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PubMed1993

Decreased bone carbonate content in response to metabolic, but not respiratory, acidosis.

In vitro cultured neonatal mouse calvariae release calcium and buffer the medium proton concentration in response to a decrease in the medium pH caused by a reduction in bicarbonate concentration ([HCO3-]), a model of metabolic acidosis, but not to an equivalent decrease in pH caused by an increase in the partial pressure of carbon dioxide (PCO2), a model of respiratory acidosis. We have postulated that the medium is in equilibrium with the carbonated apatite in bone. To determine whether bone carbonate is depleted during models of acidosis, we cultured calvariae in control medium (pH approximately 7.4, PCO2 approximately 43, [HCO3-] approximately 26) or in medium in which the pH was equivalently reduced by either a decrease in [HCO3-] (metabolic acidosis, pH approximately 7.1, [HCO3-] approximately 13) or an increase in PCO2 (respiratory acidosis, pH approximately 7.1, PCO2 approximately 86) and determined net calcium flux (JCa) and bone carbonate content. We found that compared with control, after 3, 24, and 48 h there was a decrease in bone carbonate content during metabolic but not during respiratory acidosis. Compared with control, at 3 h JCa increased with both respiratory and metabolic acidosis; however, at 24 and 48 h JCa increased only with metabolic acidosis. JCa was correlated inversely with percent bone carbonate content in control and metabolic acidosis at all time periods studied (r = -0.809, n = 23, P < 0.001). Thus a model of metabolic acidosis appears to increase JCa from bone, perhaps due to the low [HCO3-] inducing bone carbonate dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMedDate not supplied

Effects of intravenous hyperosmotic sodium bicarbonate on arterial and cerebrospinal fluid acid-base status and cardiovascular function in calves with experimentally induced respiratory and strong ion acidosis.

The objectives of this study were to determine the effects of hyperosmotic sodium bicarbonate (HSB) administration on arterial and cerebrospinal fluid (CSF) acid-base balance and cardiovascular function in calves with experimentally induced respiratory and strong ion (metabolic) acidosis. Ten healthy male Holstein calves (30-47 kg body weight) were instrumented under halothane anesthesia to permit cardiovascular monitoring and collection of blood samples and CSE Respiratory acidosis was induced by allowing the calves to spontaneously ventilate, and strong ion acidosis was subsequently induced by i.v. administration of L-lactic acid. Calves were then randomly assigned to receive either HSB (8.4% NaHCO3; 5 ml/kg over 5 minutes, i.v.; n=5) or no treatment (controls, n=5) and monitored for 1 hour. Mixed respiratory and strong ion acidosis was accompanied by increased heart rate, cardiac index, mean arterial pressure, cardiac contractility (maximal rate of change of left ventricular pressure), and mean pulmonary artery pressure. Rapid administration of HSB immediately corrected the strong ion acidosis, transiently increased arterial partial pressure of carbon dioxide (P(CO2)), and expanded the plasma volume. The transient increase in arterial P(CO2) did not alter CSF P(CO2) or induce paradoxical CSF acidosis. Compared to untreated control calves, HSB-treated calves had higher cardiac index and contractility and a faster rate of left ventricular relaxation for 1 hour after treatment, indicating that HSB administration improved myocardial systolic function. We conclude that rapid i.v. administration of HSB provided an effective and safe method for treating strong ion acidosis in normovolemic halothane-anesthetized calves with experimentally induced respiratory and strong ion acidosis. Fear of inducing paradoxical CSF acidosis is not a valid reason for withholding HSB administration in calves with mixed respiratory and strong ion acidosis.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Metabolic acidosis in patients with chronic kidney diseases: why and when to treat it?].

Metabolic acidosis is a common complication in patients with advanced chronic renal diseases and dialytic treatments are unable to correct it completely. In hemodialysis (HD) patients, severe metabolic acidosis is associated with an increased risk of death. Evidence from several experimental studies suggests that even mild metabolic acidosis is associated with systemic effects. Acidosis is implicated in endocrine changes and has negative repercussions on bone and protein metabolism. In addition, recent observations suggest that acidosis triggers inflammation and accelerates the progression of chronic kidney diseases. As a contradictory finding, acidosis can reduce circulating leptin. Clinical studies on the nutritional effects of metabolic acidosis correction have shown mildly favorable effects. Taking into account the systemic effects of metabolic acidosis it is suggested that even mild metabolic acidosis is corrected. However, the new findings concerning the systemic effects of acidosis must be evaluated in controlled trials.

Acidosis↗
PubMed2001

Compensatory role of CaMKII on ICa and SR function during acidosis in rat ventricular myocytes.

It has been suggested that the activity of Ca2+/calmodulin-dependent protein kinase II (CaMKII) increases during acidosis in cardiac muscle. Thus we have investigated the role of CaMKII during acidosis by monitoring intracellular Ca2+ (using fura-2) and ICa (using the perforated patch clamp technique) during acidosis, in the absence and presence of the CaMKII inhibitor KN-93, in rat isolated ventricular myocytes. In the absence of KN-93, acidosis (pH 6.5) increased the amplitude of the fura-2 transient and prolonged its decay, but in the presence of KN-93 acidosis did not alter the amplitude and prolonged the decay more. In the absence of KN-93, acidosis increased the amplitude of the caffeine-induced fura-2 transient but did not alter its amplitude in the presence of KN-93. ICa did not change significantly during acidosis in the absence of KN-93 but decreased during acidosis in the presence of KN-93. These results suggest that activation of CaMKII during acidosis helps to compensate for the direct inhibitory effects of acidosis on sarcoplasmic reticular Ca2+ uptake and ICa.

Acidosis↗
PubMed2004

Phospholamban is required for CaMKII-dependent recovery of Ca transients and SR Ca reuptake during acidosis in cardiac myocytes.

Initially during acidosis, Ca transient amplitude (Delta[Ca]i) and the rate constant of [Ca]i decline (k(Ca)) are decreased, but later during acidosis Delta[Ca]i and k(Ca) partially recover. This recovery in rat myocytes could be inhibited by KN-93 suggesting that CaMKII-dependent protein phosphorylation (and enhanced SR Ca uptake) may be responsible. To test whether phospholamban (PLB) is required for the Delta[Ca]i and k(Ca) recovery during acidosis, we used isolated myocytes from PLB knockout (PLB-KO) vs. wild-type (WT) mice. [Ca]i was measured using fluo-3. During the initial phase of acidosis (1-4 min), Delta[Ca]i decreased in WT myocytes (n = 8) from 1.75 +/- 0.19 to 1.10 +/- 0.13 DeltaF/F0 (P < 0.05) and k(Ca) decreased from 3.20 +/- 0.22 to 2.38 +/- 0.18 s(-1) (P < 0.05). Later during acidosis (6-12 min), Delta[Ca]i partially recovered to 1.41 +/- 0.18 DeltaF/F0 and k(Ca) to 2.78 +/- 0.22 s(-1) (i.e. both recovered by approximately 50%). CaMKII inhibition using KN-93 completely prevented this recovery of Delta[Ca]i and k(Ca) during late acidosis in WT myocytes. In PLB-KO myocytes (n = 11) Delta[Ca]i decreased during early acidosis from 2.92 +/- 0.31 to 1.33 +/- 0.17 DeltaF/F0 (P < 0.05) and k(Ca) decreased from 10.45 +/- 0.56 to 7.58 +/- 0.68 s(-1) (P < 0.05). However, Delta[Ca]i did not recover during late acidosis and k(Ca) decreased even more (6.59 +/- 0.65 s(-1)). Parallel results were seen for contractile parameters. We conclude that PLB is crucial to the recovery of Delta[Ca]i and k(Ca) during acidosis. Moreover, PLB phosphorylation by CaMKII plays an important role in limiting the decline in Ca transients (and contraction) during acidosis.

Acidosis↗
PubMed2003

Management of acidosis during lung-protective ventilation in acute respiratory distress syndrome.

In ARDS, when acidosis complicates LPV, the goal of alkali therapy is to maintain arterial pH at a safe level (> or = 7.20). A pure respiratory acidosis generally does not require alkali therapy. If the Pplat is greater than 30 cm H2O, and the respiratory rate equals the upper limit (35-40 breaths/minute), then V(E) is slowly titrated down by approximately 1 L/hour, so that PaCO2 increases by 10 mm Hg/hour or less. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics. Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. Using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation. Under these circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. When renal failure is present, CRRT is indicated to manage acidosis. When ARDS is complicated by traumatic or hemorrhagic shock, overresuscitation with Cl(-)-rich solutions should be avoided to prevent metabolic acidosis.

Acidosis↗
PubMed1999

Altered contractile response of penis under hypoxia with metabolic acidosis.

Previous studies concerning ischemic priapism revealed that hypoxia alters the erectile and contractile responses of penis. But the effects of accompanying acidosis on those responses have not been fully evaluated or understood yet. We performed this study to elucidate the role of acidosis on the trabecular smooth muscle contractility like in ischemic priapism. Under the general anesthesia, 55 mature male cats were conditioned to systemic metabolic acidosis by hypoventilation by animal ventilator. The changes of intracavernous pressure (ICP) to erectogenic agents (acetylcholine, L-arginine, prostaglandin E1: PGE1), erectolytic agents (epinephrine, thromboxane A2; TXA2), K channel-related drugs (pinacidil, 4-aminopyridine, tetraethylammonium; TEA, glibenclamide) and calcium ionophore were monitored at Set 1 (PO2 > 60 mmHg, pH > 7.25), Set 2 (PO2 < 30 mmHg, 7.25 > pH > 7.0), Set 3 (PO2 < 30 mmHg, pH < 7.0), and Set 4 (PO2 > 60 mmHg, pH < 7.0) in vivo. At Set 1 and Set 2, epinephrine, TXA2, and ionomycin decreased the ICP by acetylcholine or PGE1 (n = 9, P < 0.01). The decrease of ICP was in order of epinephrine, TXA2 and ionomycin. Acidosis reduced the increase of ICP to acetylcholine or PGE1 (n = 8, P < 0.01), TXA2 or ionomycin did not affect ICP under severe acidosis but epinephrine decreased ICP even under severe acidosis (n = 7, P < 0.05). Pretreatment of potassium channel blockers did not suppress the increase of ICP by erectogenic agents under acidosis (n = 6, P < 0.05). Pinacidil did not affect ICP under acidosis (n = 6, P < 0.01). These results suggest that acidosis impairs the contractile response of cavernous smooth muscle to erectolytic agents. It may be the results of the interference by [H+] with the intra and extracellular mechanisms that regulate the homeostasis of [Ca2]. Conclusively, besides hypoxia, acidosis is another limiting factor of trabecular smooth muscle contractility like in ischemic priapism.

Acetylcholine↗
PubMed1996

Protective effects of extracellular acidosis and blockade of sodium/hydrogen ion exchange during recovery from metabolic inhibition in neuronal tissue culture.

Acidosis is a universal response of tissue to ischemia. In the brain, severe acidosis has been linked to worsening of cerebral infarction. However, milder acidosis can have protective effects. As part of our investigations of the therapeutic window in our neuronal tissue culture model of ischemia, we investigated the effects of acidosis during recovery from brief simulated ischemia. Ischemic conditions were simulated in dissociated cortical cultures by metabolic inhibition with potassium cyanide to block oxidative metabolism and 2-deoxyglucose to block glycolysis. Lowering the extracellular pH (pH0) to 6.2 during metabolic inhibition had no effect on injury, as measured by lactate dehydrogenase release from cultures after 24 h of recovery. Lowering the pH0 during the first hour of recovery, in contrast, had profound protective effects. When the duration of metabolic inhibition was lengthened to 30 min, most of the protective effects of the NMDA receptor antagonist MK-801 were lost. However, the protective effects of acidosis were unchanged. This suggested that the protective effects of extracellular acidosis could be due to more than blockade of NMDA receptors. Intracellular acidosis might be responsible. To test this, recovery of intracellular pH (pH1) was slowed by incubation with blockers of Na+/H+ exchangers at normal pH0. The two compounds tested, dimethylamiloride and harmaline, had protective effects when present during recovery from metabolic inhibition. Measurements of pH1 confirmed that the blockers slowed recovery from intracellular acidosis; more rapid pH1 recovery was correlated with injury. The protective effects of acidosis could be reversed by brief incubation with the protonophore monensin, which rapidly normalized pH1. These results are the first demonstration of the protective effects of blocking Na+/H+ exchange in a model of cerebral ischemia. The protective effects of acidosis appear to arise either from suppressing pH-sensitive mechanisms of injury or from blocking sodium entry due to Na+/H+ exchange.

Acidosis↗
PubMed1999

Cause of metabolic acidosis in prolonged surgery.

OBJECTIVE: The intraoperative development of metabolic acidosis is frequently attributed to hypovolemia, tissue hypoperfusion, and lactic acidosis. In this study, dilutional acidosis was evaluated as a possible mechanism for the routine development of intraoperative acidosis in noncardiac, nonvascular surgery patients. DESIGN: Prospective, observational study. SETTING: University-affiliated Veteran's Affairs Medical Center and a staff model, health maintenance organization hospital. PATIENTS: Twelve patients undergoing prolonged surgical procedures expected to last > or = 4 hrs were enrolled in the study. INTERVENTIONS: Perioperative management was based on the judgment of the attending anesthesiologist and surgeon without knowledge of the study's intent. MEASUREMENTS AND MAIN RESULTS: Arterial blood gas parameters, serum electrolytes, and urine electrolytes were measured pre- and postoperatively. Pulmonary artery catheters were placed for hemodynamic measurement and oxygen delivery calculations. Plasma volume was measured both pre- and postoperatively, using the Evans blue dye dilution technique. Although significant changes in lactate level (1.1 +/- 0.6-1.8 +/- 1.0) occurred, the change was not large enough to explain the degree of change in base excess (0.8 +/- 2.3 to -2.7 +/- 2.9). Chloride levels significantly increased (106 +/- 3-110 +/- 5) with a correlation (r2 = .92; p < .0001) between the degree of change in chloride and the degree of change in base excess. Plasma volume did not change. Furthermore, a correlation between the volume of normal saline administered and the change in base excess was found (r2 = .86; p < .0001), although no correlation was found with Ringer's lactate solution. An even stronger correlation was noted when the total chloride amount administered was compared with the change in base excess (r2 = .93; p < .0001). CONCLUSIONS: In this patient population, a common source of increasing base deficit is related to chloride administration. The largest source of chloride is usually normal saline. Classically, dilutional acidosis would explain the predominance of this acidotic change; however, no increase in plasma volume occurred. The absence of plasma volume change would suggest that the mechanism postulated to result in dilutional acidosis is incomplete. The common treatment of administering more fluid for intraoperative acidosis may be inappropriate, may have caused the acidosis, and may further exacerbate the acidosis. Chloride levels should be assessed whenever a metabolic acidosis is seen perioperatively.

Acidosis↗
PubMed2003

Treatment of metabolic acidosis.

Metabolic acidosis is characterized by a decrease of the blood pH associated with a decrease in the bicarbonate concentration. This may be secondary to a decrease in the strong ion difference or to an increase in the weak acids concentration, mainly the inorganic phosphorus. From a conceptual point of view, two types of nontoxic metabolic acidosis must be differentiated: the mineral metabolic acidosis that reveals the presence of an excess of nonmetabolizable anions, and the organic metabolic acidosis that reveals an excess of metabolizable anions. Significance and consequences of these two types of acidosis are radically different. Mineral acidosis is not caused by a failure in the energy metabolic pathways, and its treatment is mainly symptomatic by correcting the blood pH (alkali therapy) or accelerating the elimination of excessive mineral anions (renal replacement therapy). On the other hand, organic acidosis gives evidence that a severe underlying metabolic distress is in process. No reliable argument exists to prove that this acidosis is harmful under these conditions in humans. Experimental data even show that hypoxic cells are able to survive only if the medium is kept acidic. The management of an acute organic metabolic acidosis is therefore primarily based on the cause of the acidosis, and no scientific argument exists to justify the correction of the acid-base imbalance in this context.

Acidosis↗
PubMed2006

Does bicarbonate correct coagulation function impaired by acidosis in swine?

BACKGROUND: Coagulopathy is an important contributor to morbidity and mortality in trauma patients. Acidosis contributes to coagulopathy. Acidosis can be neutralized with intravascular bicarbonate, but it is unclear if the coagulation defect is rapidly reversed. The effects of acidosis and bicarbonate neutralization on coagulation function were investigated in vivo. METHODS: Acidosis was induced in 12 pigs by infusing 0.2 mol/L HCl to pH 7.1. Pigs were then infused with either LR to maintain a pH of 7.1 (A-LR, n = 6) or 0.3 mol/L bicarbonate to a pH of 7.4 (A-Bi, n = 6). Blood samples were taken at baseline, 15 minutes after acidosis induction, and 15 minutes after bicarbonate neutralization. Coagulation function was assessed by prothrombin time (PT), partial thromboplastin time (PTT), thrombin generation, initial clot formation time (R), clotting rapidity (alpha), and clot strength (MA). RESULTS: Compared with baseline values, acidosis reduced fibrinogen concentration to 66% +/- 2% in A-LR and to 71% +/- 3% in A-Bi, and decreased platelet counts to 49% +/- 4% in A-LR and to 53% +/- 4% in A-Bi. Thrombin generation decreased to 60% +/- 4% in A-LR and to 53% +/- 7% in A-Bi. Acidosis prolonged PT and PTT about 20% and decreased alpha and MA. After pH neutralization, fibrinogen and platelet levels remained depleted and no reversal of acidosis-induced changes in thrombin generation, PT, PTT, alpha, and MA were observed. CONCLUSION: Acidosis impaired coagulation by depleting fibrinogen and platelets and by inhibiting clotting kinetics. The deficit associated with acidosis was not reversed with bicarbonate pH neutralization.

Acidosis↗
PubMed2000

One year period prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of non-invasive ventilation and oxygen administration.

BACKGROUND: Non-invasive ventilation (NIV) reduces mortality and intubation rates in patients with chronic obstructive pulmonary disease (COPD) admitted to hospital with respiratory acidosis. This study aimed to determine the prevalence of respiratory acidosis in patients admitted with COPD, to draw inferences about oxygen therapy, and to determine the need for NIV services for acute COPD in typical UK hospitals. METHODS: This one year prospective prevalence study identified patients with COPD aged 45-79 years inclusive who were admitted to Leeds General Infirmary, St James's University, and Killingbeck Hospitals, Leeds between 1 March 1997 and 28 February 1998. The prevalence of respiratory acidosis and the relationship with oxygenation are described. Other outcomes included intensive care use and in hospital mortality. From this data population prevalence estimates were determined for respiratory acidosis, from which the need for NIV in a typical district general hospital was modelled. RESULTS: 983 patients were admitted, 11 of whom required immediate intubation. 20% of the remaining 972 had a respiratory acidosis. Acidosis was associated with subsequent admission to the intensive care unit (ICU): pH<7.25, OR 6.10 (95% confidence interval (CI) 1.19 to 31.11); pH 7.25-7.30, OR 8.73 (95% CI 2.11 to 36.06). pH was inversely correlated with arterial oxygen tension (PaO(2)) in the 47% of patients who were hypercapnic, with a PaO(2) of >10 kPa being associated with acidosis in most hypercapnic patients. 80% remained acidotic after initial treatment, giving an age/sex specific prevalence for England and Wales of 75 (95% CI 61 to 90)/100 000/year for men aged 45-79 years and 57 (95% CI 46 to 69)/100 000/year for women. Modelling the need for NIV for all COPD patients indicates that a typical UK hospital will admit 90 patients per year with acidosis of which 72 will require NIV. CONCLUSIONS: In patients with acute COPD the PaO(2) should be maintained at 7.3-10 kPa (SaO(2) 85-92%) to avoid the dangers of hypoxia and acidosis. If all COPD patients with a respiratory acidosis (pH<7.35) after initial treatment are offered NIV, a typical UK hospital will treat 72 patients per year.

Acidosis, Respiratory↗
PubMed1995

Effects of intracellular acidosis on Ca2+ activation, contraction, and relaxation of frog skeletal muscle.

The goal of this study was to determine the effects of intracellular acidosis (pH approximately 6.3) of frog skeletal muscle on force and on intracellular Ca2+ concentration ([Ca2+]i; measured at 20 degrees C using indo 1 fluorescence). Acidosis reduced tetanic force by only 11 +/- 2% (mean +/- SE, n = 8) but increased tetanic [Ca2+]i by 33 +/- 6%, suggesting that acidosis reduced the maximum Ca(2+)-activated force. During relaxation, the [Ca2+]i at half-maximal force was doubled with acidosis, suggesting that acidosis altered the Ca(2+)-force relationship. Acidosis markedly slowed force relaxation and [Ca2+]i decline (time constants fitted to force and [Ca2+]i during relaxation increased by 133 +/- 20 and 68 +/- 13%, respectively, with acidosis), suggesting that slowed force relaxation with acidosis may arise from slowed Ca2+ clearance from the cytosol. Late in relaxation, at approximately 30% of initial force, there was a transient phase of [Ca2+]i increase that was delayed with acidosis in proportion to the slowing of force relaxation. This is consistent with previous suggestions that dissociation of cross-bridges from the thin filament during relaxation promotes Ca2+ release to the cytosol from troponin. This study concludes that in skeletal muscle acidosis has little effect on tetanic force and that the major effects are decreased Ca2+ sensitivity and slower relaxation.

Acidosis↗
PubMed2002

Electrophysiological response of rat atrial myocytes to acidosis.

The effect of acidosis on the electrical activity of isolated rat atrial myocytes was investigated using the patch-clamp technique. Reducing the pH of the bathing solution from 7.4 to 6.5 shortened the action potential. Acidosis had no significant effect on transient outward or inward rectifier currents but increased steady-state outward current. This increase was still present, although reduced, when intracellular Ca(2+) was buffered by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA); BAPTA also inhibited acidosis-induced shortening of the action potential. Ni(2+) (5 mM) had no significant effect on the acidosis-induced shortening of the action potential. Acidosis also increased inward current at -80 mV and depolarized the resting membrane potential. Acidosis activated an inwardly rectifying Cl(-) current that was blocked by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), which also inhibited the acidosis-induced depolarization of the resting membrane potential. It is concluded that an acidosis-induced increase in steady-state outward K(+) current underlies the shortening of the action potential and that an acidosis-induced increase in inwardly rectifying Cl(-) current underlies the depolarization of the resting membrane potential during acidosis.

Acidosis↗
PubMed1998

Effect of acidosis on tension and [Ca2+]i in rat cerebral arteries: is there a role for membrane potential?

The cellular mechanism responsible for the reduction of tension in cerebral small arteries to acidosis is not known. In this study the role of smooth muscle intracellular Ca2+ concentration ([Ca2+]i) and membrane potential for the relaxation to acidosis was investigated in isolated rat cerebral small arteries. Isometric force was measured simultaneously with [Ca2+]i (fura 2) or with membrane potential (intracellular microelectrodes), and acidosis was induced by increasing PCO2 or reducing HCO3- of the bathing solution. Both hypercapnic and normocapnic acidosis were associated with a reduction of intracellular pH [measured with 2',7'-bis-(carboxyethyl)-5 (and -6)-carboxyfluorescein], caused relaxation, and reduced [Ca2+]i. However, whereas hypercapnic acidosis caused hyperpolarization, normocapnic acidosis was associated with depolarization. It is concluded that a reduction of [Ca2+]i is in part responsible for the direct effect of the acidosis on the vascular smooth muscle both during normo- and hypercapnia. The mechanism responsible for the reduction of [Ca2+]i differs between the hypercapnic and normocapnic acidosis, being partly explained by hyperpolarization during hypercapnic acidosis, whereas it is seen despite depolarization during normocapnic acidosis.

Acidosis↗
PubMed1981

Effect of metabolic acidosis on renal response to parathyroid hormone in phosphorus-deprived rats.

Both metabolic acidosis and phosphorus (Pi) deprivation have been shown to alter not only renal Pi metabolism independent of parathyroid hormone (PTH), but also the phosphaturic response to PTH. In the present studies, we examined the interaction between metabolic acidosis and Pi deprivation on renal handling of Pi in an animal model in which metabolic acidosis was superimposed on 3 days of dietary Pi deprivation. The effect of metabolic acidosis was evaluated after acute (for 3 h) and chronic (for 3 days) administration of HCl. In Pi-deprived and thyroparathyroidectomized rats, chronic acidosis increased both plasma Pi and the basal fractional excretion of Pi (FEPi). Furthermore, chronic acidosis partially restored the phosphaturic response to PTH, which was totally absent in nonacidotic Pi-deprived rats. These effects metabolic acidosis were not demonstrable in acutely acidotic animals. Determination of PTH-dependent cAMP generation and cAMP-dependent protein kinase activation revealed that neither of these parameters was altered by chronic metabolic acidosis in vivo. These results show that in Pi-deprived rats chronic metabolic acidosis induced by HCl administration further modifies the renal handling of Pi associated with Pi deprivation. Further, the renal interaction between acidosis and Pi deprivation is at a step (or steps) after cAMP generation and protein kinase activation.

Acidosis↗
PubMed1986

Effect of respiratory acidosis on intracellular pH of the proximal tubule.

In contrast to chronic metabolic acidosis, chronic respiratory acidosis does not result in an adaptation in either renal ammonia or glucose production. To examine the possibility that this might be explained by a difference in proximal tubule intracellular pH, the response of two pH-sensitive metabolites, citrate and alpha-ketoglutarate, were assessed. Metabolic acidosis of 3 days duration, induced by drinking 1.5% NH4Cl, significantly reduced urinary citrate excretion (172 to 15 mumol/day) and renal cortical citrate (1.33 to 0.88 mumol/g) and alpha-ketoglutarate (0.90 to 0.46 mumol/g) concentrations in comparison with normal rats. Chronic respiratory acidosis, produced by 3 days in a 10% CO2 environment, lowered systemic pH similar to metabolic acidosis but had no effect on either urinary citrate excretion or renal cortical citrate and alpha-ketoglutarate concentrations. By contrast, acute respiratory acidosis (3, 6, or 24 h duration) reduced urinary citrate excretion and renal cortical citrate and alpha-ketoglutarate concentrations in a fashion similar to acute metabolic acidosis. These data suggest that acute acidosis of either respiratory or metabolic origin lowers the intracellular pH of the proximal tubule. However, when the acid-base abnormality enters the chronic phase, proximal tubular intracellular pH remains low with metabolic acidosis but returns to normal values with respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1997

Effect of chronic metabolic acidosis on thyroid hormone homeostasis in humans.

The effects of metabolic acidosis on thyroid function are unknown. We investigated the effects of chronic extrarenal acidosis on the hypothalamic-pituitary-thyroid axis. Chronic metabolic acidosis was induced by administering NH4Cl (4.2 mmol.kg body wt-1.day-1) to six normal male volunteers during metabolic balance conditions. Plasma bicarbonate concentration decreased from 25.0 +/- 0.4 to 15.5 +/- 0.9 mmol/l (P < 0.001). Metabolic acidosis significantly decreased serum-free 3,5,3'-triiodothyronine (T3) concentrations from 373 +/- 18 (control) to 251 +/- 13 pg/dl (P < 0.001) and decreased serum-free L-thyroxine (T4) from 1.55 +/- 0.42 to 1.25 +/- 0.37 ng/dl (P < 0.002), whereas serum total reverse T3 did not change significantly. Consequently, the reverse T3-to-free T4 ratio increased. Serum thyroid-stimulating hormone (TSH) levels increased significantly from 0.70 +/- 0.07 during control to 1.30 +/- 0.12 mU/l during acidosis (P < 0.003). The TSH response to thyrotropin (TRH, 2 mg intranasally) was exaggerated in acidosis: the partial area under the concentration curve for the TSH response (210 min post-TRH) was 902 +/- 167 during control compared with 1.394 +/- 209 mU.min.l-1 during acidosis (P = 0.0139). Chronic metabolic acidosis, as produced by the model employed here, induces a decrease in thyroid hormone secretion and might exert additional effects on thyroid hormone metabolism in humans. The acidosis-induced decrease in thyroid function might modulate some of the reported effects of metabolic acidosis, such as on nitrogen balance, protein synthesis, lean body mass, insulin-like growth factor I levels, renal acidification, and cardiac contractile function.

Acidosis↗