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PubMed1994

[The mechanism and clinical significance of decreased anion gap in patients with COPD and acid-base imbalance].

The blood-gas and electrolytes of 427 blood samples from patients with COPD and acid-base imbalance were analysed. The results showed that 14 types of acid-base imbalance were present in patients with COPD and the anion gap decreased in 8 types of acid-base imbalance, especially in respiratory acidosis, metabolic alkalosis and coexistence of both. The anion gap in respiratory acidosis and metabolic alkalosis were 0.8 +/- 6.6mmol/L and 2.1 +/- 7.3mmol/L, respectively. The anion gap in respiratory acidosis with metabolic alkalosis was negative. In all patients the HCO3- increased, and the total anion and total cation diminished. The anion gap decreased owing to the diminution of unmeasured anion. Clinically, the criterion for judging metabolic acidosis with increased anion gap is a value of anion gap over 16 mmol/L. But in case respiratory acidosis (or metabolic alkalosis) and metabolic acidosis coexist in a patient, the anion gap for judging metabolic acidosis should be decreased appropriately.

Acid-Base Equilibrium↗
PubMed1990

Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs.

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.

Acidosis↗
PubMed1986

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats.

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1993

Interrenal function in larval Ambystoma tigrinum. III. Acid-base balance responses.

Larval Ambystoma tigrinum (59-199 g) were treated with the drug aminoglutethimide (6 mg/day) in order to abolish steroid hormone synthesis. Steroid deprivation prevented the increase in plasma aldosterone concentration observed in sham-infused larvae during respiratory acidosis. It also blocked the normal compensatory response to respiratory acidosis of elevated plasma [HCO3-] and inhibited cutaneous Na+ transport. Aldosterone (10 micrograms/day) and, to a lesser extent, corticosterone (240 micrograms/day) restored the compensatory response. Aldosterone replacement also stimulated cutaneous Na+ transport in AG-inhibited larvae. The results suggest that aldosterone, at about 1000 pg/ml, supports the compensatory ionic responses to respiratory acidosis in this species.

Acid-Base Equilibrium↗
PubMedDate not supplied

Control of energy production in cardiac muscle: effects of ischemia in acidosis.

Evidence is summarized indicating that mitochondrial respiration and citric acid cycle activity in the intact heart are controlled by the cytosolic phosphate potential and mitochondrial NAD oxidation-reduction state. Data are presented showing that the effect of respiratory acidosis is greater than that of metabolic acidosis in inhibiting left ventricular pressure development in the perfused rat heart, because of a greater fall of intracellular pH under the former conditions. Respiratory acidosis is shown to be readily associated with tissue hypoxia as a result of an increased vascular resistance and diminished flow rate through the coronary circulation. In nonischemic respiratory acidosis, the rate of ATP production is well balanced by the rate of ATP utilization, and tissue ATP and creatine-P levels remain approximately normal. Partially ischemic respiratory acidosis was associated with low tissue levels of ATP and creatine-P and high tissue levels of lactate and NADH. Ischemic areas with sharp border zones were visualized during and after an abrupt decrease of perfusion fluid pH by directly photographing NADH fluorescence from the surface of perfused hearts. Reversal of the hypodynamic state with partially ischemic respiratory acidosis could not be achieved by augmenting the coronary flow by means of an external pump. The demonstration of the existence of sharp zones of high pyridine nucleotide fluorescence adjacent to normal zones indicates a great heterogeneity of coronary perfusion and the existence of steep oxygen gradients in the intact heart.

Acidosis↗
PubMed2001

Bone loss in patients with untreated chronic obstructive pulmonary disease is mediated by an increase in bone resorption associated with hypercapnia.

This study sought to determine whether the bone loss in untreated chronic obstructive pulmonary disease (COPD) is associated with hypercapnia and/or respiratory acidosis. Bone mineral density (BMD) measured at the distal forearm of the nondominant arm (with peripheral quantitative computed tomography [pQCT]) and serum markers of bone turnover were determined in 71 male patients with untreated COPD and 40 healthy male subjects who matched the patients in age, weight, and body mass index (BMI). The COPD patients, compared with controls, had reduced pulmonary functions, lower arterial pH, and elevated arterial partial pressure of CO2 (PCO2) The BMD (in T score) was significantly lower in COPD patients than that in control subjects (-1.628 +/- 0.168 vs. -0.058 +/- 0.157; p < 0.001). The BMD of COPD patients correlated positively with arterial pH (r = 0.582; p < 0.001), negatively with PCO2 (r = -0.442; p < 0.001), and negatively with serum cross-linked telopeptide of type I collagen (ICTP), a bone resorption marker (r = -0.444; p < 0.001) but not with serum osteocalcin, a bone formation marker. Serum ICTP, but not osteocalcin, correlated with PCO2 (r = 0.593; p < 0.001) and arterial pH (r = -0.415; p < 0.001). To assess the role of hypercapnia, COPD patients were divided into the hypercapnic (PCO2 > 45 mm Hg; n = 35) and eucapnic (PCO2 = 35-45 mm Hg) group (n = 36). Patients with hypercapnia had lower BMD, lower arterial pH, and higher serum ICTP than did patients with eucapnia. Arterial pH and serum ICTP of eucapnic patients were not different from those of controls. To evaluate the role of uncompensated respiratory acidosis, COPD patients with hypercapnia were subdivided into those with compensatory respiratory acidosis (pH > or = 7.35; n = 20) and those with uncompensated respiratory acidosis (pH < 7.35; n = 15). The BMD and serum ICTP were not different among the two subgroups. In conclusion, this study presents the first associative evidence that the bone loss in COPD is at least in part attributed to an increased bone resorption that is associated primarily with hypercapnia rather than uncompensated respiratory acidosis.

Acidosis, Respiratory↗
PubMed1985

Influence of chronic respiratory acid-base disorders on acute CO2 titration curve.

We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). Chronic respiratory alkalosis and acidosis, as well as the acute CO2 titrations, were produced in unanesthetized dogs within a large environmental chamber. For comparison with our data on chronic metabolic acidosis and alkalosis, plasma bicarbonate levels, which are secondarily altered in chronic respiratory acid-base disorders, were used as an index of chronic acid-base status of the animals. Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1997

[Mechanical ventilation therapy with permissive hypercapnia on ARDS].

OBJECTIVE: Study of mechanical ventilation (MV) therapy of ARDS (acute respiratory distress syndrome). METHODS: Ten cases of ARDS were observed. Depending on patients' kidney compensation for respiratory acidosis, low tidal volume (VT, mean = 6.5 ml/kg) was used and certain respiratory acidosis was permitted in order to decrease airway plateau pressure and lung barotrauma. On the premise of keeping patients' PaO2 about 7.3 kPa (1 kPa = 7.5 mmHg), lowest possible FiO2 (mean = 0.51) and PEEP (mean = 0.92 kPa, 1 kPa = 10.2 cmH2O) were used. RESULTS: Seven of the ten survived. Three of them had respiratory acidosis and two had lung barotrauma during MV. CONCLUSION: Using lower VT and permitting certain respiratory acidosis are worthy to be considered in MV therapy of ARDS.

Adult↗
PubMed1996

Toxic doses of rac-, (-)-(S)- and (+)-(R)-propranolol in rats and rabbits.

The contribution of the individual enantiomers ([+]-[R]- and [-]-[S]-propranolol) to rac-propranolol intoxication was studied in anaesthetized, spontaneously breathing (SB) rats and artificially ventilated (AV) rats and rabbits. In the SB rat, propranolol (30 mg.kg-1.h-1 i.v.) decreased heart rate and mean arterial blood pressure and caused hypoventilation, serious hypoxaemia, respiratory acidosis, and death by respiratory arrest. Survival time (ST) in the (+)-(R)-propranolol group (ST 91 +/- 5 min) was significantly longer than in the rac-propranolol group (ST. 68 +/- 6 min). In AV rats and rabbits toxic doses of rac-, (-)-(S)- and (+)-(R)-propranolol, 30 mg.kg-1.h-1 and 15 mg.kg-1.h-1 i.v., respectively, induced comparable effects on haemodynamic variables as in the SB rat. Artificial ventilation lengthened ST by a factor of three to four in rats. In the AV rat, ST's were not significantly different between the rac-, (-)-(S)- and (+)-(R)-propranolol groups. In the rabbit, as in the SB rat, ST in the (+)-(R)-propranolol group was significantly longer than ST's in the rac- and (-)-(S)-propranolol groups. The acute respiratory acidosis in SB rats and the prolonged ST in AV rats suggest that respiratory failure is the primary and cardiovascular failure the secondary cause of death in propranolol intoxication. The potentiation of the toxic effect of the enantiomers observed after dosing the racemate instead of the pure enantiomers could not be explained by a stereoselective difference in plasma propranolol concentration.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of acute acid-base disturbances on renal tubule reabsorption of magnesium in the rat.

The effects of acute metabolic and respiratory acidosis and acute metabolic alkalosis on magnesium excretion and on fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron and the end-descending limb of the juxtamedullary nephron were examined by micropuncture in anesthetized thyroparathyroid-intact rats. Compared with normal control rats, acute metabolic acidosis (HCl infusion) did not produce any significant change. Acute respiratory acidosis (15% CO2 in inspired air) significantly increased the absolute but not the fractional excretion of magnesium and did not alter fractional delivery of magnesium to the end-accessible superficial proximal tubule or juxtamedullary end-descending limb. Acute metabolic alkalosis (NaHCO3 infusion) significantly reduced absolute and fractional magnesium excretion and fractional magnesium delivery to the end-descending limb of the juxtamedullary nephron but did not affect fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron. Tubule fluid-to-ultrafilterable magnesium ratio was a function of tubule fluid-to-plasma inulin ratio in the end-descending limb when all groups were combined. These results suggest that although acute metabolic or respiratory acidosis has no significant effect, acute metabolic alkalosis enhances magnesium reabsorption in the juxtamedullary proximal nephron--possibly in the pars recta.

Absorption↗
PubMed1986

Furosemide pharmacodynamics: effect of respiratory and acid-base disturbances.

The aims of this study were to investigate the effect of changes in arterial blood gases and pH on furosemide pharmacodynamics and kinetics. Five groups of conscious rabbits were used: a control group breathing air with normoxia and normocarbia; a second group with hypercapnia and respiratory acidosis; a third with hypoxemia; a fourth with hypercapnia and respiratory acidosis combined with hypoxemia (HCHO); and the fifth group with metabolic acidosis. All experimental conditions, except hypoxemia, increased sodium tubular reabsorption and therefore, decreased urinary excretion of sodium. Renal blood flow was decreased by HCHO and metabolic acidosis. In response to 5 mg/kv i.v. of furosemide, natriuresis and diuresis were decreased by an average of 44% in animals with HCHO (P less than .05). The kinetics of furosemide were not affected by any of the experimental conditions except HCHO, in which the renal clearance of furosemide was reduced from 7.5 +/- 1.4 ml/min/kg (controls) to 2.7 +/- 0.7 ml/min/kg (P less than .05). The reduction in renal clearance of furosemide was associated with a decrease in urinary excretion of sodium (P less than .05). The reduction in renal clearance of furosemide was probably secondary to the decrease in renal blood flow and an increase in furosemide tubular reabsorption. Finally, HCHO did not decrease plasma volume, suggesting that the reduction in renal blood flow was secondary to blood flow distribution. In conclusion, only hypercapnia and respiratory acidosis combined with hypoxemia decreases the natriuretic and diuretic effect of furosemide.

Acidosis, Respiratory↗
PubMed1987

Effects of acid-base imbalance on pulmonary angiotensin-converting enzyme in vivo.

The effects of acid-base balance disturbances on pulmonary endothelial angiotensin-converting enzyme (ACE) were studied in anesthetized mechanically ventilated rabbits. Enzyme function was estimated from [3H]benzoyl-Phe-Ala-Pro ([3H]BPAP) utilization under first-order reaction conditions during a single transpulmonary passage and expressed as 1) substrate metabolism (M), 2) Amax/Km (Amax being equal to the product of enzyme mass and the constant of product formation), and 3) (Amax/Km)/100 ml blood flow. When respiratory acidosis/alkalosis was produced by altering respiratory rate at constant airway pressure, substrate (BPAP) utilization varied proportionally to arterial pH and inversely proportionally to arterial PCO2 (PaCO2) (P less than 0.05). Percent BPAP metabolism (%M) ranged from 92 +/- 3 (respiratory alkalosis) to 85 +/- 3 (normal), 82 +/- 3 (respiratory acidosis), and 78 +/- 2% (severe respiratory acidosis). Amax/Km similarly decreased from 899 +/- 129 to 825 +/- 143, 601 +/- 74, and 450 +/- 34 ml/min, respectively, and (Amax/Km)/100 ml blood flow was reduced from 176 +/- 26 to 131 +/- 22, 111 +/- 12, and 97 +/- 5, respectively. However, when respiratory acidosis/alkalosis was produced by altering both respiratory rate and airway pressure, no changes were observed in either %M, Amax/Km or (Amax/Km)/100 ml blood flow. Similarly metabolic alkalosis or acidosis did not alter M, Amax/Km or (Amax/Km)/100 ml blood flow. These results indicate that pulmonary endothelial ACE function can be affected by acid-base disturbances, probably indirectly through changes in perfused microvascular surface area.

Acid-Base Imbalance↗
PubMed1995

Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis.

The acid-base balance of 199 patients with cystic fibrosis, seen from 1987 through 1992 at the Bern Outpatient Clinic, were evaluated. Simple metabolic alkalosis was demonstrated in 16 and mixed metabolic alkalosis and respiratory acidosis in 9 patients. When compared with 10 patients with simple respiratory acidosis and 16 with normal hydrogen ion balance, those with simple metabolic alkalosis were significantly younger. The need for pancreatic enzymes was significantly higher and the relative underweight significantly more severe in patients with either simple or mixed metabolic alkalosis and respiratory acidosis. The results indicate the rather common occurrence of chronic metabolic alkalosis in cystic fibrosis. It is observed in young patients, in patients who need high doses of pancreatic enzymes and in the those with poor nutritional status.

Acidosis, Respiratory↗
PubMed1976

Intracellular and extracellular acid-base changes in hemorrhagic shock.

Each of 21 dogs was bled until mean arterial blood pressure fell to 50 torr; this hemorrhagic shock state was then maintained for two hours. During hemorrhagic shock, the blood lactate concentration increased sixfold. The severe metabolic acidosis in arterial blood was partially compensated by a decreased PCO2 caused by increased ventilation. However, in mixed venous blood, the metabolic acidosis was combined with a respiratory acidosis. This hypercapnia in venous blood was indicative of the increased PCO2 in tissues poorly perfused following hemorrhage. The increase in the PCO2 of the femoral venous blood was greater than that in mixed venous blood, suggesting that some tissue beds were better perfused than those of the hind limb during shock. The intracellular lactate concentration of hind limb skeletal muscle was greatly increased in the shock state, and tissue PCO2 rose. Intracellular pH of skeletal muscle was only slightly decreased and bicarbonate concentration was unchanged during this combined metabolic and respiratory acidosis. This capacity of skeletal muscle to maintain a high HCO-3 concentration in intracellular fluid during metabolic acidosis may be an enhanced response of the mechanism responsible for maintaining (HCO-3)i normally at a level approximately ten times that which would be expected if HCO-3 were distributed passively.

Acid-Base Equilibrium↗
PubMed1993

Preoperative pulmonary function evaluation for laparoscopic cholecystectomy.

OBJECTIVE: Hypercarbia with respiratory acidosis is a recognized complication of laparoscopic cholecystectomy. This study was performed to identify preoperatively those patients who may develop hypercarbia and acidosis during the procedure. DESIGN: Retrospective analysis of preoperative variables. PATIENTS: Thirty-one consecutive patients underwent laparoscopic cholecystectomy at one institution who were receiving both preoperative pulmonary function tests and arterial blood gas analysis. RESULTS: More than 80 demographic, laboratory, and perioperative variables were entered into a univariate analysis to identify predictors of intraoperative acidosis (pH, < 7.35). Patient age, duration of the procedure, and preoperative blood gas values were not predictors of intraoperative acidosis. Several univariant predictors for patients experiencing carbon dioxide pneumoperitoneum-induced hypercarbia were identified; these included an elevated American Society of Anesthesiologists classification and significant decreases in forced expiratory flow at 25% of maximum, maximal forced expiratory flow, maximal voluntary ventilation, vital capacity, inspiratory capacity, and diffusing capacity of the lung for carbon monoxide. CONCLUSIONS: This study suggests that neither age nor preoperative arterial blood gas values are predictive of intraoperative hypercarbia and acidosis during periods of carbon dioxide pneumoperitoneum. However, preoperative pulmonary function measures of decreased flow, limited capacity, and compromised diffusion do correspond to the development of intraoperative acidosis. Preoperative evaluation with pulmonary function tests demonstrating forced expiratory volumes less than 70% of predicted values and diffusion defects less than 80% of predicted values can identify those patients who are at risk of developing hypercarbia and acidosis.

Acidosis, Respiratory↗
PubMed2002

Rapid correction of early metabolic acidaemia in comparison with placebo, no intervention or slow correction in LBW infants.

BACKGROUND: Metabolic or mixed (metabolic and respiratory) acidosis are commonly encountered problems in the low birth weight (LBW) infant after delivery, and they may contribute to mortality and morbidity. Causes for the lactic acidosis are multiple and include maternal, placental and fetal factors. It is unclear whether metabolic acidaemia in the first 24 hours of life in LBW infants should be corrected by rapid infusion of alkali. OBJECTIVES: The main objective was to assess the short and long-term effects of the rapid correction of early (first 24 hours) metabolic acidaemia in LBW (<2500g birth weight) neonates. SEARCH STRATEGY: Searches were undertaken of MEDLINE from October 2001 back to 1966 and the Cochrane Controlled Trials Register (Cochrane Library, Issue 4, 2001). The title and abstract of each retrieved study were examined to assess eligibility. If there was uncertainty, the full paper was examined. SELECTION CRITERIA: Types of studies All randomised controlled trials where short or long term effects of treatment with alkalising agents by rapid infusion were compared with placebo or no treatment, or where rapid infusion of alkalising agents was compared with slow infusion. Types of participants Newborn infants with birth weight <2500g and less than 24 hours of age with proven metabolic acidaemia (on arterial blood gas). Types of interventions Rapid correction of acidaemia with alkalising agents (sodium bicarbonate and/or THAM) given as a bolus over 5 minutes or less compared with either placebo, no intervention or slow infusion (>5 minutes). Types of outcome measures 1) maximal oxygen requirement in first 24 hours 2) duration of oxygen therapy 3) need for and duration of assisted ventilation 4) intraventricular haemorrhage and/or periventricular leucomalacia 5) survival to discharge 6) long term survival (to 24 months of age) 7) neurological and developmental outcome at 24 months of age DATA COLLECTION AND ANALYSIS: Each reviewer assessed eligibility, trial quality and extracted data separately, then compared and resolved differences. Study authors were contacted for additional information if necessary. MAIN RESULTS: No studies were found meeting the criteria for inclusion in this review. REVIEWER'S CONCLUSIONS: There is no evidence available from randomised controlled trials to support or refute the rapid correction of metabolic acidaemia, in LBW infants in the first 24 hours of life, as compared with slow or no correction.

Acidosis↗
PubMed1975

Ventilatory acclimatization and csf acid-base balance in carotid chemodenervated dogs at 3550 m.

In three awake dogs in a hypobaric chamber at 140 m and at 3550 m, resting ventilation, pulmonary gas exchanges, respiratory gases and pH of the arterial blood, acid-base status in the cerebrospinal fluid (csf), and ventilatory responses to transient O2-inhalation were studied before (intact) and after chronic bilateral carotid body denervation (cbd). 1. The hypoxic chemoreflex drive of ventilation was reduced by about half in cbd dogs. 2. At low altitude, sino-carotid body denervation resulted in hypoventilation and respiratory acidosis in the arterial blood and csf. 3. At high altitude, initial hypoxic hyperventilation, and the related alkalosis in blood and csf, occurred within 30 min in intact dogs, but was not observed in cbd ones. 4. Further increase in ventilation was achieved upon 3 hrs of altitude exposure in intact animals, while a delayed hyperventilation occurred after 24 hrs in cbd ones. 5. Neither in intact nor in cbd dogs, the ventilatory changes at altitude were related to the changes in csf pH. It is concluded that the rate of ventilatory acclimatization to altitude is dependent upon the strength of the arterial chemoreceptor drive. Integrity of this chemoreflex drive of breathing is essential in determining the eupneic level of ventilation and normal acid-base status of the blood and csf at low altitude and at high altitude.

Acclimatization↗