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

The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.
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PMID:Intracellular pH regulation of normal and hypertrophic rat myocardium. 4 27

The individual importance of peripheral chemosensitive afferents was studied using a transient hypercapnia (inhalation of a 5% or a 10% CO2 in air gas mixture respectively during 4 or 2 breaths) in human conscious subjects chosen for their different eupnoeic ventilatory patterns. Calculation of the speed of change in end-tidal CO2 pressure in tracheal gas (sPETCO2) and of the rate of change in tidal volume (sVI) gave assessment for quantifying the sensitivity of arterial chemoreceptors to hypercapnia (sCO2=SVI/SPETCO2). Our results showed that, independently of any outside influence of the eupnoeic ventilatory pattern on the components of the chemical stimulus, sVI and sCO2 were found to be much smaller in subjects whose pattern of breathing was slow (i.e. having a large tidal volume). The possible causes of the weak importance of peripheral chemosensitive afferents in such subjects were discussed.
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PMID:Relationships between eupnoeic pattern of breathing and ventilatory control in man II. Early response to transient hypercapnia. 6 39

In order to study the influence of hypercapnia on the content of glutamate and glutamine in the developing brain, pregnant rats and their offspring were kept in CO2 rich (6-10%) atmosphere and the litters were killed at different ages between 4 and 28 days. In the hypercapnic rats the content of both amino acids in the brain increases with age with almost the same time course as in normocapnic rats. At any age the glutamate content is lower in the hypercapnic animals than in control rats, whereas the glutamine content, beyond the first 8 days of life is increased. Both effects are rapidly reversible on return to air breathing. Although the glutamate-glutamine system is in full development, the influence of hypercapnia can be compared to that observed in adult rats. Hypercapnia did not change the glutaminase and the glutamine synthetase activity of the brain.
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PMID:Glutamate and glutamine in the brain of the neonatal rat during hypercapnia. 7 Oct 88

The pattern of change in ventilatory variables after inhalation of pure N2 for two breaths was studied in normal children and adults. In six subjects the trends of change were compared to the ventilatory response to transient hypercapnia. We observed differences in the patterns of increasing ventilation with an initial abrupt increase of tidal volume for transient hypoxia and a progressive change for hypercapnia. In both cases respiratory frequency was progressively but unsystematically enhanced. A highly significant positive correlation was demonstrated between individual sensitivities to CO2 and O2, with a greater response to hypercapnia (5.6 time) than to hypoxia. Finally, a very short-latency decrease in expiratory duration occurred in the first breath after inhalation of hypercapnic mixture, supporting the recent data of Cunningham et al. (1977).
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PMID:Pattern of the ventilatory response to transient hypoxia in man: differences from transient hypercapnic test. 9 21

The experiments on 18 guinea pigs were divided into two groups and each group was arranged in such a way that the effect of hypercapnia (generated by breathing 10% CO2-90% O2) was investigated with and without inhibition of carbonic anhydrase by methazolamide, 25 mg/kg, in the first group and acetazolamide, 50 mg/kg, in the second group, administered intravenously. The endocochlear potentials (EP) and endocochlear PO2 were recorded by microelectrodes introduced into the scala media, and cochlear microphonics (CM) were monitored by a silver-wire electrode from the round window. In the first exposure to hypercapnia (20-40 min) EP increased about + 6 mV. At the same time CM decreased; the reason for this is not yet known. During the second period of hypercapnia (80-100 min) when carbonic anhydrase was inhibited with methazolamide and acetazolamide, EP did not elevate as during the first period when carbonic anhydrase was not inhibited. In this work, under specific conditions, it was observed for the first time that carbonic anhydrase affects the generation of EP.
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PMID:Carbonic anhydrase in the generation of cochlear potentials. 10 17

The effects of elevated plasma CO2 partial pressure (PCO2) and [HCO3-] on cerebrospinal fluid (CSF) HCO3- accession have been reviewed in the context of the basal route of CSF HCO3- formation. The basal rate of 53 mM/h appears to be a consequence entirely of formation, via the reaction CO2 + OH- leads to HCO3-. Two-thirds of this rate is catalyzed by carbonic anhydrase, and the remainder uncatalyzed. The HCO3- accession matches 37% that of sodium, so that the HCO3- rate is involved with CSF turnover. When PCO2 is elevated twofold, the rate of HCO3- formation increase 10%, and results in elevation of CSF [HCO3-] by 5 mM in 1 h. Also, when plasma [HCO3-] is elevated 15 mM, CSF [HCO3-] rises about 5 mM/h; this is transfer of HCO3- "as such" by diffusion from plasma. The effects of hypercapnia and metabolic alkalosis on CSF HCO3- accumulation are additive, but they occur by separate processes. The effect of hypercapnia is an exaltation of the normal process due to increased substrate (CO2), but that of increased plasma HCO3- is due to imposition of an abnormal diffusion gradient for this ion between plasma and CSF. The effect of hypercapnia in elevating brain HCO3- operates to maintain brain pH and is also based on the formation of HCO3- from CO2. Brain HCO3- may also be a source of CSF HCO3-. Relations have been sought between the chemically calculated rates of HCO3- formation in CSF and those observed. The chemically calculated catalytic rate is 1,600 times greater than that observed, agreeing with the fact that more than 99.9% of choroid plexus carbonic anhydrase must be inhibited to yield a decrease in fluid formation or ion transport from plasma to CSF. The calculated uncatalyzed rate agrees closely with what is observed after complete inhibition of the enzyme. These considerations support the idea that all the HCO3- reaching the CSF is formed from CO2, rather than by transfer of the ion from plasma to CSF.
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PMID:Effect of varying CO2 equilibria on rates of HCO3- formation in cerebrospinal fluid. 11 42

Ten healthy subjects were tested for their peripheral respiratory chemosensitivities by the withdrawal technique two times on separate days. Hypoxic hypercapnia of PET, O2 75, 65 AND 55 mmHg with PET, CO2, 5 mmHg higher than the control level was replaced by 100% O2 two times with spontaneous respiration. Then, breath-by-breath depression calculated in minute ventilation (delta V) was observed during the period 5-20 sec after the first O2 inhalation. The results were analyzed by the linear relationship between PET, O2 and 1n delta V, and PaO2 and 1n delta V. Delta V at P02 50 mmHg, delta V50, was 9.09 +/- 6.81 liters/min (mean +/- SD) in PET, O2-1n delta V analysis and 9.22 +/- 7.46 liters/min in PaO2-1n delta V analysis, respectively. The averaged day to day variation of delta V50 expressed by SE in % was 5.3% in PET, O2-1n delta V analysis and 11.5% in PaO2-1n delta V analysis, respectively.
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PMID:A quantitative evaluation for peripheral respiratory chemosensitivities by the withdrawal test in man. 12 Apr 62

Effectiveness and haemodynamic tolerance of M.A.V. in conscious patients with a severe respiratory insufficiency is mainly due to the proper adaptation to ventilator with low frequency and adequate V.T. Thus M.A.V. is an eventual complement to directed ventilation exercises which in addition reduce the "rebound" of hypoxia and hypercapnia after a M.A.V. session. A proper adaptation ensures haemodynamic tolerance. Expiratory time should be sufficient in such obstructive patients. A post inspiratory pause can improve V.C.O2. Nevertheless, it should not shorten inspiratory time to less than one second and for each patient the best ventilatory profile should be properly established taking into account blood gases, circulatory, expired CO2 and clinical monitoring.
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PMID:[Immediate effects and conditions of effectiveness of a session of mechanical assisted ventilation (M.A.V.) in severe respiratory insufficiency (PaCO2 greater than 50 mmHg) out of intensive care conditions (author's transl)]. 12 82

Intravenous injection of CT 1341 (a mixture of alphaxalone and alphadolone dissolved in cremophor el) induced a decrease in cerebral blood flow (CBF) measured by 133Xe clearance in cats with artificial respiration (the mean reduction in CBF was 2 ml/100 g/mn for 1,2 mg/kg or CT 1341. So, CBF was decreased by 22% when CT 1341 (7,2 mg/kg) was intravenously injected, (mean Pa CO2 equals 30 mm Hg). Changes in CBF following CT 1341 intravenous injection seems to be caused by cerebral vascular constriction evidenced by the direct observation of pial vessels. Following intravenous injection of CT 1341 (from 7, 2 mg/kg to 19,2 mg/kg), the cerebrovascular reactivity to hypercapnia or hypocapnia was not affected, but autoregulation of cerebral blood flow was transiently abolished. In animals with free respiration, CBF was increased in relation with the elevation in Pa CO2 caused by the depression of respiration.
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PMID:[Effects of combination alfaxalone and alfadolone, anesthetic derivatives of pregnanedione, on cerebral hemodynamics in cats]. 12 19

In the unanesthetized rabbit autoregulation of cerebral blood flow was evaluated by continuous recording of local cerebral blood flow during progressive hypotension induced by exsanguination. Under hypercapnia induced by CO2, 8 per cent in air, autoregulation was not suppressed but an increase of the threshold under which autoregulation disappears was noted.
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PMID:[Influence of moderate normoxic hypercapnia on the autoregulation of the cerebral circulation in the unanesthetized rabbit]. 13 40


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