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At least 19 recordsLinked to original sources
PubMed2001

Respiratory acidosis.

Respiratory acidosis, or primary hypercapnia, is the acid-base disorder that results from an increase in arterial partial pressure of carbon dioxide. Acute respiratory acidosis occurs with acute (Type II) respiratory failure, which can result from any sudden respiratory parenchymal (eg, pulmonary edema), airways (eg, chronic obstructive pulmonary disease or asthma), pleural, chest wall, neuromuscular (eg, spinal cord injury), or central nervous system event (eg, drug overdose). Chronic respiratory acidosis can result from numerous processes and is typified by a sustained increase in arterial partial pressure of carbon dioxide, resulting in renal adaptation, and a more marked increase in plasma bicarbonate. Mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space. Although the symptoms, signs, and physiologic consequences of respiratory acidosis are numerous, the principal effects are on the central nervous and cardiovascular systems. Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology.

Acidosis, Respiratory↗
PubMed1994

Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes.

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.

Acidosis, Respiratory↗
PubMed2000

Metabolic acidosis and respiratory acidosis impair gastro-pyloric motility in anesthetized pigs.

UNLABELLED: Acidosis impairs smooth muscle function in various organs. However, the effects of acidosis on the gastroduodenal tract are unknown while its dysfunction has potential perioperative harmful consequences. We investigated the effects of metabolic (MA) and respiratory acidosis (RA) on upper gut motility in tracheally ventilated pigs whose anesthesia was induced with halothane and maintained with alpha-chloralose-urethane administration (IV). Increased dead space and perfusion of hydrochloric acid 1 N (150 mL over 30 min) were used to induce RA and MA, respectively. Measurements of fundic tone using an electronic barostat, antro-pyloroduodenal phasic motility with perfused manometry and antro-duodenal electric control activity by electromyography were used to evaluate gastroduodenal function. Acidosis increased the fundic tone as reflected by a decrease in barostat volumes from 275+/-83 to 194+/-88 mL for MA and from 278+/-93 to 236+/-106 mL for RA. Pyloric and duodenal basal tones were not affected by either acidosis. A decrease in pyloric contraction amplitude from 95+/-24 to 62+/-26 mm Hg during MA and from 94+/-26 to 64+/-20 mm Hg during RA was observed. Both acidosis altered antral control activity that became dysrhythmic. Acidosis could be implicated in perioperative complications, such as gastroparesis, emesis, and regurgitation of gastric contents. IMPLICATIONS: Metabolic and respiratory acidosis mainly affects gastric antral rhythms and has a major effect on fundic tone. Acidosis could be implicated in perioperative complications, such as gastroparesis, emesis, and regurgitation of gastric contents.

Acidosis↗
PubMed1993

Role of protein kinase C in the adaptive increase in Na-H antiporter in respiratory acidosis.

Chronic respiratory acidosis stimulates the Vmax of the renal brush border Na-H antiporter. The activation of protein kinase C (PKC) by phorbol esters stimulates the activity of the renal Na-H antiporter. In this study, the hypothesis that PKC plays a role in the adaptive increase of the renal brush border Na-H antiporter activity to respiratory acidosis was tested. In vivo respiratory acidosis was associated with an increase in in vitro Na-H antiporter activity and also with an increase in brush border membrane PKC activity, without changes in PKC activity in cytosol or basolateral membranes. Na-H antiporter activity, assessed as the amiloride-sensitive component of 22Na uptake, was measured in cultured proximal tubule cells exposed to 10% CO2 for 48 h. Na-H antiporter activity was significantly higher in cells exposed to 10% CO2 than in those exposed to 5% CO2. To evaluate the role of PKC, cultured cells were depleted of PKC by exposure to the active phorbol ester phorbol 12-myristate 13-acetate (PMA; 10(-7) or 10(-6) M) for 48 h before exposure to 10% CO2. In the presence of 10% CO2, Na-H antiporter activity was significantly lower in PKC-depleted cells than in control. In addition, sphingosine, an inhibitor of PKC, also prevented the adaptation of the Na-H antiporter to 10% CO2 as compared with 5% CO2. In cells treated with the inactive analog 4 alpha-PMA, 22Na uptake was not different than that in control. PMA-treated cells also had a decrease in Na-H antiporter activity during exposure to 5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1990

[Water-electrolyte and acid-base disorders. VIII. Respiratory acidosis].

Acute respiratory acidosis will result from many processes that acutely interfere with the excretion of CO2 by the lungs. CO2 excretion by the lungs can be interfered with by processes that inappropriately decrease minute ventilation, processes that impair the transport of CO2 from the site of production to the lungs for export, and by processes that impair the transfer of CO2 from the blood through the alveolar space to the atmosphere. The underlying clinical syndrome generating the primary hypercapnia will determine the duration of the acidosis as well as the anticipated clinical manifestations attributable to the acidosis.

Acidosis, Respiratory↗
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↗
PubMed1984

Effects of 'DIDS', an anion transport blocker, on CSF [HCO3-] in respiratory acidosis.

During acute respiratory acidosis increments in cisternal cerebrospinal fluid (CSF) [HCO3-] approximate decrements in CSF [Cl-] with CSF [Na+] remaining unchanged; the mechanisms mediating this reciprocal anionic relationship are unclear. In the present study we investigated the effects of DIDS (4,4'-diisothiocyano-disulfonic stilbene), a known inorganic anion exchange blocker, on CSF ionic regulation in acute respiratory acidosis. In two groups of anesthetized paralyzed dogs we injected either mock CSF (group I, n = 8) or mock CSF containing DIDS (group II, n = 9) into the lateral cerebral ventricles. After 45 min, acute respiratory acidosis was induced for 6 h. During acute respiratory acidosis, CSF PCO2 rose in average by 38 mm Hg in both groups; increments in CSF [HCO3-], however, were significantly lower by about 2 mEq/L in DIDS-treated animals than in controls throughout the experimental period. Such differences were not due to changes in CSF lactate concentration which were similar in both groups. Furthermore, CSF [Na+] remained unchanged in both groups. Since disulfonic stilbene derivatives combine selectively with the carrier involved in anion transport and inhibit inorganic anion exchange, the data in the present study suggest that in the central nervous system a DIDS-inhibitable carrier is involved in the rise of CSF [HCO3-] observed during acute respiratory acidosis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2004

Role of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog.

Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased (P < 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater (P < 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater (P < 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by > 0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded (P < 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.

Acidosis↗
PubMed1991

Myocardial uptake and pharmacodynamics of quinidine and propafenone in isolated rabbit hearts: metabolic versus respiratory acidosis.

The influence of metabolic and respiratory acidosis on the myocardial accumulation and pharmacodynamics of quinidine and propafenone was studied in isolated perfused rabbit hearts. Three pH groups were evaluated: physiologic buffer, pH 7.4; metabolic acidosis, pH 7.0; and respiratory acidosis, pH 7.0. Myocardial accumulation of quinidine and propafenone was significantly reduced during acidosis. Although myocardial quinidine concentrations were similar in the metabolic acidosis group (14.4 +/- 1.2 micrograms/g) and the respiratory acidosis group (14.5 +/- 1.3 micrograms/g), the myocardial propafenone concentration was significantly less during metabolic acidosis (8.9 +/- 2.0 micrograms/g) as compared with respiratory acidosis (12.7 +/- 2.4 micrograms/g, p less than 0.05). The myocardial concentration-effect relationships were linear over the observed myocardial concentration ranges. The slopes of the linear concentration-effect relationships describing QRS duration were increased twofold by both types of acidosis as compared with normal pH (p less than 0.05). In contrast, the slopes of the concentration-effect relationships describing changes in ventricular repolarization and refractoriness were increased only during metabolic acidosis as compared with pH 7.4 (p less than 0.05). Thus, for any given concentration of drugs, the effects of quinidine and propafenone on ventricular conduction time are dependent on the pH of the perfusate, whereas these drug effects on ventricular repolarization and refractoriness are dependent on the buffer composition.

Acidosis↗
PubMed1992

Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs.

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.

Acidosis, Respiratory↗
PubMed1989

Hydrochloric acid infusion for treatment of metabolic alkalosis associated with respiratory acidosis.

Hypercapnia due to respiratory failure can be more severe when accompanied by coexistent metabolic alkalosis. We therefore tested the hypothesis that hydrochloric acid (HCl) infusion could improve PaCO2 in 15 critically ill patients admitted with mixed respiratory acidosis and metabolic alkalosis, and a pH of between 7.35 and 7.45. HCl was infused at a constant rate of 25 mmol/h until the bicarbonate concentration decreased less than 26 mmol/L, or until the pH decreased less than 7.35 (initial pH greater than 7.40) or 7.30 (initial pH less than 7.40). Administration of 170 +/- 53 mmol of HCl decreased the bicarbonate concentration from 34 +/- 3 to 25 +/- 2 mmol/L (p less than .001), the pH from 7.41 +/- 0.03 to 7.33 +/- 0.02 (p less than .001), and the PaCO2 from 54 +/- 8 to 48 +/- 8 torr (p less than .001). Postinfusion PaCO2 could be predicted accurately from the initial status of the patients (r = .95, p less than .001) except in one patient with fixed hypercapnia. PaCO2 increased from 77 +/- 19 to 94 +/- 24 torr (p less than .001) and PaO2/PAO2 increased from 59 +/- 17 to 66 +/- 17% (p less than .001). The effects of HCl were still present 12 h after the end of the infusion. No complications related to the acid infusion were noted. These results indicate that, even in the absence of alkalemia, active correction of metabolic alkalosis by HCl infusion can improve CO2 and oxygen exchange in critically ill patients with mixed respiratory acidosis and metabolic alkalosis.

Acidosis, Respiratory↗
PubMed1985

Adaptive changes in renal acidification in response to chronic respiratory acidosis.

To examine whether chronic respiratory acidosis results in adaptive changes in renal acidification, rats were housed for 3 days in an environmental chamber with an ambient CO2 content of 10% and their kidneys were perfused in vitro according to two protocols. To assess hydrogen ion secretory capacity of the distal nephron, perfusions were carried out with a low bicarbonate concentration, in the absence of ammoniagenic substrate, and with saturating quantities of the buffer creatinine. Under these conditions, the titration of creatinine at a pH less than 6.0 (TA pH 6.0) reflects the H+ secretory capacity of a discrete functional segment of the distal nephron. Kidneys from rats with chronic respiratory acidosis exhibited a significantly lower urine pH and higher rate of TA pH 6.0 than controls perfused in this fashion, indicative of an adaptive increase in the distal nephron capacity for proton transport. This adaptation was comparable with that reported previously for rats exposed to chronic metabolic acidosis. Furthermore, evidence of adaptation persisted in the presence of amiloride (10(-5) M), suggesting that it reflects, at least in part, a sodium-independent mechanism of proton transport. Hydrogen ion secretion by the proximal nephron was assessed by performing standard bicarbonate titration curves with kidneys from rats with chronic respiratory acidosis, chronic metabolic acidosis, and controls using a perfusate equilibrated with 95% O2/5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1976

Plasma renin activity in acute respiratory acidosis.

Plasma renin activity in acute respiratory acidosis and the effect of hexamethonium bromide was studied. Fourteen mongrel dogs were anesthetized with sodium pentobarbiturate and given 5% and 15% carbon dioxide in room air, successively. Hexamethonium bromide was given to 8 dogs prior to carbon dioxide inhalation. Arterial carbon dioxide partial pressure, oxygen partial pressure and pH were measured in addition to the determination of plasma renin activity. Plasma renin activity was elevated in moderate respiratory acidosis induced by 5% carbon dioxide inhalation from 37.5 +/- 8.8 ng/ml to 52.8 +/- 7.0 ng/ml. In severe respiratory acidosis produced by 15% carbon dioxide inhalation, plasma renin activity elevated further to 85.8 +/- 8.6 ng/ml. Plasma renin activity of the hexamethonium bromide treated dogs was 19.0 +/- 3.5 ng/ml during room air breathing. The activity was elevated to 26.0 +/- 6.4 ng/ml by 5% carbon dioxide inhalation and further to 57.3 +/- 5.9 ng/ml by 15% carbon dioxide inhalation. These findings may suggest that the elevation of plasma renin activity in acute respiratory acidosis induced by carbon dioxide inhalation is independent from sympathetic stimulation.

Acidosis, Respiratory↗
PubMed1998

Regulation of renal Na-HCO3 cotransporter: VIII. Mechanism Of stimulatory effect of respiratory acidosis.

We examined the effect of respiratory acidosis on the Na-HCO3 cotransporter activity in primary cultures of the proximal tubule of the rabbit exposed to 10% CO2 for 5 min, 2, 4, 24 and 48 hr. Cells exposed to 10% CO2 showed a significant increase in Na-HCO3 cotransporter activity (expressed as % of control levels, 5 min: 142 +/- 6, 2 hr: 144 +/- 13, 4 hr: 145 +/- 11, 24 hr: 150 +/- 15, 48 hr: 162 +/- 24). The increase in activity was reversible after 48 hr. The role of protein kinase C (PKC) on the stimulatory effect of respiratory acidosis on the cotransporter was examined in presence of PKC inhibitor calphostin C or in presence of PKC depletion. Both calphostin C and PKC depletion prevented the effect of 10% CO2 for 5 min or 4 hr to increase the activity of the cotransporter. 10% CO2 for 5 min or 4 hr increased total and particulate fraction PKC activity. To examine the role of phosphotyrosine kinase (PTK) on the increase in cotransporter activity we studied the effect of two different inhibitors, 2-hydroxy-5-(2,5-dihydroxylbenzyl) aminobenzoic acid (HAC) and methyl 2,5-dihydroxycinnamate (DHC) which inhibit phosphotyrosine kinase in basolateral membranes. Cells were pretreated either with vehicle or HAC or DHC and then exposed to 10% CO2 for 5 min or 4 hr. In cells treated with vehicle, 10% CO2 significantly increased cotransporter activity as compared to control cells exposed to 5% CO2. This stimulation by 10% CO2 was completely prevented by HAC or DHC at 5 min (5% CO2: 1.8 +/- 0.2, 10% CO2: 2.6 +/- 0.2, 10% CO2 + HAC: 1.6 +/- 0.2, 10% CO2: +DHC: 2.0 +/- 0.3 pH unit/min) and also at 4 hr. The protein synthesis inhibitors actinomycin D and cycloheximide appear to prevent the effect of 10% CO2 for 4 hr on the cotransporter. Our results show that early respiratory acidosis stimulates the Na-HCO3 cotransporter through PKC and PTK-dependent mechanisms and the late effect appears to be mediated through protein synthesis.

Acidosis, Respiratory↗
PubMed2001

Metabolic, but not respiratory, acidosis increases bone PGE(2) levels and calcium release.

A decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO(3)(-)]; metabolic acidosis) or to an increase in PCO(2) (respiratory acidosis). In mammals, metabolic, but not respiratory, acidosis increases urine calcium excretion without altering intestinal calcium absorption, indicating that the additional urinary calcium is derived from bone. In cultured bone, chronic metabolic, but not respiratory, acidosis increases net calcium efflux (J(Ca)), decreases osteoblastic collagen synthesis, and increases osteoclastic bone resorption. Metabolic acidosis increases bone PGE(2) production, which is correlated with J(Ca), and inhibition of PGE(2) production inhibits this acid-induced J(Ca). Given the marked differences in the osseous response to metabolic and respiratory acidosis, we hypothesized that incubation of neonatal mouse calvariae in medium simulating respiratory acidosis would not increase medium PGE(2) levels, as observed during metabolic acidosis. To test this hypothesis, we determined medium PGE(2) levels and J(Ca) from calvariae incubated at pH approximately 7.1 to model either metabolic (Met; [HCO(3)(-)] approximately 11 mM) or respiratory (Resp; PCO(2) approximately 83 Torr) acidosis, or at pH approximately 7.5 as a control (Ntl). We found that after 24-48 and 48-51 h in culture, periods when cell-mediated J(Ca) predominates, medium PGE(2) levels and J(Ca) were increased with Met, but not Resp, compared with Ntl, and there was a direct correlation between medium PGE(2) levels and J(Ca). Thus metabolic, but not respiratory, acidosis induces the release of bone PGE(2), which mediates J(Ca) from bone.

Acidosis↗
PubMed1999

In vitro metabolic and respiratory acidosis selectively inhibit osteoblastic matrix gene expression.

Clinically, a decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO(-)(3)], metabolic acidosis) or an increase in PCO(2) (respiratory acidosis). In mammals, metabolic acidosis induces a far greater increase in urine calcium excretion than respiratory acidosis. In cultured bone, metabolic acidosis induces a marked increase in calcium efflux and a decrease in osteoblastic collagen synthesis, whereas isohydric respiratory acidosis has little effect on either parameter. We have shown that metabolic acidosis prevents the normal developmental increase in the expression of RNA for matrix Gla protein and osteopontin in chronic cultures of primary murine calvarial bone cells (predominantly osteoblasts) but does not alter expression of osteonectin. To compare the effects of isohydric metabolic and respiratory acidosis on expression of these genes, bone cell cultures were incubated in medium at pH approximately 7.2 to model metabolic ([HCO(-)(3)], approximately 13 mM) or respiratory (PCO(2), approximately 80 mmHg) acidosis or at pH approximately 7.4 as a control. Cells were sampled at weeks 4, 5, and 6 to assess specific RNA content. At all time periods studied, both metabolic and respiratory acidosis inhibited the expression of RNA for matrix Gla protein and osteopontin to a similar extent, whereas there was no change in osteonectin expression. In contrast to the significant difference in the effects of metabolic and respiratory acidosis on bone calcium efflux and osteoblastic collagen synthesis, these two forms of acidosis have a similar effect on osteoblastic RNA expression of both matrix Gla protein and osteopontin. Thus, although several aspects of bone cell function are dependent on the type of acidosis, expression of these two matrix genes appears to be regulated by extracellular pH, independently of the type of acidosis.

Acidosis↗