SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources

PubMed1991

Acid-base disturbances in cardiogenic pulmonary edema.

Eighty-one consecutive cases of uncomplicated cardiogenic pulmonary edema (CPE) were retrospectively graded for severity of chest roentgenogram (CXR) changes and grouped according to primary acid-base abnormalities, either single or mixed. Mean age was 72, 50 male, 31 female. Twenty-three percent had no acid-base disturbances (ABD). Isolated respiratory alkalosis was most common (41%), followed by metabolic acidosis, 22%; metabolic alkalosis, 10%, and respiratory acidosis, 9%. Age, sex, race distribution, morbidity and mortality were not significantly different between the groups. Overall mortality was 17%. Significantly higher mortality was associated with age over 70, pH less than 7.4, and presence of acute myocardial infarction. CXR scores did not correlate with pH, pCO2 or pO2, mortality or morbidity. Some patients with the most severe ABDs recovered while others, who had no ABD on presentation, eventually died. Thus, in 81 consecutive episodes of uncomplicated CPE, isolated respiratory alkalosis was the commonest ABD, occurring in 41%. No correlation was found between ABD and severity of CPE, morbidity or mortality.

Acid-Base Imbalance↗

PubMed1980

Ventilatory acclimatization to high altitude is prevented by CO2 breathing.

The hypoxia of high altitude stimulates ventilation. If the resultant respiratory alkalosis inhibits the initial increase in ventilation, then with prevention of alkalosis, ventilation should rise immediately to a stable plateau. 4 subjects inspired CO2 (3.77%) from ambient air in a hypobaric chamber (PB = 440-455 Torr) during 100 h at high altitude. Ventilation (for given oxygen uptakes at rest and during exercise) increased promptly and remained stable. 4 control subjects exposed to high altitude without CO2 supplementation showed the expected progressive increases in ventilation with time. The hyperoxic CO2 ventilatory response curve shifted progressively to the left with time in the control subjects, but not in those given supplemental CO2. The latter group also failed to increase the ventilatory response to isocapnic hypoxia. Thus, CO2 supplementation at high altitude prevented the so-called "ventilatory acclimatization' from occurring. Prevention of respiratory alkalosis at high altitude probably permitted maintenance of [H+] at some central nervous system locus, thus allowing an uninhibited hypoxic stimulation of ventilation.

Acclimatization↗

PubMed1972

The effect of glutamine administration on urinary ammonium excretion in normal subjects and patients with renal disease.

The effect of acute changes in the delivery rate of glutamine to the kidney on urinary ammonium excretion was studied in man. Healthy subjects and patients with intrinsic renal disease were studied under three different acid-base conditions: unaltered acid-base balance; NH(4)Cl-induced acidosis; and NaHCO(3)-induced alkalosis. Anhydrous L-glutamine was administered orally in a single dose of 260 mmoles during each of these three acid-base states. We found that endogenous venous plasma glutamine concentration fell during acidosis and rose during alkalosis in both healthy subjects and patients with renal disease. In healthy subjects, orally administered glutamine raised plasma glutamine concentration markedly over a 2-3 hr period. This was accompanied by an increase in urinary ammonium excretion and a rise in urine pH under normal acid-base conditions and during metabolic acidosis. No increase in ammonium excretion occurred when glutamine was administered during metabolic alkalosis in spite of an equivalent rise in plasma glutamine concentration. In patients with renal disease, endogenous venous plasma glutamine concentration was lower than in healthy subjects, perhaps as a result of mild metabolic acidosis. Acute oral glutamine loading failed to increase urinary ammonium excretion significantly during either unaltered acid-base conditions or after NH(4)Cl-induced acidosis, even though plasma glutamine rose as high as in healthy subjects. We conclude from these observations that glutamine delivery to the kidney is a rate-limiting factor for ammonium excretion in healthy subjects, both before and after cellular enzyme adaptation induced by metabolic acidosis. In contrast, in patients with renal disease, glutamine delivery is not rate-limiting for ammonium excretion. Presumably other factors, such as surviving renal mass and the activity of intracellular enzymes necessary for ammonia synthesis limit ammonium excretion in these patients.

Acidosis↗

PubMed1983

Influence of steady-state alterations in acid-base equilibrium on the fate of administered bicarbonate in the dog.

Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-3] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-3] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCl-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min. The results obtained from animals with metabolic acid-base disturbances demonstrated an inverse relationship between bicarbonate space and initial plasma pH, confirming the previous findings of others. By contrast, the results obtained in animals with respiratory acid-base disturbances demonstrated a direct relationship between bicarbonate space and initial plasma pH. The pooled data revealed that bicarbonate space is, in fact, quite independent of the initial pH but is highly correlated with the initial level of extracellular [HCO-3]; dogs with low extracellular [HCO-3] (congruent to 10 meq/liter) whether acidemic or alkalemic, have a bicarbonate space that is 25% larger than normal and some 50% larger than in dogs with high extracellular [HCO-3] (congruent to 50 meq/liter). We conclude from these results that the increased bicarbonate space in metabolic acidosis (and respiratory alkalosis) does not reflect the availability of more hydrogen ions for release during bicarbonate administration, but merely evidences the wider range of titration (delta pH) of nonbicarbonate buffers that occurs during alkali loading whenever plasma [HCO-3] is low.

Acid-Base Equilibrium↗

PubMed1986

Intracellular and extracellular acid-base status and H+ exchange with the environment after exhaustive exercise in the rainbow trout.

Exhaustive exercise induced a severe short-lived (0-1 h) respiratory, and longer-lived (0-4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood 'lactate' load exceeded blood 'metabolic acid' load from 1-12 h after exercise. Over-compensation occurred, so that by 8-12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8-12 h, H+ excretion was reduced to resting levels and at 12-24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.

Acid-Base Equilibrium↗

PubMed2002

Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD.

STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and cerebral blood volume (CBV), to short-term changes in arterial PCO(2) was measured. PATIENTS AND METHODS: Seventeen patients with chronic hypercapnia and COPD (PaCO(2) > 6.0 kPa) and 16 normocapnic patients with COPD (PaCO(2) < or = 6.0 kPa) [FEV(1) 27% predicted] were studied under baseline metabolic conditions and after 1 week of treatment with oral furosemide, 40 mg/d, or acetazolamide, 500 mg/d. Hypercapnia (change in end-tidal carbon dioxide > 1 kPa) was induced by administering adequate amounts of carbon dioxide in the inspired air. CBV was measured using near-infrared spectroscopy. RESULTS: Compared with baseline metabolic condition, chronic metabolic acidosis and alkalosis did not change ventilatory (Delta VI/Delta PaCO(2)) and cerebrovascular (Delta CBV/Delta PaCO(2)) reactivity. Base excess (BE) decreased by 6.8 +/- 1.1 mEq/L and 6.9 +/- 1.6 mEq/L, respectively, in the normocapnic and chronic hypercapnic COPD groups during metabolic acidosis, resulting in a not-quite-significant leftward shift of both the ventilatory and cerebrovascular carbon dioxide response curve. BE increased by 2.3 +/- 1.2 mEq/L and 1.2 +/- 1.3 mEq/L, respectively, during chronic metabolic alkalosis in both COPD groups, without concomitant shift. Poor correlations between ventilatory and cerebrovascular carbon dioxide responsiveness (Delta CBV/Delta PaCO(2) and Delta VI/Delta PaCO(2), Delta CBV/Delta PaCO(2) and Delta P(0.1)/Delta PaCO(2), respectively) were found irrespective of baseline, respiratory condition, and induced metabolic state. CONCLUSIONS: Normocapnic and chronic hypercapnic COPD patients have the same ventilatory and cerebrovascular carbon dioxide responsiveness irrespective of induced metabolic state.

Acetazolamide↗

PubMed1987

Management of acid-base balance with red blood cell carbonic anhydrase (RCA). II. Control of acid-base balance with acetazolamide.

Acetazolamide, a carbonic anhydrase (CA) inhibitor, was used to normalize metabolic alkalemia. A dosage of acetazolamide for normalizing metabolic alkalemia has not yet been experimentally determined. The dosage of acetazolamide for this purpose is experimentally calculated in this paper. The correlation between various concentration of acetazolamide mixed with blood and the base excess (BE) levels in blood at the start of normalizing metabolic alkalosis was studied in vitro. The change rate of the BE level was calculated from BE levels noted before and after tonometry of the blood with and without acetazolamide. A dosage of acetazolamide which can cause the change rate of the BE level to decrease is considered to be an effective dosage. Metabolic alkalosis in vitro was produced by adding bicarbonate into the blood. An effective dosage of acetazolamide for metabolic alkalemia of which the BE range was from 0 to + 30 mEq/liter was calculated. CA activities in the kidney and the blood of dogs administered acetazolamide were examined. The effective dosage of acetazolamide obtained from in vitro experiments inhibited the CA activities not only in the blood but also in the kidneys. An effective dosage of acetazolamide to normalize a BE of + 10 mEq/liter in vitro was converted into about 7-12 mg/kg in vivo. This dosage inhibited the red blood cell carbonic anhydrase (RCA) activity to 20-40%, whereas the normal physiological variation range is 25%. An effective dosage of acetazolamide in the blood did not proportionally increase with an increase of HCO3- during severe alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗

PubMed2006

Acid-base status determines the renal expression of Ca2+ and Mg2+ transport proteins.

Chronic metabolic acidosis results in renal Ca2+ and Mg2+ wasting, whereas chronic metabolic alkalosis is known to exert the reverse effects. It was hypothesized that these adaptations are mediated at least in part by the renal Ca2+ and Mg2+ transport proteins. The aim of this study, therefore, was to determine the effect of systemic acid-base status on renal expression of the epithelial Ca2+ channel TRPV5, the Ca2+-binding protein calbindin-D28K, and the epithelial Mg2+ channel TRPM6 in relation to Ca2+ and Mg2+ excretion. Chronic metabolic acidosis that was induced by NH4Cl loading or administration of the carbonic anhydrase inhibitor acetazolamide for 6 d enhanced calciuresis accompanied by decreased renal TRPV5 and calbindin-D28K mRNA and protein abundance in wild-type mice. In contrast, metabolic acidosis did not affect Ca2+ excretion in TRPV5 knockout (TRPV5-/-) mice, in which active Ca2+ reabsorption is effectively abolished. This demonstrates that downregulation of renal Ca2+ transport proteins is responsible for the hypercalciuria. Conversely, chronic metabolic alkalosis that was induced by NaHCO3 administration for 6 d increased the expression of Ca2+ transport proteins accompanied by diminished urine Ca2+ excretion in wild-type mice. However, this Ca2+-sparing action persisted in TRPV5-/- mice, suggesting that additional mechanisms apart from upregulation of active Ca2+ transport contribute to the hypocalciuria. Furthermore, chronic metabolic acidosis decreased renal TRPM6 expression, increased Mg2+ excretion, and decreased serum Mg2+ concentration, whereas chronic metabolic alkalosis resulted in the exact opposite effects. In conclusion, these data suggest that regulation of Ca2+ and Mg2+ transport proteins contributes importantly to the effects of acid-base status on renal divalent handling.

Acidosis↗

PubMedDate not supplied

[Acid-base equilibrium in cerebrospinal fluid following intracranial surgery].

In 48 patients the acid-base equilibrium in the CSF and blood was determined on the 2nd day after intracranial operation. In the postopertive period various disturbances of this equilibrium were found which were probably various stages of metabolic acidosis compensation in the CSF which was a reflection of metabolic (lactate) acidosis developing primarily in the damaged brain area. On the basis of determinations it was found that changes in the CSF of the type of metabolic acidosis (21 cases) corresponded most frequently to respiratory alkalosis in the blood (11 cases). Changes of the type of respiratory acidosis in the CSF(13 cases) corresponded usually to metabolic alkalosis in the blood (7 cases). The development of metabolic acidosis in patients in severe and moderately severe condition (19 cases) was associated with poor prognosis as to survival since the mortality in this group was 10 (about 53%). The favourable effect of dehydrating treatment may be due also to facilitation of passage of bicarbonates from the blood into the cerebral tissue and CSF since their level is increased in the blood during metabolic alkalosis (during a decrease in the extracellular space) resulting from dehydration.

Acid-Base Imbalance↗

PubMed1975

[The effect of potassium chloride and organic potassium salts on the acid-base equilibrium in normo and hypokalemic rats].

The effects of intravenous infusions of potassium chloride, potassium acetate, potassium aspartate and potassium malate on plasma electrolytes and acid-base balance were investigated in normokalemic or hypokalemic alkalotic rats. Animals who obtained equal volumes of isotonic sodium chloride solution served as controls. All of these potassium solutions increased the plasma potassium concentrations to the same extent. Potassium chloride shifted the acid-base balance to acidotic values in normal rats or corrected metabolic alkalosis in hypokalemic rats. The potassium salts of organic acids, however, caused an increase in alkalosis, acetate acting stronger than aspartate and malate. In potassium deficiency combined with metabolic alkalosis the administration of potassium chloride is preferable to the organic potassium salts since it corrects both the electrolyte disturbances at the same time.

Acetates↗

PubMed2002

[Licorice--not just candy].

BACKGROUND: Liquorice is widely used as a flavour and also as a medical drug. Possible side effects include hypertension, hypokalaemia and metabolic alkalosis. MATERIALS AND METHODS: We present a case history and a review on liquorice intoxication based on relevant literature found from searches on Medline. RESULTS AND INTERPRETATION: A 19-year-old girl was admitted to hospital with severe hypertension, hypokalaemia and metabolic alkalosis. Urine analysis showed inhibition of 11-beta-hydroxysteroid dehydrogenase. It turned out that she ingested a lot of liquorice; after she stopped eating it she became normotensive without any medication. Three months later there were no signs of inhibition of the enzyme. The active component of liquorice is glycyrrhetinic acid, which inhibits the enzyme 11-beta-hydroxysteroid dehydrogenase. This enzyme promotes the conversion of cortisol to cortisone and is thereby responsible for the specificity of the mineralocorticoid receptor to aldosterone in the collecting tubules. Inhibition of the enzyme allows cortisol to act as the major endogenous mineralocorticoid producing a marked elevation in mineralocorticoid activity, resulting in hypertension, hypokalaemia and metabolic alkalosis.

Adult↗

PubMed2003

Role of acid-base physiology on the pathogenesis of parturient hypocalcaemia (milk fever)--the DCAD theory in principal and practice.

The hypocalcemia associated with the clinical disease known as milk fever is due to a failure of the calcium homeostatic mechanisms in the cow to restore normal blood calcium concentration in a timely manner at the onset of lactation. The defect in calcium homeostasis appears to reside in the sensitivity of bone and kidney tissues to parathyroid hormone (PTH) stimulation. Evidence suggests the acid-base status of the cow dictates the sensitivity of the tissues to PTH stimulation, and that metabolic alkalosis is responsible for blunting tissue PTH responsiveness. Hypomagnesemia can also reduce tissue PTH responsiveness but hypomagnesemia can be corrected in most rations. Excessive dietary potassium is very common and is the most important factor causing metabolic alkalosis in dairy cows. Formulation of rations to reduce metabolic alkalosis and/or induce a compensated metabolic acidosis in the pre-partal cow has proved a useful strategy for prevention of milk fever. The concept of dietary cation-anion difference manipulation and the physiologic effects this can have in the cow are presented, with special emphasis on the Strong Ion Difference theory of acid-base physiology.

Acid-Base Imbalance↗

PubMed1993

In vivo experimental models on the evaluation of haemoperfusion.

We described some experimental models that were performed in rabbits and in swine in order to evaluate the efficacy of haemoperfusion treatment in hypochloremic alkalosis, uraemia and cytotoxic drug poisoning. In all the models, an extracorporeal circuit was used constituted mainly by a hematic sampling line and a cartridge, containing an anion exchange resin. Access to the blood stream was achieved by isolation and catheterization of the vessels either of the neck or of the leg, or both. The experimental model for the evaluation of haemoperfusion in hypochloremic alkalosis was carried out in rabbits by a pyloric stenosis because its size and weight are similar to new-born humans and its stomach is a simple monogastric one. The hypochloremia and alkalosis were achieved in only 4 hours. The other two experimental models were carried out in pigs because, in these cases, it was better to choose a large size animal with a nutritional similarity to humans, and with the capability to produce a stable chronic renal failure. The pigs were submitted to a bilateral ureter ligature to create a chronic renal failure or to a bilateral renal vessel ligature to avoid the physiologic precipitation of some drugs in renal tubules.

Alkalosis↗

PubMed2006

Proteomic identification of alterations in metabolic enzymes and signaling proteins in hypokalemic nephropathy.

Hypokalemic nephropathy caused by prolonged K(+) deficiency is associated with metabolic alkalosis, polydipsia, polyuria, growth retardation, hypertension, and progressive tubulointerstitial injury. Its pathophysiology, however, remains unclear. We performed gel-based, differential proteomics analysis of kidneys from BALB/c mice fed with high-normal-K(+) (HNK), low-normal-K(+) (LNK), or K(+)-depleted diet for 8 wk (n = 6 in each group). Plasma K(+) levels were 4.62 +/- 0.35, 4.46 +/- 0.23, and 1.51 +/- 0.21 mmol/L for HNK, LNK, and KD mice, respectively (p < 0.0001; KD vs. others). With comparable amounts of food intake, the KD mice drank significantly more water than the other two groups and had polyuria. Additionally, the KD mice had growth retardation, metabolic alkalosis, markedly enlarged kidneys, renal tubular dilation, intratubular deposition of amorphous and laminated hyaline materials, and tubular atrophy. A total of 33 renal proteins were differentially expressed between the KD mice and others, whereas only eight proteins were differentially expressed between the HNK and LNK groups, as determined by quantitative intensity analysis and ANOVA with Tukey's post hoc multiple comparisons. Using MALDI-MS and/or quadrupole-TOF MS/MS, 30 altered proteins induced by K(+)-depletion were identified as metabolic enzymes (e.g., carbonic anhydrase II, aldose reductase, glutathione S-transferase GT41A, etc.), signaling proteins (14-3-3 epsilon, 14-3-3 zeta, and cofilin 1), and cytoskeletal proteins (gamma-actin and tropomyosin). Some of these altered proteins, particularly metabolic enzymes and signaling proteins, have been demonstrated to be involved in metabolic alkalosis, polyuria, and renal tubular injury. Our findings may lead to a new road map for research on hypokalemic nephropathy and to better understanding of the pathophysiology of this medical disease when the functional and physiological significances of these altered proteins are defined.

Animals↗

PubMed1978

Disturbances in acid-base balance during hypophosphatemia and phosphate depletion.

Phosphate depletion leads to bone resorption, resulting in the accession of alkali to the blood and urine. There may also be a release of lactic acid from liver, resulting from ATP depletion and intracellular alkalosis. In general, the net result of these tissue effects is an alkali load discharged into the extracellular fluid. In the kidneys, phosphate depletion causes impaired proximal tubular reabsorption of bicarbonate, and perhaps other substrates, owing in all likelihood to both intracellular alkalosis and depletion of ATP. This impaired proximal capacity to reclaim bicarbonate results in hyperchloremic acidosis. The distal nephron may contribute to acidosis by virtue of inability to produce titratable acid (phosphate-free urine) and perhaps impaired ammonia production. Severe phosphate depletion, therefore, tends to produce hyperchloremic acidosis as a result of a diminished capacity for bicarbonate reclamation in the proximal tubule and probably some impairment of bicarbonate regeneration in the distal nephron. These effects, when marked, ultimately outweigh the contribution of alkali coming from bone breakdown. In the liver, phosphate depletion may stimulate lactic acid production by reducing hepatic ATP stores (Pasteur effect) and producing intracellular alkalosis. ATP depletion may also limit hepatic uptake of lactate. Finally, in muscle cells ATP depletion, resulting from either profound hypophosphatemia or the metabolism of massive fructose loads, may eventuate in frank rhabdomyolysis.

Acid-Base Imbalance↗

PubMed2004

Effect of bicarbonate on retinal vasculature and acidosis-induced retinopathy in the neonatal rat.

BACKGROUND: Systemic acidosis induces preretinal neovascularization (NV) analogous to retinopathy of prematurity (ROP) in the neonatal rat. Sodium bicarbonate is used in human neonates to treat acidosis. The effects of alkali administration on the developing retinal vasculature and on acidosis-induced retinopathy (AIR) are unknown. We investigated the effect of sodium bicarbonate gavage on the retinal vasculature of normal and acidotic neonatal rats to determine (1) whether bicarbonate treatment is associated with preretinal NV and (2) whether AIR can be prevented with systemic bicarbonate treatment. METHODS: The extent of acidosis and alkalosis were initially determined from carotid arterial blood samples. In the bicarbonate-alone study, newborn rats were randomized into litters of 25 and received bicarbonate doses of 15 mmol/kg twice daily and 20 mmol/kg once daily from days 2 to 7. Control animals received saline gavage. In the AIR treatment study, acidosis was induced in neonatal rats by intraperitoneal injection of acetazolamide 200 mg/kg from days 2 to 7. Acetazolamide-treated rats received either additional bicarbonate gavage or no additional treatment. Eyes were enucleated on day 13, and the retinal vasculature was assessed for NV using ADPase staining techniques and light microscopy. RESULTS: Systemic alkalosis (peak pH 7.55+/-0.02; mean +/- SD) was confirmed with bicarbonate gavage, and partial reversal of acidosis was confirmed when acetazolamide-treated rats received bicarbonate. Surviving rats receiving bicarbonate 15 mmol/kg twice daily (28% survival) and 20 mmol/kg bicarbonate once daily (45% survival) had an incidence of preretinal NV of 9% and 8%, respectively. No NV was seen in saline-control rats. In the acetazolamide-treated rats, the incidence of preretinal NV in surviving rats was numerically lower in bicarbonate-treated rats than acetazolamide-only controls (8% versus 24%, p=0.065) but with only 19% survival in the bicarbonate-treated rats. CONCLUSIONS: In the neonatal rat, alkalosis induced by bicarbonate gavage is associated with a low incidence of mild, preretinal NV similar to ROP. Although treating acidotic rats with bicarbonate may reduce the incidence of preretinal NV, treatment was associated with an unacceptable mortality rate.

Acetazolamide↗

PubMed1989

The effect of hypocapnia on extinction of conditioned fear responses.

Conditioning models have been very helpful in the understanding of the etiology and maintenance of anxiety. Such laboratory models, however, leave unexplained why in many cases of naturally occurring anxiety, as in the case of agoraphobia, the fear responses do not extinguish. Literature on experimental anxiety provocation suggests that a systemic alkalosis might play a role in the maintenance of phobic fear. It was hypothesized that a subject in a state of respiratory alkalosis would show delayed extinction to classical conditioned anxiety. In a differential classical conditioning paradigm, consisting of a habituation-, an acquisition-, and an extinction-phase, slides and electric shocks were used as conditioned stimuli (CS) and unconditioned stimuli (US) respectively. The skin conductance response was taken as (U)CR. Subjects were randomly assigned to two groups: hyperventilation or control. It was shown that the extinction was not delayed when subjects were hypocapnic during the extinction. These data support the view that a respiratory alkalosis per se is not a sufficient condition for the maintenance of neurotic fears. The data of the present study are discussed in the context of existing literature on a psychological interpretation of the maintenance of anxiety.

Adult↗

PubMed1977

Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis.

Changes in acid-base equilibrium and blood lactate and pyruvate concentrations were studied during recovery (breathing room air) after three days hypercapnia (FICO2 = 0.10) in awake dogs. Fast return to FICO2 = 0 produced a slight alkalosis in arterial blood and an increase in lactate and pyruvate concentrations which seemed to be maximum at the 15th minute. These changes were inhibited by previous injection of acetazolamide (50 mg/kg body weight). During progressive return to FICO2 = 0, over 1 hour, the peak value of blood lactate and pyruvate was delayed until the end of that hour, at the same time as a slight blood alkalosis appeared. These phenomen are most probably explained by a stimulation, due to alkalosis, of glycolysis at the level of phosphofructokinase.

Acetazolamide↗