.
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PMID:Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog. 3 75

The present studies were done to determine whether preventing the respiratory alkalosis, which is known to occur with acute "hypoxic" stimuli, would lead to alterations in plasma concentrations of erythropoietin (Ep). Rats were subjected to two acute stresses, hypoxia and blood loss, separately and in combination, with and without the added stress of hypercarbia. Hypercarbia in all experimental groups was associated with a decrease in plasma concentrations of Ep. This reduction in plasma Ep with hypercarbia could not be fully explained by the higher arterial pO2S or p50S of the hypercarbic rats. Hypercarbia may have indirectly suppressed Ep production by increasing blood flow to the site of Ep production. Alternatively, the cell of origin of Ep could be sensitive to changes in pH and/or PCO2. It was further demonstrated that neither the onset nor the degree of reticulocytosis could be predicted by the plasma Ep concentrations. It is likely that the removal of red blood cells led to a decrease in marrow transit time with the early emergence of reticulocytes after acute blood loss.
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PMID:Modulation of erythropoietin concentrations by manipulation of hypercarbia. 12 67

Using the stop flow microperfusion technique with simultaneous capillary perfusion the secretory rate of H+ ions in the proximal tubule was evaluated by measuring the level flow reabsorption as well as the static head concentration difference of 3H labeled glycodiazine. At ambient glycodiazine concentration of 21 mmol/l the level flow reabsorption is in the same range as that of bicarbonate. In the early proximal loops the reabsorption is 20% greater than in the late proximal loops. The carbonic anhydrase inhibitors acetazolamide and 3,4-methylene-dioxyphenyl-sulfonamide (both 10(-4) M) as well as furosemide (10 (-3) M) inhibit the glycodiazine reabsorption 43%, 27% and 22% respectively. Thiocyanate (2-10(-2) M), however, exerted only an insignificant inhibition (12%). When Na+ in the ambient perfusion solutions was replaced by Li+ or choline+ the glycodiazine transport was strongly reduced. Ouabain (5-10(-2) M) inhibited too, but amiloride (10(-3) M) had no effect on glycodiazine transport. The glycodiazine transport was 28% reduced in metabolic alkalosis and to a smaller although significant extent (17%) in metabolic acidosis; it was unchanged in chronic hypercapnia. In chronic K+ depletion the glycodiazine reabsorption was accelerated by 12% only in the early proximal loops. Chronic parathyroidectomy as well as acute substitution with parathyroid hormone had no effect on the glycodiazine absorption. The main conclusions are: Proximal H+ transport proceeds with suitable buffers. Although independent of HCO3- and carbonic anhydrase, it could be partially inhibited by CA inhibitors. H+ transport is supposed to proceed as countertransport with Na+ ions. In chronic alkalosis the H+ transport is reduced.
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PMID:Renal proximal tubular buffer-(glycodiazine) transport. Inhomogeneity of local transport rate, dependence on sodium, effect of inhibitors and chronic adaptation. 12 86

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

The Authors produce a further contribution on metabolic post-hypercapnic alkalosis on the basis of clinical observation of a patient with severe hypercapnia and respiratory failure undergoing intensive care as well as treatment with iron lung (Pulmolife). The improvement of respiratory acid-base umbalance was associated with alteration of electrolytic assessment, especially of the plasmatic chloride ratio. The Authors consider this remark as a starting point for a physiopathological pattern and a more complete analysis of the pathways which generate the metabolic post-hypercapnic alkalosis condition in such patients.
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PMID:[Physiopathological and clinical data on post-hypercapnic metabolic alkalosis. A case of severe hypercapnia treated with drugs and in an "iron lung"]. 43 33


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