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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that furosemide would cause metabolic alkalosis and thus alveolar hypoventilation, normal rabbit pups were given either furosemide (4 mg/kg/day) or saline solution for the first 8 to 10 days of life. Pups given furosemide developed primary metabolic alkalosis and reduced ventilation, which resulted in secondary respiratory acidosis. Lung compliance was improved by furosemide, and the ventilatory response to CO2 was unaffected. KCl injection in alkalotic pups increased ventilation and decreased pH. The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water. When these effects occur in infants with chronic lung disease, the beneficial effect of furosemide may be obscured.
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PMID:Furosemide decreases ventilation in young rabbits. 391 2

To examine the nature of the electroneutral sodium chloride absorptive process affected by arterial carbon dioxide tension (PCO2), we measured the effects of amiloride on colonic sodium absorption at concentrations (0.75 mM) known to inhibit cell membrane sodium-hydrogen ion exchange. During sequential in situ perfusions of distal colon with amiloride-free and amiloride-containing solutions, water and electrolyte transport was measured in anesthetized, mechanically ventilated rats during normocapnia, respiratory alkalosis, or respiratory acidosis. During amiloride-free perfusions, alkalosis decreased and acidosis increased net water, sodium, and chloride absorption without changing the transmural potential difference. Perfusion of amiloride (0.75 mM) caused a similar fractional decrease in net sodium absorption in alkalotic (-53.3 +/- 10.2%), normocapnic (-46.3 +/- 6.5%), and acidotic rats (-57.2 +/- 5.2%). Net water (-43%) and chloride absorption also exhibited equivalent fractional reductions in the three acid-base states during amiloride perfusion, although net chloride absorption was reduced only about 20%. These results suggest that the specific colonic sodium absorptive process affected by arterial PCO2 is an amiloride-sensitive, sodium-hydrogen ion exchange process. Arterial PCO2 probably also affects a mucosal chloride-bicarbonate exchange process that results in its overall effect on electroneutral sodium chloride absorption by the distal colon.
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PMID:Effect of arterial carbon dioxide tension on amiloride-sensitive sodium absorption in the colon. 609 83

In 1975 H. Rahn put forward a new concept of hydrogen ions regulation which explains acid-base regulation in relation to body temperature and applies to all animal species. At the root of this concept is the finding that maintenance of intracellular neutrality is governed by water dissociation and regulated by imidazole-rich protein buffers. The pH of the extracellular fluid, which receives acid by-products of cell activity, is kept higher than that of the intracellular fluid (relative alkalinity). The difference between extracellular pH and neutrality is constant for each species and ranges from 0.6 to 0.8 pH units. It is unaffected by changes in temperature, and the total CO2 content of extracellular fluid remains constant. The authors were able to confirm the value of this new concept in man by experimental studies of in vitro and in vivo blood of patients undergoing aorto-coronary bypass under controlled hypothermia. They draw the following practical conclusions: (1) in subjects under moderate or deep hypothermia for surgical purposes, the acid-base status can be controlled and the extracellular pH adjusted by ensuring intracellular neutrality; this is done by keeping PCO 2 at such a level that the arterial blood pH measured at 37 degrees C remains around 7.40; (2) the problem of correcting acid-base values (pH-PCO 2) according to body temperature is solved simply by using pH and PCO 2 values measured at 37 degrees C and interpreting them, as usual, in terms of metabolic or respiratory acidosis or alkalosis.
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PMID:[Relations between acid-base equilibrium and body temperature. Physiological concepts and practical applications]. 622 30

To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.
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PMID:Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs. 674 23

In the unanesthetized dogfish, Scyliorhinus canicula, oxygen and carbon dioxide partial pressures and concentrations in inspired and expired water and the acid-base balance of arterial blood, pHa and PcCO2, were determined. Each dogfish was exposed to waters differing in oxygenation and in CO2 levels, which was controlled with a pH-CO2-stat device, for successive 2- to 3-h periods. The four ambient conditions were: normoxia-normocapnia (inspired PO2, PIO2 ca 160 Torr; PICO2 ca 0.3 Torr), hyperoxia-normocapnia (PIO2 ca 730 Torr), hyperoxia-hypercapnia (PICO2 ca 1.0 Torr); normoxia-hypercapnia. At both low and high ambient CO2, the inspired-expired O2 and CO2 concentration differences increased in hyperoxia. Ventilation was depressed, and concomitantly, PACO2 increased and the arterial plasma pH decreased. The hypercapnic acidosis was rapidly but only partially compensated by an increase of the plasma bicarbonate concentration. Due to the buffer action of carbonate in sea water, low and high ambient CO2 levels corresponded respectively to high and low values of the CO2 capacitance coefficient, betaWCO2. At both ambient oxygenation levels, the expired-inspired PCO2 difference was greater at low than at high betaWCO2. At a given ambient CO2 level, expired PCO2, PECO2, wash higher in hyperoxia than in normoxia; an effect more marked at low than at high betaWCO2. Thus, the water capacitance coeffcient betaWCO2 is an important factor determining PECO2 values and probably arterial blood acid-base balance. As a general conclusion, the acid-base balance of the arterial blood in the dogfish is very much dependent on the conditions of the oxygenation and acid-base balance of the ambient water which consequently should be carefully controlled.
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PMID:Blood acid-base balance as a function of water oxygenation: a study at two different ambient CO2 levels in the dogfish, Scyliorhinus canicula. 677 56

We studied the response of blood, cerebrospinal fluid (CSF), and brain ionic composition and acid-base status as well as ventilation to acute respiratory acidosis (FICO2 0.08) in lightly anesthetized newborn puppies. Control puppy plasma ions and CSF-plasma ionic distribution ratios were essentially adultlike while in blood a mild, compensated respiratory acidosis was present, and in CSF, PCO2 and [HCO3-] were slightly higher than in adults. Brain tissue water content was higher in puppy vs. adult; the Cl- space was greater; the content of [Na+], [Cl-], and [HCO3-] were higher and [K+] lower. During respiratory acidosis, CSF [HCO3-] increased 2.0 mmol/l by 15 min and 6.2 mmol/l by 3 h, a response quantitatively like that observed in the adult. The quantity, CSF [Na+] -- [Cl-], increased stoichiometrically with CSF [HCO3-], indicating the mechanistic involvement of these ions in the CSF [HCO3-] response. In brain tissue, water content, [Cl-], and the [Cl-] space were unchanged, but by 3 h [Na+] and [HCO3-] were increased. Ventilation was stimulated but the response expressed as ml.min-1.Torr-1.body wt-1 was less in puppy than in adult.
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PMID:CSF acid-base regulation and ventilation during acute hypercapnia in the newborn dog. 678 36

Compared to littermate controls, unstressed Jimpy mice have higher brain water, sodium, potassium and chloride contents and lower carbonic anhydrase activity. When stressed by CO2 to produce a respiratory acidosis or by injection of distilled water to produce brain edema, the Jimpy mouse brain has water and ionic responses essentially like those in controls.
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PMID:Brain water and electrolytes in response to respiratory acidosis and brain edema in the mutant mouse, jimpy. 680 28

The mechanism by which proximal volume reabsorption is reduced during hyperchloremic metabolic acidosis was studied using free-flow micropuncture techniques in Munich-Wistar rats. Compared with control hydropenic conditions, absolute rates of proximal total CO2 and water reabsorption rates during NH4Cl-induced metabolic acidosis were diminished: from 557 +/- 35 to 204 +/- 19 pmol/min and from 13.0 +/- 1.0 to 9.7 +/- 0.6 nl/min, respectively. Inhibition of proximal volume reabsorption during metabolic acidosis was not attributable to alterations in the reabsorptive Starling forces, since peritubular capillary oncotic and hydraulic pressures were normal, or to acidemia itself, since acute respiratory acidosis was not found to decrease reabsorption. When partial repair of the acidosis was achieved by NaHCO3 infusion, absolute reabsorption of both total CO2 (390 +/- 48 pmol/min) and water (12.2 +/- 1.1 nl/min) significantly increased despite modest extracellular volume expansion. NaCl infusion in acidotic animals had no restorative effect on volume reabsorption. Mean values for single nephron glomerular filtration rate were similar under all conditions. Absolute chloride reabsorption tended to correlate better with absolute bicarbonate reabsorption and, hence, with the magnitude of the chloride concentration gradient developed than with the filtered chloride load. In conclusion, absolute proximal volume reabsorption during metabolic acidosis and its partial repair correlated with the absolute magnitude of bicarbonate filtered and reabsorbed. It is proposed that proximal volume reabsorption may be regulated, at least in part, by the anion composition of the glomerular ultrafiltrate.
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PMID:Proximal reabsorption during metabolic acidosis in the rat. 680 35

Western Painted Turtles, Chrysemys picta bellii (N = 5), were maintained submerged and apneic for 90 days: days 0-21 in severely hypoxic water (PO2 = 0-5 mmHg), days 22-43 in aerated water (PO2 approximately 160 mmHg), and days 44-90 again in hypoxic water. From day 90 onward, the water was aerated and the turtles were allowed access to the air; water and air temperatures were maintained at 3 degrees C. Arterial blood samples were taken periodically and analysed for PO2, PCO2, pH, [Na+], [K+] [Cl-], [lactate-], [glucose] and haematocrit. Plasma [HCO3-] was calculated for all samples and total plasma calcium was measured on samples from two animals. Each exposure to low PO2 water caused progressive lactic acidosis and a transient respiratory acidosis with an accompanying fall in plasma [Cl-] and rise in plasma [K+] and [calcium]. During the intervening period in aerated water, blood pH recovered significantly (from 7.33 to 7.74 in 7 days), due primarily to a fall in PCO2 (from 23.5 to 10.6 mmHg), while [lactate-] remained unchanged (at about 50 mM), and [HCO-3] rose slightly. Plasma [K+] promptly returned to nearly normal values. When permitted to breathe on day 90, the three surviving turtles rapidly restored pH to normal by pronounced hyperventilation (PCO2 less than 5 mmHg). Metabolic acidosis, however, disappeared slowly with a t1/2 for [lactate-] and [HCO-3] restoration of about 2 weeks. We conclude that a wintering turtle can stabilize or even slightly improve its acid-base and ionic status by moving from an anoxic environment to well-oxygenated water. Further improvements can be gained by breathing air, but recovery proceeds at a very slow rate if the animal remains at 3 degrees C.
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PMID:Long-term submergence at 3 degrees C of the turtle Chrysemys picta bellii in normoxic and severely hypoxic water. III. Effects of changes in ambient PO2 and subsequent air breathing. 680 28

The partial pressure of CO2 (PCO2) in certain areas of the aquatic habitat of the salamanders Siren lacertina and Amphiuma means frequently rises to values of up to 60 mm Hg. This ambient hypercapnia occurs due to hindrance of gas exchange between water and air caused by dense water-surface vegetation. In order to investigate the acid-base regulation in response to the respiratory acidosis, which wound be expected to result from the high CO2 conductance of the amphibian skin, specimens of both species were subjected to water PCO2 of 47 mm Hg while having free access to normocapnic air in a closed water recirculation system. Arterial PCO2 rose considerably from 12 to 35 mm Hg in Siren and from 17 to 36 mm Hg in Amphiuma. The resultant fall in plasma pH remained uncompensated, whereas intracellular pH of white muscle and heart muscle of Siren were little affected owing to elevated intracellular bicarbonate concentrations. The bicarbonate accumulated in the intracellular compartments was in part produced by intracellular and extracellular nonbicarbonate buffering, and in part gained from the environment in exchange for Cl- ions. Elevated water bicarbonate concentration or bicarbonate infusion into Siren had no effect on the acid-base regulation. These data suggest that the availability of bicarbonate is not a limiting factor for extracellular compensation of increased PCO2, but that the threshold of the bicarbonate-regulating structures is simply not readjusted in hypercapnia. This type of regulation may have evolved as a result of the specific environmental conditions of these animals and may be considered as an energetically efficient way of maintaining a constant milieu for the pH-sensitive intracellular structures.
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PMID:Acid-base regulation in response to environmental hypercapnia in two aquatic salamanders, Siren lacertina and Amphiuma means. 681 49


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