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

Decreased ventilatory response to hypoxia has been reported in patients with CO2 retention. The CO2 retention increases cerebrospinal fluid (CSF) [HCO3-], which could modify the ventilatory response to hypoxia. In order to evaluate the effect of increased CSF [HCO3-] as a consequence of hypercapnia on the response to hypoxia, phrenic nerve output during 5 min of progressive hypoxia was measured in anesthetized vagotomized and mechanically ventilated dogs when their acid-base was normal and when CSF [HCO3-] had increased. Peak phrenic nerve activity (PPNA), inspiratory time (TI), and expiratory time (TE) were recorded in 2 groups of dogs. Two hypoxic tests were conducted 2.5 h apart in each group. One group had normal acid-base status and the second group after the first hypoxic challenge breathed 10% CO2 for 2 h, and then ventilation was adjusted to bring CSF pH back to normal. The CSF [HCO3-] then had increased by 5.2 mEq/L and CSF PCO2 was 14.6 mmHg higher. With CSF [HCO3-] elevation, PPNA activity in response to hypoxia was significantly depressed, compared with that in animals with normal acid-base balance, TI was increased indicating slowing of nerve discharge, and TE was minimally increased indicating lessening of frequency of neural bursts. We conclude that the metabolic component of acid-base balance in the central nervous system can influence the neural output of the respiratory centers in response to hypoxia as manifested by phrenic nerve output, and increased CSF [HCO3-] seen with hypercapnia is associated with depressed hypoxic response.
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PMID:Modification of phrenic nerve output to hypoxia after two hours of hypercapnia and increased cerebrospinal fluid [HCO3-]. 709 12

Ventilatory adaptation to CO2 has been related to a return toward normal pH via an increase in CSF and arterial [HCO3(-)]. To examine whether the overall brain tissue can contribute HCO3(-) to surrounding fluids, we measured the in vitro CO2 buffer value (beta CO2) of control and hypercapnic rat brain homogenates and compared values with reported in vivo data. Hypercapnic rats were exposed to 7% CO2 for 3 days or 1 week. Brain homogenate was continuously tonometered for 3 h at 37 degrees C with 2%, 5% and 15% CO2 in O2. In addition, we used KOH to determine the brain buffering in the pH range 6.8-10.25. During CO2 titration, [HCO3(-)] increased gradually with time up to 90 min by about 10-15%, but the increase was blocked by a metabolic inhibitor, NaF, beta CO2, estimated per kg brain tissue from the dilute homogenate, ranged between 23.4 +/- 2.7 (SD) in controls and 26.0 +/- 1.3 meq/pH in the 7 day group, which were not significantly different. Over the same 7 days, CO2 dissociation curves were shifted upwards with similar slopes by about 6 ml/100 g tissue in association with a rise in pH of about 0.06, consistent with an accumulation of HCO3(-) without any change in buffers. No significant differences between groups were found from KOH titration curves, either in slope or position, consistent with lack of alteration in buffers as well. In vitro brain tissue beta CO2 (about 25) was less than reported in vivo values in the literature (around 40), possibly because H+ adjustments by whole body occur so rapidly in vivo. In addition, other investigators demonstrated that a major part of the increased brain cell [HCO3(-)] in prolonged hypercapnia could not be accounted for by the fixed acid production (Acta Physiol. Scand. 83: 344, 1971). By assuming the in vitro beta CO2 measures the available non-carbonic buffers, the data may be interpreted as showing that the overall brain tissue accumulates HCO3(-) from surrounding fluid during hypercapnia.
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PMID:In vitro buffer value of brain tissue during prolonged hypercapnia. 715 28

Shifts of Na+, K+, Cl- and HCO3- between the cells and extracellular fluid of nephrectomized mammals in acute response to hypercapnia and to HCl or KCl infusion are simulated in steady state models involving just intracellular buffering and a simply defined interdependence of ionic gradients. Such models integrate diverse kinds of data and suggest new interpretations. In respiratory acidosis K+, HCO3- and water leave some cells and move both to where chemical buffering is least (ECF and other cells) and to cells that regulate pH particularly well by active transport. Buffering by erythrocytes is important, but the effects of distinguishing erythrocytes from other cells in a model is mainly just to emphasize Cl- movements. Effects of departures from the mammalian norm of body composition are explored.
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PMID:The role of intracellular buffers in acid-base disturbances: mathematical modelling. 736 Oct 19

Recent results have demonstrated that intracellular pH (pHi) in nerve and glial cells is not regulated back to normal during CO2 exposure if extracellular pH (pHe) is reduced. This raises the question about regulation of pHi and pHe in vivo. In order to successively reduce pHe we exposed animals to incremental increases in CO2 tension (11, 27.5, 42.5%) and studied regulation of pHi during the first 90 min of hypercapnia. Extracellular pH, as well as Na+, K+, and Cl- concentrations, were also measured, as were whole tissue contents of Na+, K+, and Cl-. At all CO2 tensions studied, pHe slowly increased during CO2 exposure. In animals breathing 11% CO2 (delta pHe approximately 0.2 units), pHi increased slowly. However, in animals exposed to 27.5% CO2 or 42.5% CO2 (delta pHe > 0.4 units), no regulation of pHi was observed. Extracellular HCO3- concentrations increased substantially already during the first 15 min of hypercapnia (not significant in animals breathing 42.5% CO2), and then gradually rose. These increases were accompanied by a decrease in Cl- and an increase in Na+ concentration, K+ concentration remaining constant. The total tissue content of these ions remained constant, suggesting that extracellular HCO3- concentration increases by Cl-/HCO3- antiport and/or by Na+.2HCO3- symport, the HCO3- emanating from intracellular sources. The results challenge the dogma of the supremacy of mechanisms regulating pHi, and suggest that brain cells, possibly astrocytes, regulate pHe at the expense of their own pH homeostasis. By inference, we further conclude that regulation of pHi normally occurs only if pHe is first regulated back close to normal value.
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PMID:Regulation of intra- and extracellular pH in the rat brain in acute hypercapnia: a re-appraisal. 792 89

In order to determine the relationship between chronic hypercapnia and anthropomorphic data, pulmonary function tests and slopes of ventilatory responses to hypercapnia (HVCR) and hypoxia (HVR), we studied 55 patients with sleep apnea-hypopna syndrome (SAHS). Patients were divided into hypercapnic, PaCO2 > or = 45 mm Hg (Group I, n = 23, PaO2 = 61 +/- 10 and PaCO2 = 50 +/- 5 mm Hg, and [HCO3-] = 30 +/- 4 mEq/l [means +/- SD]) and normocapnic (or eucapnic), PaCO2 < 45 mm Hg (Group II, n = 32, PaO2 = 76 +/- 10 and PaCO2 = 39 +/- 4 mm Hg and [HCO3-] = 25 +/- 3 mEq/l [means +/- SD]) groups. When compared to the normocapnic group, hypercapnic patients were significantly heavier (with greater body surface area) and had significantly more severe restrictive and obstructive defects and impaired HVR and HCVR. The means (+/- SD) of some of the data follow (* indicates p < 0.05 when Group I is compared to Group II): [table: see text] When subgroups of hypercapnic and eucapnic patients with similar lung functions were compared, the subgroups differed significantly in their weights; conversely, in subgroups with comparable weights, lung function tests differed significantly. These data suggest that the mechanisms of chronic hypercapnia are multifactorial, and we hypothesize that, in the face of repetitive apneas and hypopneas, increased weight and abnormal lung function tests interact and contribute to the generation and maintenance of hypercapnia.
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PMID:Chronic hypercapnia in obstructive sleep apnea-hypopnea syndrome. 799 52

1. Triflocin, applied at millimolar concentration hyperpolarizes the basolateral membrane of Necturus proximal convoluted tubular cells, in vivo. 2. Barium, 2.5 x 10(-3) M, ouabain, 10(-3) M, or amiloride 10(-4) M, fail to prevent this hyperpolarization. 3. Triflocin has no effect on the intracellular chloride activity. 4. In physiological acid base conditions, Triflocin increases intracellular pH. 5. Upon an acute isohydric hypercapnia, Triflocin depolarizes the basolateral membrane potential. 6. It is concluded that, Triflocin inhibits the basolateral electrogenic Na-(HCO3)n > 1 cotransport in proximal tubules.
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PMID:Triflocin, a novel inhibitor for the Na-HCO3 symport in the proximal tubule. 807 65

This study reports variations observed under general anesthesia through small-bore endotracheal tubes in PO2, PCO2, HCO3, percentage saturation of O2, and pH levels in 39 patients who underwent laryngeal microsurgery lasting from 10 to 100 minutes. The tendency to an increase in PCO2 levels reached statistical significance only at the 100th minute but did not constitute a risk for patients as values remained within the limits of "permitted hypercapnia." PO2, percentage saturation of oxygen, and HCO3 levels did not vary significantly. pH values tended to fall (respiratory acidosis) in correlation to the increase in PCO2. Small-bore endotracheal tubes can safely be used for laryngeal microsurgery when operating times are not longer than 100 minutes.
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PMID:Laryngeal microsurgery under general anesthesia using small-bore endotracheal tubes: blood gas analysis. 812 90

To examine whether changes in respiratory chemosensitivity during the menstrual cycle are related to worsening of airway functions, hypoxic and hypercapnic ventilatory and P0.1 responses, airway function, and serum progesterone levels were studied in 11 female asthmatic patients in both the follicular and luteal phases. Plasma progesterone levels were 30-fold higher in the luteal phase than in the follicular phase (p < 0.0001). The PaCO2 decreased from 37.1 +/- 0.98 (SE) mm Hg to 35.1 +/- 0.89 mm Hg (p = 0.05) and HCO3- decreased from 22.4 +/- 0.44 mEq/L to 20.8 +/- 0.61 mEq/L (p < 0.001), from the follicular phase to the luteal phase, respectively. From the follicular to the luteal phase, delta VE/delta PACO2 tended to increase from 1.57 +/- 0.12 L/min/mm Hg to 1.91 +/- 0.26 L/min/mm Hg (p = 0.08) and delta P0.1/delta PACO2 increased from 0.25 +/- 0.05 cm H2O/mm Hg to 0.37 +/- 0.08 cm H2O/mm Hg (p = 0.05). During hyperoxic hypercapnia in the luteal phase, VE, f, and mean inspiratory flow increased and TI and TE decreased (p < 0.05). There were no differences in the hypoxic ventilatory and P0.1 responses and airway functional parameters (FEV1, PEF, V50, V25, and Raw) of the two phases. The increases in hypercapnic ventilatory and P0.1 responses were correlated to the improvement in FEV1 and PEF (p = 0.05 and p < 0.01, respectively). These results suggest that, although there is an augmentation of hypercapnic chemosensitivity during the luteal phase in female asthmatic patients, this is not associated with the decline in airway functions.
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PMID:Female asthmatics have increased hypercapnic chemosensitivity during the luteal phase which is not associated with decline in airway function. 825 50

We have investigated the effects of acidic stimuli upon [Ca2+]i in isolated carotid body type I cells from the neonatal rat using indo-1 (AM-loaded). Under normocapnic, non-hypoxic conditions (23 mM HCO3-, 5% CO2 in air, pHo = 7.4), the mean [Ca2+]i for single cells was 102 +/- 5.0 nM (SEM, n = 55) with 58% of cells showing sporadic [Ca2+]i fluctuations. A hypercapnic acidosis (increase in CO2 to 10%-20% at constant HCO3-, pHo 7.15-6.85), an isohydric hypercapnia (increase in CO2 to 10% at constant pHo = 7.4) and an isocapnic acidosis (pHo = 7.0, constant CO2) all increased [Ca2+]i in single cells and cell clusters. The averaged [Ca2+]i response to both hypercapnic acidosis and isohydric hypercapnia displayed a rapid rise followed by a secondary decline. The averaged [Ca2+]i response to isocapnic acidosis displayed a slower rise and little secondary decline. The rise of [Ca2+]i in response to all the above stimuli can be attributed to no single factor other than to a fall of pHi. The hypercapnia-induced rise of [Ca2+]i was almost completely abolished in Ca(2+)-free solution, suggesting a role for Ca2+ influx in triggering and/or sustaining the [Ca2+]i response. These results are consistent with a role for type I cell [Ca2+]i in mediating pH/PCO2 chemoreception.
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PMID:Effects of acidic stimuli on intracellular calcium in isolated type I cells of the neonatal rat carotid body. 827 80

The role of carbonic anhydrase (CNA) in the dynamics of carotid body (CB) function was tested by studying the effects of the membrane-permeable CNA inhibitor methazolamide on the chemosensory responses of the cat CB, perfused and superfused in vitro with cell-free and modified Tyrode solution at 36.5 +/- 0.5 degrees C in the presence of CO2-HCO3- (PO2 = 120 Torr, PCO2 = 32 Torr, pH = 7.40). The bulk of CO2 flow to the CB from the external milieu was overwhelmingly large relative to the metabolic production of CO2 in the CB. Accordingly, the relative contribution of the endogenous CO2 to the CB responses was small. The chemosensory nerve discharges were recorded from the whole desheathed carotid sinus nerve. The responses to acidic hypercapnia (PCO2 = 50-60 Torr, pH = 7.20-7.10), hypoxia (PO2 = 25 and 50 Torr), perfusate flow interruption, and bolus injections of sodium cyanide (20-40 nmol) were tested. To contrast, we also measured the effects of nicotine (2-4 nmol), which may act at sites other than those for O2 and CO2. Methazolamide (30 mg/l) in the perfusate at constant PCO2 and pH reduced the baseline activity and delayed the responses to step changes in PCO2 (and concomitantly pH) and PO2 and to cyanide but not to nicotine. The steady-state responses to these stimuli, measured as differences from control, were reduced, but not significantly. The initial overshoots seen with step changes in both high PCO2 and low PO2 were eliminated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dynamics of carotid body responses in vitro in the presence of CO2-HCO3-: role of carbonic anhydrase. 828 7


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