Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF "metabolic" acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.
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PMID:Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions. 11 88

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

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

Five anesthetized dogs were made severely hypercapnic by stepwise addition of CO2 to their inspired air. Blood PCO2 levels greater than 400 Torr were reached. During hypercapnia, the steady-state end-tidal PCO2 (PaCO2) was always higher than the simultaneous measured arterial PCO2 (PaCO2). The mean ratio PaCO2/PACO2 was 0.861 +/- 0.01. These results are consistent with the predictions of the Charged Membrane Hypothesis, that gas-to-blood PCO2 differences should be directly proportional to the blood H+ activity. The results cannot be explained by delayed equilibration of CO2 between plasma and red blood cells. The latter hypothesis predicts that, under the conditions of these experiments, the PCO2 of arterial blood should be higher than the PCO2 of end-tibal gas. The blood HCO3- during hypercapnia did not increase as much as would be predicted if the blood were exposed to CO2 in vitro. This may reflect movement of blood HCO3- generated by the buffering of carbonic acid into intracellular compartments during hypercapnia.
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PMID:Gas-to-blood PCO2 differences during severe hypercapnia. 46 74

Experiments were designed to determine the contribution of increased extracellular HCO3- concentration, [HCO-3e], to the net extracellular-to-intracellular HCO3- flux observed in hearts during hypercapnia. Isolated rabbit hearts were perfused by recirculating for 15-min periods a small volume of Ringer solution in which [HCO-3e] and carbon dioxide tension (PCO2) could be independently altered. A net HCO-3 flux was evidenced by a decrease in [HCO-3e] during recirculation. [HCO-3e] was randomly increased from 19 mM over a range of 19-42 mM at a constant PCO2 of 38.7 Torr. The resulting flux increased linearly with the [HCO-3e] existing at the start of recirculation. The same relationship was observed at 95.8 Torr PCO2. The disappearance of HCO-3 from the perfusate could not be explained by dilution in the interstitium or by lactate accumulation. When PCO2 was increased from 40 Torr over a range of 40-160 Torr at a constant [HCO-3e] of 20 or 30 mM, a small flux was observed only at the highest PCO2 levels. Essentially the same results were obtained when recirculation time was prolonged to 30 min. These results suggest that the major determinant of the HCO-3 flux is a change in extracellular HCO-3 concentration.
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PMID:Determinants of transmembrane bicarbonate flux during acid-base changes. 60 97

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (VE), end-tidal carbon dioxide tension (PETCO2), venous bicarbonate concentration [HCO3-], oxygen consumption (VO2), hypercapnic ventilatory response (deltaVE/deltaPCO2), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 +/- 2.0 mg/dl. VE increased (P less than 0.05, PETCO2 decreased (P less than 0.05), and [HCO3-] did not change significantly during drug ingestion. deltaVE/deltaPCO2 increased gradually to a value 37% greater than control by day 3 and remained constant (P less 0.01). A increased by 251% and VO2 by 18% within 2 h and remained constant for the remainder of the ASA period (P less than 0.01). All values returned to base line within 24 h following cessation of ASA. We conclude that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanically linked to changes in metabolic rate.
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PMID:Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion. 60 1

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71

Cerebral hemodynamics, vascular reactivity, and metabolic alterations were studied in anesthetized, spontaneously respiring dogs for 4-6 hr of gram-negative endotoxin shock. Cerebral venous outflow (cerebral blood flow) was measured directly from the cannulated confluence of the sagittal, straight, and lateral sinuses, with the lateral sinuses occluded. Cerebral blood flow and cerebral perfusion pressure decreased immediately upon administration of 1,2, or 5 mg/kg endotoxin and consistently remained below control values. By the fourth hour of shock, cerebral blood flow was decreased 37, 48, and 45% respectively. Cerebral vascular resistance initially decreased, then progressively increased to levels significantly above control, and it was primarily responsible for the reduced cerebral blood flow in the later stages of shock. Cerebral autoregulatory and "venous-arteriolar" responses were well maintained, although cerebral vascular reactivity to arterial hypercapnia was depressed. Cerebral venous blood pH and pO2 decreased, and arterial-venous differences of percentage oxygen saturation, total CO2, and HCO3 increased. These alterations in cerebral vascular hemodynamics and tissue acid-base balance indicate that cerebral ischemia and resulting acidosis occur during canine endotoxin shock.
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PMID:Cerebral hemodynamics, vascular reactivity, and metabolism during canine endotoxin shock. 92 8

Ten mongrel dogs (mean weight: 27 kg) awake and with an implanted femoral catheter have been maintained for three days in a controlled chamber (10% CO2 and 21% O2). Arterial blood samples, taken before admission and after one, two, four, six, 24, 48 and 72 hours of exposure, allowed to study blood gases and acid-base equilibrium. Glycemia, phosphatemia, erythrocyte concentration of glucose-6-phosphate (G-6-P), fructose-6-phosphate (F-6-P), fructose-1,6-diphosphate (F-1,6-DP), 2,3-diphosphoglycerate (2,3-DPG), pyruvate, lactate and ATP were also titrated by various enzymatic methods. In addition, nine reference subjects were studied in air (without CO2). During the hypercapnia, [H+] rapidly increases to 70 nmol/1, then progressively decreases after 24 hours, while [HCO3-] slowly rises. The glycemia stays high during the whole exposure. There is also an increase in inorganic phosphate, G-6-P and F-6-P, but during the first 24 hours only. F-1,6-DP, pyruvate and lactate remain lowered during the whole exposure. The 2,3-DPG diminishes after the sixth hour. These phenomena, related to the acidosis and probably to the phosphofructokinase inhibition don't arise in the reference subjects. However the latter present after a two and four hour-stay in the chamber a small decrease in pyruvicemia and lactacidemia.
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PMID:[Intermediates of erythrocyte glycolysis during three days hypercapnia in the dog (author's transl)]. 101 72

The total CO2 is titrated in liver, abdominal and leg's muscles, brain and thigh-bone of rats exposed to 8 +/- 1% of carbon dioxide under normoxic (20-23% of O2) and normobaric conditions during zero, two, four or six weeks. Total (H2Ot) and extracellular (H2Oe) water is measured in these organs by the 3H-inulin method. The CO2 storage in organs is expressed in relation to the PaCO2 increase (mmol-kg-1 fresh tissue-torr-1). During a four week hypercapnia, this CO2 increase is very important in bone and brain compared with that of other organs and of the whole body. With regard to the whole body, the bone CO2 content is still increasing after four weeks. The increase in extracellular bicarbonate (delta[HCO3-e]/delta PaCO2) is negligible (1/100 th) in comparison with the whole carbonic increase (delta CO2/delta PaCO2). The bone extracellular compartment diminishes in relation with the experimentation duration, without any significant change in H2Oi (Student's analysis). A factorial analysis (BENZECRI) shows that the weight of H2Oe in the information diminishes for all organs, both with the duration of normal subjects observation (ageing) and with the hypercapnia duration.
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PMID:[CO2 storage in various organs during chronic experimental hypercapnia (author's transl)]. 101 73


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