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PubMed1982

A study of the effects of hypoxia on acid-base status of rainbow trout blood using an extracorporeal blood circulation.

(1) The use of an extracorporeal blood circulation method has made it possible to obtain information on the time course of possible modifications in acid-base status of trout blood during hypoxia. (2) Two series of experiments are described: (a) Continuous measurement of arterial pH, PCO2 and PO2 during 24 h of moderate hypoxia (60 Torr). (b) Continuous measurement of acid-base status during 24 h of deep hypoxia (40 Torr). (3) The results of the first series show that hypoxia provokes a stimulation of ventilatory frequency and amplitude which is associated with an increased output of CO2 from the blood which induces respiratory alkalosis. This alkalosis is compensated during the following 24 h, and results in a return to the initial pH, a decrease in concentration of HCO-3 + CO2-(3) and an increase in lactate levels and Cl- ion concentration. (4) The second set of experiments show that in deep hypoxia the respiratory alkalosis is preceded by a brief stage of deep metabolic acidosis during which lactate levels suddenly increase dramatically.

Acid-Base Equilibrium↗
PubMed1989

Arterial blood gas changes in panic disorder and lactate-induced panic.

Lactate infusions were conducted in 12 male panic patients and 8 male normal controls with arterial catheters in place to reassess previously reported acid-base changes based on venous blood samples. The analysis of arterial pH, carbon dioxide pressure, and bicarbonate concentration confirmed most venous findings. At baseline, before the infusion, venous blood shows evidence of mixed chronic and acute respiratory alkalosis in patients while arterial blood gasses are most consistent with developing acute respiratory alkalosis. During the infusion both bloods are consistent with mixed metabolic and respiratory alkalosis with the patients hyperventilating more than normal controls and panicking patients hyperventilating more than nonpanicking patients. Arterial blood seems more sensitive than venous blood in detecting baseline differences between panicking and nonpanicking patients. A baseline arterial carbon dioxide pressure of 40 mmHg or higher and an arterial pH below 7.40 may predict no subsequent panic to lactate infusion.

Acid-Base Equilibrium↗
PubMed1984

The hypokalemic, bowel, bladder, headache relationship; a new syndrome. The role of the potassium ammonia axis.

A conceptual approach that relates vascular headaches, bowel and bladder dysfunction to abnormalities of the "ammonia potassium axis" is presented. Hypokalemia alters smooth muscle function of both the bowel and bladder and results in the elaboration of an alkaline urine. The occurrence of an alkaline urine, along with bladder dysfunction and urinary stasis, predisposes to recurrent urinary tract infections. Hypokalemia and/or alkalosis increases the renal return of ammonia, exposes the brain to chronically higher concentration of ammonia and facilitates its passage into the central nervous system. Increased levels of blood ammonia predispose to hyperventilation which results in a superimposed respiratory alkalosis on a pre-existing hypokalemia and/or alkalosis therefore causing intense cerebral vasoconstriction. Varying degrees of cerebral ischemia and hypoxia occur and give rise to higher brain concentrations of ammonia. Vasodilatation occurs during the headache phase and may be a consequence of the sudden increase of brain ammonia and/or due to the release of other vasoactive mediators. As a consequence of increased blood ammonia, a reduction of protein intake may result in the alterations of amino acid precursors for brain uptake and therefore further interferes with the modulation of cerebral blood flow and brain function.

Adult↗
PubMed1986

Cardiac cell action potential duration is dependent upon induced changes in free Ca2+ activity during pH changes in vitro.

We examined how changes in solution pH alter myocardial cell action potentials (AP) with and without changes in free [Ca2+] caused by pH induced effects on calcium binding. Guinea pig ventricular tissue was isolated, superfused either with Krebs-Ringer (K-R) bicarbonate, phosphate buffered solution, or with Hepes buffered solution, and electrically paced during control (5% CO2 in O2), acidic (12% CO2), and alkalotic (0% CO2) conditions. Action potentials were recorded with intracellular microelectrodes. Extracellular free [Ca2+] was measured with a calcium ion selective electrode and total soluble calcium was measured by ultrafiltration and spectrophotometry. With a total [CaCl2] of 2.5 mM in the K-R solution, we found a free [Ca2+] of 2.14 mM at pH 7.44 (control), 2.48 mM at pH 6.97 and 1.60 mM at pH 8.19; total soluble calcium concentration was 2.00 mM at pH 8.19. In the Hepes solution, free [Ca2+] was only slightly altered (2.42 to 2.55 mM) within this pH range. Equivalent acidosis of either K-R or Hepes suffusate significantly, and similarly, prolonged the AP and its refractory period. Alkalosis of the Hepes suffusate shortened the AP; but equivalent alkalosis of the K-R suffusate prolonged the AP as did a reduction of [CaCl2] in Hepes suffusate from 3.0 to 1.5 mM at pH 7.43. Our study demonstrates that a paradoxical increase in APD occurs because free Ca2+ ion activity falls in K-R solution and overrides the effect of alkalosis alone to decrease APD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Metabolic complications of the use of stomach for urinary reconstruction.

A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. Resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. Serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.

Acid-Base Imbalance↗
PubMed1996

Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome.

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.

Acute Kidney Injury↗
PubMed2001

Expression of rat thick limb Na/H exchangers in potassium depletion and chronic metabolic acidosis.

BACKGROUND: Regulation of renal transporter expression has been shown to support adaptation of transporter activities in several chronic situations. Basolateral and apical Na/H exchangers (NHE) in medullary thick ascending limb (MTAL) are involved in NH4+ and HCO3+ absorption, respectively. The NH4+ absorption rate in Henle's loop is increased in chronic metabolic acidosis (CMA) and potassium depletion (KD), which may be secondary to the increased NH4+ concentration in luminal fluid and/or to an increased NH4+ absorptive capacity of MTAL. HCO3- absorptive capacity in Henle's loop is increased in CMA and decreased in metabolic alkalosis, but is unchanged in KD despite the presence of metabolic alkalosis. The present study compared the effects of NH4Cl-induced CMA and KD on the expression of basolateral NHE-1 and the effect of KD on the expression of apical NHE-3 in MTAL. METHODS: NHE-1 and NHE-3 mRNAs and proteins were assessed by a competitive reverse transcription-polymerase chain reaction (RT-PCR) method and semiquantitative immunoblots, respectively, in MTAL-purified suspensions from rats with CMA and KD. RESULTS: NHE-1 protein abundance was similarly increased (approximately 90%) at two and five weeks of KD, while NHE-1 mRNA amount in MTAL cells was increased at two weeks of KD and returned to normal values by five weeks of KD. In contrast, NHE-1 mRNA and protein abundance did not change in CMA. NHE-3 protein abundance remained unchanged in both two and five weeks of KD, while NHE-3 mRNA was unchanged by two weeks of KD and reduced by approximately 50% at five weeks of KD. CONCLUSIONS: The results suggest the following: (1) in KD, where the increased NH4+ concentration of luminal fluid that favors NH4+ absorption is counterbalanced by a decrease in BSC1 expression and activity, the increased NHE-1 expression may support an increased MTAL NH4+ absorptive capacity in CMA, NHE-1 expression is not specifically regulated and remains unchanged, suggesting that the increase in NH4+ concentration in luminal fluid is the main determinant of increased NH4+ absorption in MTAL. (2) In KD, NHE-3 expression did not decrease despite the presence of metabolic alkalosis, in agreement with the unchanged HCO3- absorptive capacity of Henle's loop.

Acidosis↗
PubMed1999

Bicarbonate/chloride exchange regulates intracellular pH of embryos but not oocytes of the hamster.

The ability to regulate intracellular pH (pH(i)) is essential for normal cell development and differentiation. This study was an investigation of the regulatory system used by the hamster oocyte and preimplantation embryo to regulate pH(i) in the alkaline range. Recovery from alkalosis by late 1-cell and 2-cell embryos was rapid, and physiological pH(i) levels could be restored within 10 min. Recovery from an induced alkaline load was dependent on the chloride concentration in the external medium and sensitive to a stilbene derivative 4,4'-diisothiocyanatostilbene-2,2'-di-sulfonic acid that inhibits bicarbonate and chloride exchange. Therefore the recovery from alkalosis by hamster embryos appears to be via activity of the HCO(3)(-)/Cl(-) exchanger that was activated above a pH(i) set point of 7.24. In contrast, hamster oocytes and early 1-cell embryos (collected 3-4 h post-egg activation) could not recover from an intracellular alkalosis, and pH(i) remained elevated. Therefore, the hamster oocyte and the early 1-cell embryo still undergoing pronuclear formation lack an active HCO(3)(-)/Cl(-) exchanger for the restoration of pH(i). Inability to restore pH(i) from an alkali challenge resulted in a reduced ability of embryos to develop to the morula/blastocyst stages in culture, indicating that HCO(3)(-)/Cl(-) exchange is involved in physiological regulation of pH(i).

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1984

Acid-base interactions with noradrenaline-induced contractile response of the rabbit isolated aorta.

The effect of acidosis and alkalosis on vascular smooth muscle contractions evoked by noradrenaline was studied. Helical strips of rabbit aorta were mounted for isometric tension recording. Acidosis (pH 7.24-6.51) was obtained by either increasing the PCO2 (hypercapnic) and/or lowering the HCO3-concentration (hypobicarbonatic). Acidosis shifted the noradrenaline concentration-response curve to the right in a competitive manner. The maximal developed tension was unchanged at pH 7.24-6.90 and decreased by 30% at pH 6.51. Alkalosis (pH 7.61-8.04) did not alter noradrenaline-evoked contractions. The results suggest that hydrogen ions during acidosis (pH less than 7.40) but not during alkalosis (pH greater than 7.40) exert alpha-adrenoceptor blocking properties.

Acid-Base Equilibrium↗
PubMed1994

Kinetics of 13CO2 elimination after ingestion of 13C bicarbonate: the effects of exercise and acid base balance.

In order to investigate the effects of muscular work and preceding exercise on the retention of exogenous labelled bicarbonate, we studied the effects of oral administration of [13C]bicarbonate (0.1 mg kg-1) in five subjects at rest before exercise and during and after 1 h of treadmill walking at 73% VO2max on three separate occasions. Elimination of CO2 from labelled bicarbonate was 62.6 +/- 8.1% at rest, 103.6 +/- 11.3% during exercise (P < 0.01) and 43.0 +/- 4.7% during recovery from exercise (P = 0.01). During exercise mean residence time (MRT) was shorter than at rest (35 +/- 7 min vs. 54 +/- 9 min, P < 0.02) and CO2 pool size was larger (998 +/- 160 ml CO2 kg-1, vs. 194 +/- 28 ml CO2 kg-1, P < 0.001). Compared to values obtained at rest, during recovery from exercise, MRT and CO2 pool size were reduced (34 +/- 5 min, P < 0.05; 116 +/- 19 ml CO2 kg-1, P < 0.02, respectively). In an additional five subjects acidosis and alkalosis were induced prior to administration of oral [13C]bicarbonate at rest. Elimination of bicarbonate was lower during acidosis (46.1 +/- 5.6%, P < 0.01) but was unaltered (50.9 +/- 5.6%, NS) during alkalosis, compared to the values obtained at resting pH. During acidosis MRT and CO2 pool size decreased (37 +/- 3 min, P < 0.01 and 123 +/- 10 ml CO2 kg-1, P < 0.01, respectively) whereas in alkalosis MRT was unchanged (65 +/- 8 min NS) but CO2 pool size was increased (230 +/- 23 ml CO2 kg-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1987

Effects of salbutamol and hyperventilation on the rise in serum potassium after succinylcholine administration.

It is known that circulating catecholamines stimulating beta 2-receptors and the acid-base balance play important roles in the regulation of serum potassium (K+). The present study was undertaken to investigate the effect of salbutamol (SB), a highly selective beta 2 agonist, and hyperventilation (HV)-induced alkalosis on the change in serum K+ after succinylcholine (SCh) administration in dogs. Pretreatment with SB (0.4 microgram.kg-1.min-1 for 30 min) produced sustained decreases in serum K+ and mean arterial pressure, and transient increases in cardiac output and serum insulin concentration. Maintaining respiratory alkalosis with HV (PaCO2 = 2.6-3.3 kPa) produced sustained decreases in serum K+ and cardiac output. Although both pretreatment with SB and HV-induced alkalosis significantly reduced the absolute increases in serum K+ after SCh, the effect of SB was more remarkable than that of HV. These results suggest that the degree of beta 2-receptor activity can strongly modulate the change in serum K+ after SCh administration.

Albuterol↗
PubMed1990

Influence of temperature and extracellular pH on contractile responses in isolated human hand veins.

The effects of moderate cooling and extracellular pH changes on concentration-response relationships for noradrenaline (NA), 5-hydroxytryptamine (5-HT) and prostaglandin F2 alpha (PGF2 alpha) were investigated in isolated human hand veins. pH changes were achieved by altering the NaHCO3 content of the Krebs solution. Cooling to 24 degrees reduced the maximum contractile responses to K+ (124 mM), NA and PGF2 alpha by 20-30%, whereas that to 5-HT was unchanged. The NA and 5-HT potencies were increased 8-10 times, whereas the PGF2 alpha potency was unaffected. A shift from alkalotic (pH 7.6) to acidotic (pH 6.9) conditions did not influence the contractile response to 124 mM K+, whereas the responses to NA, 5-HT and PGF2 alpha were inhibited with regard to both potency and maximum contraction. When related to neutral pH, acidosis significantly reduced only the 5-HT potency (4 times), whereas alkalosis selectively increased the NA and PGF2 alpha potencies (3 times). In the presence of prazosin (10(-7) M) cooling to 24 degrees significantly increased the NA potency, whereas no such increase was seen in the presence of rauwolscine (10(-7) M). Alkalosis significantly increased the NA potency in the presence of either antagonist. In conclusion, temperature and extracellular pH influenced the contractile responses to NA, 5-HT and PGF2 alpha in a differentiated manner. Alkalosis appeared to increase the response to both alpha 1- and alpha 2-adrenoceptor stimulation, whereas cooling preferentially increased that to alpha 2-adrenoceptor stimulation.

Adult↗
PubMed1977

Kinetics of luminal acidification in cortical tubules of the rat kidney.

1. Some kinetic aspects of renal tubular acidification were studied in proximal and distal tubules of the rat kidney by combining stationary microperfusion methods and continuous measurements of luminal pH changes of phosphate or bicarbonate buffers by means of antimony electrodes. The analysis included the measurement of steady-state pH, steady-state buffer concentrations and acidification half-times. From these data, net rates of tubular bicarbonate reabsorption and of H ion secretion were obtained since it was shown that the rate of phosphate acidification provides a realistic estimate of H ion secretion. 2. Experiments were performed in control rats, in animals undergoing metabolic acidosis or alkalosis and in control and acidotic rats receiving the carbonic anydrase inhibitor Diamox. 3. In all experiments, the rates of tubular bicarbonate reabsorption and of phosphate acidification (H ion secretion) were proportional to luminal buffer levels. The changes of luminal acid concentrations followed first-order kinetics. 4. Steady-state transepithelial pH differences were reduced in metabolic alkalosis and after diamox but augmented during metabolic acidosis. 5. Acidification half-times were prolonged in metabolic acidosis and after Diamox but remained similar to control levels in metabolic alkalosis. 6. From the observation that both bicarbonate reabsorption and phosphate acidification are similarly affected by these experimental manoeuvres, it is concluded that H ion secretion plays a key role in both transport processes.

Acid-Base Equilibrium↗
PubMed1994

Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: HCO3- dependence.

1. HCO3(-)-dependent mechanisms involved in the regulation of intracellular pH (pHi) were characterized using double-barrelled pH-sensitive microelectrodes in smooth muscle cells of the isolated guinea-pig ureter. 2. Removal of external Cl- in the presence of CO2-HCO3- caused a transient alkalosis, consistent with the presence of Cl(-)-HCO3- exchange, before pHi slowly recovered. Recovery from acidosis in the presence of CO2-HCO3- was not affected, at a time when intracellular Cl- would have been maximally depleted, indicating that a counter transport of Cl- and HCO3- was not involved. The recovery was also not affected by amiloride, indicating that Na(+)-H+ exchange was not involved. 3. A transient hyperpolarization was associated with the recovery from acidosis in the presence of CO2-HCO3-, consistent with rheogenic coupling of Na(+)-HCO3- cotransport. However, depolarization caused by elevation of the extracellular potassium (K+o) concentration, which should favour inward transport by the rheogenic mechanism, caused a fall in pHi and decreased the rate of recovery from acidosis. Furthermore, ouabain abolished the transient hyperpolarization without affecting the recovery of pHi. It is concluded that Na(+)-HCO3- cotransport in the ureter is electroneutral. 4. Recovery from acidosis in the presence of CO2-HCO3- was insensitive to DIDS even after prolonged pre-equilibriation and extreme acidosis. The results suggest that Na(+)-HCO3- cotransport in the ureter is insensitive to DIDS and that Cl(-)-HCO3- exchange does not reverse to contribute to the extrusion of acid equivalents. A HCO3- conductance may account for the Na(+)-independent, HCO3(-)-dependent recovery from extreme acidosis. 5. Recovery from experimentally induced alkalosis was inhibited by Cl(-)-free conditions and by DIDS, indicating that Cl(-)-HCO3- exchange was involved. 6. It is concluded that pHi in the smooth muscle of guinea-pig ureter is controlled by three transport mechanisms. By far the most important is an electroneutral Na(+)-HCO3- cotransporter. Na(+)-H+ exchange appears to play little role in the presence of the physiological buffer. Both of these mechanisms extrude acid equivalents and so protect the cell against its fairly substantial intrinsic intracellular acid loading. Cl(-)-HCO3- exchange, on the other hand, is stimulated by intracellular alkalosis to transport acid equivalents into the cell and so restore a more normal pHi.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Localised pulmonary metastatic calcification associated with pulmonary artery obstruction.

BACKGROUND: Metastatic pulmonary calcification, a complication of uraemia and disordered calcium metabolism, may be diffuse or localised. The factors that determine calcium precipitation are complex, but tissue alkalosis is thought to be important. As obstruction of the pulmonary artery theoretically causes local alkalosis a retrospective necropsy study was carried out to examine the relation between metastatic pulmonary calcification and vascular obstruction. METHODS: Five patients with focal and two with diffuse metastatic calcification in the lungs were identified over eight years. Lungs were studied macroscopically and by light microscopy, haematoxylin and eosin and histochemical stains being used for calcium. RESULTS: Underlying risk factors for calcification in these patients included renal failure in six and disseminated malignancy in five. In the five patients with localised calcification obstruction of the pulmonary artery by thrombus or tumour was found proximal or adjacent to areas of calcium deposition. In two patients metastatic calcification was confined to a lung with unilateral pulmonary artery thromboembolic occlusion. Calcification was not specifically associated with infarction, pneumonia, or diffuse alveolar damage. Lesions of the pulmonary artery were not seen in the two patients with diffuse bilateral metastatic calcification. CONCLUSION: In this small series there was a spatial association between pulmonary artery obstruction and localised metastatic calcification. It is proposed that pulmonary artery obstruction alters the microchemical environment of the lung, favouring tissue alkalosis and thereby enhancing parenchymal calcification in patients predisposed to this condition.

Adult↗
PubMed1998

PKC activation is required by EGF-stimulated Na(+)-H+ exchanger in human pleural mesothelial cells.

Epidermal growth factor (EGF) stimulates the Na(+)-H+ exchanger, leading to enhanced cell proliferation. In human pleural mesothelial cells (PMCs), the intracellular signaling mechanism mediating the EGF-induced stimulation of the Na(+)-H+ exchanger has not yet been identified. Using a pH-sensitive fluorescent probe, 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein, to measure changes in intracellular pH (pHi), we found that 1) EGF and 12-O-tetradecanoylphorbol 13-acetate (TPA; a phorbol ester) both stimulate the ethylisopropyl amiloride-sensitive Na(+)-H+ exchanger; 2) TPA-induced alkalosis can be blocked by protein kinase C (PKC) inhibitors (chelerythrine and staurosporine) or by PKC down-regulation, indicating that PKC activation is involved in the stimulation of the Na(+)-H+ exchanger. However, TPA-induced alkalosis is not blocked by tyrosine kinase inhibitors; and 3) the stimulatory effect of EGF on the Na(+)-H+ exchanger acts via stimulation of tyrosine kinase-receptor activity because it is inhibited by tyrosine kinase inhibitors (genistein, lavendustin A, and herbimycin A). It also involves PKC activation because EGF-induced alkalosis was blocked by PKC inhibitors. These results suggest that PKC activation is one of the downstream signals for EGF-induced activation of the Na(+)-H+ exchanger in primary cultures of human pleural mesothelial cells.

Cells, Cultured↗
PubMed1988

Effect of systemic pH on pHi and lactic acid generation in exhaustive forearm exercise.

To investigate whether changes in systemic pH affect intracellular pH (pHi), energy-rich phosphates, and lactic acid generation in muscle, eight normal volunteers performed exhaustive forearm exercise with arterial blood flow occluded for 2 min on three occasions. Subjects ingested 4 mmol/kg NH4Cl (acidosis; A) or NaHCO3 (alkalosis; B) or nothing (control; C) 3 h before the exercise. Muscle pHi and phosphocreatine (PCr) content were measured with 31P-nuclear magnetic resonance (31P-NMR) spectroscopy during exercise and recovery. Lactate output during 0.5-7 min of recovery was calculated as deep venous-arterial concentration differences times forearm blood flow. Before exercise, blood pH and bicarbonate were lower in acidosis (7.303 +/- 0.009, 18.6 +/- 0.5 meq/l) than alkalosis (7.457 +/- 0.010, 32.2 +/- 0.7 meq/l) and intermediate in control (7.389 +/- 0.007, 25.3 +/- 0.6 meq/l). Lactic acid output during recovery was less with A (245 +/- 39 mumol/100 ml) than B (340 +/- 55 mumol/100 ml) (P less than 0.05) and intermediate in C (293 +/- 31 mumol/100 ml). PCr utilization and resynthesis were not affected by extracellular pH changes. pHi did not differ before exercise (A, 7.04 +/- 0.01; B, 7.09 +/- 0.01; C, 7.06 +/- 0.01) or at its end (A, 6.28 +/- 0.07; B, 6.28 +/- 0.11; C, 6.31 +/- 0.09). Hence systemic acidosis inhibited and alkalosis stimulated lactic acid output. These findings suggest that systemic pH regulates cellular acid production, protecting muscle pH, at the expense of energy availability.

Adult↗
PubMed1989

Bicarbonate reabsorption by the kidney of the newborn rabbit.

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.

Animals↗