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

Systemic hypoxia [PaO2 27.3 +/- 1.8 (SE) mmHg] in anesthetized paralyzed rats reversibly increased within seconds the arterial pressure and activities of the sympathetic nerves and the reticulospinal vasomotor neurons of the rostral ventrolateral medulla (RVL). After peripheral chemodenervation, hypoxia also increased activity of the sympathetic nerves and doubled discharges of the vasomotor neurons while inhibiting a majority of the RVL respiratory neurons. Systemic hypercapnia was not effective in eliciting sympathoexcitatory responses. Iontophoresis of sodium cyanide stimulated the vasomotor and inhibited the respiratory neurons. In contrast, iontophoreses of H+, HCO3-, and lactate were without effects on activity of the vasomotor neurons. We conclude 1) hypoxia excites the vasomotor neurons by activating the arterial chemoreceptors and by activating intrinsic cellular mechanisms probably unrelated to accumulation of metabolic byproducts; 2) hypoxia may be the adequate stimulus exciting the RVL-spinal vasomotor and inhibiting the respiratory neurons during the cerebral ischemic response; and 3) these vasomotor neurons may be central oxygen detectors.
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PMID:Hypoxia selectively excites vasomotor neurons of rostral ventrolateral medulla in rats. 830 47

Uremic acidosis accompanies chronic renal failure in hemodialysis patients because of a retention of nonvolatile acids. Standard bicarbonate (39 mEq/L) and acetate (38 mEq/L) dialysates do not completely correct the acidosis. The acid-base and biochemical effect of a high-bicarbonate (42 mEq/L) dialysate was evaluated in 38 patients during high-efficiency and high-flux dialysis over 12 wk. All patients were dialyzed on standard bicarbonate dialysate before the study and for 8 wk after the study. In order to monitor potential excessive alkalosis, predialysis and postdialysis arterial blood gases were measured in seven patients who initially had a normal predialysis pH. Serum chemistries revealed no significant changes in predialysis BUN, calcium, ionized calcium, or phosphorus during the 12-wk study. There was no change in postdialysis ionized calcium or phosphorus. Predialysis and postdialysis serum total CO2 (STCO2) increased over the 12-wk study (P < 0.0001). By week 12, 75% of the hemodialysis patients had an STCO2 > 23 mEq/L and no patient had an STCO2 > 30 mEq/L predialysis. After the 8-wk washout, all chemistries were no different from prestudy concentrations. Predialysis blood gases in seven patients with normal predialysis HCO3 revealed a significant increase (P < 0.009) in PCO2 and HCO3 over the 12-wk study; predialysis pH and PO2 did not change. There was no significant change in postdialysis blood gases. It was concluded that: (1) a high-bicarbonate dialysate corrects predialysis acidosis in 75% of hemodialysis patients without causing progressive alkalemia, hypoxia, or hypercarbia; and (2) predialysis BUN, calcium, ionized calcium, and phosphorus are unaffected by high-bicarbonate dialysate.
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PMID:Normalization of uremic acidosis in hemodialysis patients with a high bicarbonate dialysate. 813 52

Electrogenic cotransport of Na+ with HCO3- has been reported in numerous tissues. It has always been shown with a net transfer of negative charge, but in some situations achieves net outward transport of both species with a stoichiometry of at least three HCO3- ions per Na+ ion (3:1), and in other situations achieves net inward transport of both species and has a stoichiometry of at most two HCO3- ions per Na+ ion (2:1). This suggests either that there may be more than one protein responsible for Na(+)-HCO3- cotransport in different tissues or that if there is a single protein, its stoichiometry may differ depending on the orientation of net transport. The present study, using conventional or double-barreled ion-selective microelectrodes to follow basolateral membrane potential and intracellular pH or Na+ activity in Necturus proximal convoluted tubule in vivo, shows that the orientation of the basolateral Na(+)-HCO3- cotransporter can be reversed upon switching from a perfusate simulating normal acid-base conditions to one that imposes peritubular isohydric hypercapnia. Moreover, accompanying the reversal of orientation is a change of apparent stoichiometry from 3:1 to 2:1. Given that the observed change of orientation and accompanying change of apparent stoichiometry occur within seconds and in the same preparation, these results suggest that a single transport protein is responsible for both types of behavior.
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PMID:Change of apparent stoichiometry of proximal-tubule Na(+)-HCO3- cotransport upon experimental reversal of its orientation. 834 63

These studies were conducted in neurosurgical patients to determine brain tissue nonbicarbonate buffering of pH changes during hypercapnia. Following a craniotomy, a sensor which continuously measures oxygen pressure, carbon dioxide pressure, pH and temperature was inserted into cortex tissue of nine subjects. Bicarbonate concentration was calculated from the Henderson-Hasselbach equation. Following baseline measures, PaCO2 was increased 10mmHg for 10 min. Tissue pCO2 increased 9 mmHg (p < 0.05) without a change in tissue pO2. In six patients, tissue bicarbonate concentration increased from 18 to 20 meq L-1 (p < 0.05), indicating a 40-50% attenuation of the increase in hydrogen ion (H+) by nonbicarbonate buffering mechanisms. Three patients showed no increase in tissue bicarbonate during hypercapnia; 2 had baseline tissue pH less than 6.5 and one displayed signs of tissue hypoxia during the CO2 challenge. In all patients, increases in tissue H+ during hypercapnia were related to baseline tissue bicarbonate concentration. Marked increases in H+ were seen when baseline bicarbonate decreased below 10 meq L-1. These results suggest that when tissue bicarbonate is depleted, the risk of H+ induced injury during hypercapnia is increased.
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PMID:Brain tissue acid-base response to hypercapnia in neurosurgical patients. 862 93

Acute hyperosmolality results in an extracellular dilution acidosis and hypercarbia that does not stimulate ventilatory compensation. The osmotic stress is also associated with shifts in water and electrolyte balance and an increase in intracellular pH. The alkaline intracellular pH was hypothesized to have a role in preventing a normal respiratory response to the extracellular acidosis and hypercarbia. Therefore, this study examined the effect of ion-exchange blockade on intra- and extracellular pH and ventilation during acute hyperosmolality in the Pekin duck (Anas platyrhynchos) by using 31P-nuclear magnetic resonance spectroscopy. Both 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and amiloride inhibited the development of the intracellular alkalosis that normally develops in muscle during acute hyperosmolality. Instead, exposure to hyperosmotic stress during ion-exchange blockade resulted in a significant acidosis both intracellularly and extracellularly. Arterial pH decreased 0.10 +/- 0.04 pH unit with a sucrose infusion after either blocker, and intracellular pH decreased 0.11 +/- 0.06 and 0.16 +/- 0.04 pH units with a sucrose infusion after DIDS and amiloride, respectively. Ventilation increased 79 +/- 28 and 122 +/- 100%, respectively, during acute hyperosmolality after ion-exchange blockade with either DIDS or amiloride. The results suggest that intracellular pH may play a role in the ventilatory response to acid-base perturbations. The data also indicate that both Cl-/HCO3- and Na+/H+ exchanges are involved in the development of the intracellular alkalosis during hyperosmotically induced extracellular acidosis.
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PMID:Dilution acidosis: evidence for a role of intracellular pH in the control of ventilation. 872 70

The serum anion gap is decreased in hyperchloremic (HCl) acidosis and increased in diuretic-induced alkalosis. These anion gap changes have been largely attributed to titration-induced variations in the net negative charge of the serum proteins, which are the predominant non-HCO3 buffers of serum. It has recently been shown, however, that albumin has all of the net protein charge, and titration-induced changes in charge are smaller than have been widely believed. Because the non-HCO3 buffers are also titrated in acute hypocapnia and hypercapnia, these disorders were induced in 16 anesthetized dogs for 10 min in order to assess the effect of acute changes in pH on the anion gap. Although the mean arterial pH varied from 7.04 to 7.65, the calculated mean albumin charge only varied from 6.8 to 9.0 mEq/L. When the anion gap was computed with HCO3 (AGHCO3 = Na + K - Cl - HCO3), the change in AGHCO3 per 0.1 change in pH (delta AGHCO3/ delta pH) was only 0.15 mEq/L per 0.1 pH. When the anion gap was computed with total CO2 content (AGTCO2 = Na + K - Cl - TCO2), delta AGTCO2/delta pH was larger (0.51 mEq/L per 0.1 pH) because of the effect of variable PCO2 levels on TCO2. In a review of 22 previous studies in humans and dogs, similar estimates of delta AG/delta pH were obtained (after adjusting for the lower albumin level in dogs). These results show that simple titration processes that occur within 10 min of a change in pH cause minimal changes in the anion gap. Titration of the known non-HCO3 buffers of serum does not explain the much larger anion gap changes of HCl acidosis and diuretic alkalosis.
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PMID:Effect of acute pH change on serum anion gap. 878 9

We examined effects of central hypoxia on tracheal smooth muscle (TSM) tone, phrenic nerve activity (PNA) and blood pressure (BP) in decerebrated, paralysed, and artificially ventilated dogs. Central hypoxia was induced by injection of N2-saturated saline (5 ml; PO, 25-32 torr) through a catheter in the vertebral artery. The effects of central hypoxia were compared with the responses to central chemoreceptors stimulation, namely central hypercapnia induced by intravertebral injection of high CO2 saline (5 ml; PCO2 90-100 torr, PO2 80-120 torr, pH 7.38-7.42) buffered by HCO3-. Central hypoxia caused relaxation of TSM accompanied by depression of PNA and elevation of BP. In contrast, central hypercapnia evoked tracheal constriction along with respiratory excitation and pressor response. The tracheal relaxation in response to central hypoxia occurred with onset and peak latencies similar to those observed in PNA depression and BP elevation. This suggests a common source for the synaptic inputs to three distinct control systems involved in cardiovascular, respiratory and airway functions. Such neuronal substrate is considered to be activated by central hypoxia.
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PMID:Response of tracheal smooth muscle tone to lower brain stem hypoxia in dogs. 891 75

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.
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PMID:A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. 902 82

Concentrations of H+ and HCO3- rise in fluid lining hypercapnic airways. Effects of these ions on pulmonary endocrine cells were studied in 119 fetal rat lung organ cultures by semiquantitative staining for calcitonin gene-related peptide (CGRP)-like immunoreactive material. Intracellular CGRP was determined in cultures under "no-release" baseline conditions and after incubation in control or test media. After exposure to HCO3(-)-free medium at pH 7.4 (incubation control), CGRP fell moderately from no-release levels. Bombesin (1 ng/ml) promoted further significant loss of peptide, which was dependent on extracellular Ca2+ and inhibited by somatostatin and [D-Arg(1),D-Pro(2),D-Trp(7,9),Leu(11)]substance P, a bombesin receptor antagonist. CGRP staining of explants incubated with 24 mM HCO3- maintained no-release levels at and above pH 7.1 but decreased significantly at pH 6.8. The drop was blocked by somatostatin or exclusion of HCO3- and was not augmented by bombesin or 48 mM HCO3-. Results suggest that pulmonary endocrine cells may respond to hypercapnia by releasing bioactive peptides like CGRP, thus stimulating afferent nerves and altering patterns of ventilation and perfusion.
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PMID:Effects of hydrogen and bicarbonate ions on endocrine cells in fetal rat lung organ cultures. 912 67

We investigated whether neurons in two chemosensitive areas of the medulla oblongata [nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM)] respond to hypercapnia differently than neurons in two nonchemosensitive areas of the medulla oblongata [inferior olive (IO) and hypoglossal nucleus (Hyp)]. Medullary brain slices from preweanling Sprague-Dawley rats were loaded with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, and intracellular pH (pHi) was followed in individual neurons at 37 degrees C with the use of a fluorescence imaging system. Most neurons from the NTS and VLM did not exhibit pHi recovery when CO2 was increased from 5 to 10% at constant extracellular HCO3- concentration [extracellular pH (pHo) decreased approximately 0.3 pH unit] (hypercapnic acidosis). However, when CO2 was increased from 5 to 10% at constant pHo (isohydric hypercapnia), pHi recovery was seen. In contrast, all neurons from the IO and Hyp exhibited pHi recovery during hypercapnic acidosis. All pHi recovery in the four areas studied was inhibited by 1 mM amiloride and unaffected by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. These data indicate that 1) pHi regulation differs between neurons in chemosensitive (NTS and VLM) and nonchemosensitive (IO and Hyp) areas of the medulla, 2) pHi recovery is due solely to Na+/H+ exchange in all four areas, and 3) Na+/H+ exchange is more sensitive to inhibition by extracellular acidosis in NTS and VLM neurons than in IO and Hyp neurons.
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PMID:Intracellular pH response to hypercapnia in neurons from chemosensitive areas of the medulla. 924 82


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