Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous infusion in conscious rabbits of Hacetate decreases both arterial CO2 partial pressure PaCO2 and cerebrospinal fluid (CSF) HCO3- more than observed with HCl or HNO3 infusion. These acids did not affect CSF HCO3- in isocapnic conditions, and this study asks whether Hacetate infusion will do so. Arterial, central venous, and cisterna magna catheters were implanted in pentobarbital-anesthetized rabbits and all subsequent measurements were performed in the conscious state. Hacetate was infused intravenously over 6 h to decrease plasma HCO3- the same amount in a group allowed to decrease its PaCO2 in response to the acid (hypocapnic) and one in which PaCO2 was maintained at control levels (isocapnic). CSF HCO3- decreased significantly in isocapnia, although the change was less than in hypocapnia. Stoichiometrically by 6 h the measured CSF HCO3- change was balanced by an increase in acetate in hypocapnia and the sum of an increase in acetate and a decrease in chloride in isocapnia. Mechanistically, net acetate entry into CSF appears to involve an exchange for chloride as proposed for NO3-/Cl- and a process that lowers CSF HCO3-. This process could be competitive replacement of HCO3- by acetate in the CSF production mechanism or nonionic diffusive entry of Hacetate into CSF with subsequent titration of HCO3-. The decreases in CSF HCO3- result from the acetate mechanism and the hypocapnic effect on Cl- and HCO3-. The greater ventilatory response results from the greater CSF acidification or a specific effect of acetate per se.
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PMID:CSF acid-base regulation and ventilation in iso- and hypocapnic Hacetate acidosis. 309 54

Studies have demonstrated that the protective effect of secondary hypocapnia on plasma acidity during chronic HCl-acidosis is undermined by a renal-mediated decrement in plasma bicarbonate concentration induced by the hypocapnia itself. The present study was designed to assess whether the protection of "whole body" intracellular pH (pHi) is similarly undermined by this maladaptive response of the kidney. Whole body pHi was estimated by the 5,5 dimethyl-2,4-oxazolidinedione (DMO) method in seven unanesthetized dogs under each of three conditions: control, chronic HCl-acidosis (10 mEq H+/kg/day) with spontaneous secondary hypocapnia, and chronic HCl-acidosis with a normal level of carbon dioxide tension (maintained by the use of an environmental chamber). pHi was 6.71 +/- 0.02 during control, and 6.57 +/- 0.03 and 6.57 +/- 0.02 during the two acidosis periods, respectively. These results indicate that sustained secondary hypocapnia fails to render the intracellular compartment less acidic because of a maladaptive reduction in intracellular bicarbonate concentration.
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PMID:Secondary hypocapnia fails to protect "whole body" intracellular pH during chronic HCl-acidosis in the dog. 640 72

Ventilation and acid-base balance were studied in 6 conscious dogs during chronic eucapnic and hypocapnic metabolic acidosis. The dogs had tracheostomas for respiratory studies, exteriorized carotid arteries for obtaining arterial blood and cannulae for sampling cisternal cerebrospinal fluid (CSF). Measurements were obtained on a control diet, and then, during metabolic acidosis induced by adding HCl (7 mmol/kg per day). Initially during metabolic acidosis, PaCO2 was maintained normal by having the dogs breathe 3% CO2 (eucapnia); then the dogs breathed air (hypocapnia). Chronically, arterial and CSF [HCO-3] were related to PCO2. No respiratory compensation occurred during chronic hypocapnic metabolic acidosis since [HCO-3] decreased more than PCO2; consequently, the acidosis worsened. At any [H+], ventilation was related to PCO2. Thus, during hypocapnic metabolic acidosis, ventilation was not increased relative to increase in arterial and CSF [H+]. Modulation of ventilation by PCO2 during severe acidosis may be crucial because stimulation of ventilation by [H+] of arterial blood or CSF would have progressively reduced PCO2 and [HCO-3], resulting in a worsening of the metabolic acidosis.
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PMID:PCO2 modulation of ventilation and HCO3- buffer during chronic metabolic acidosis. 642 Aug 62


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