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PubMed1990

Betaxolol, a cardioselective beta-adrenoceptor antagonist, attenuates ischemic myocardial acidosis in dogs.

The effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on ischemic myocardial acidosis were studied in dog hearts, in which the left anterior descending coronary artery was partially occluded for 90 min, and were compared with those of atenolol and propranolol. Myocardial ischemia produced a decrease in myocardial pH (measured by a micro glass pH electrode) and an elevation of the ST segment of epicardial ECG (assessed by a surface electrode). Betaxolol (0.01, 0.03 or 0.1 mg/kg), atenolol (0.03 or 0.1 mg/kg) or propranolol (0.03 or 0.1 mg/kg), when injected i.v. 30 min after ischemia, restored myocardial pH and the ST segment of ECG that had been altered by partial occlusion. However, the effect of betaxolol on myocardial acidosis was more potent than that of atenolol or propranolol. The decrease in (+)dp/dt by betaxolol (0.03 mg/kg) was less potent than that by atenolol (0.1 mg/kg) and equivalent to that by propranolol (0.1 mg/kg), although the restorations of myocardial acidosis by the drugs were almost equivalent. These results have confirmed that beta-adrenoceptor antagonists attenuate the ischemia-induced myocardial acidosis and have shown that among three beta-adrenoceptor antagonists, betaxolol is the most effective in improving myocardial acidosis with a relatively weak effect on myocardial contractile function.

Acidosis↗
PubMed1989

Umbilical cord blood coagulability, acidosis and intracranial hemorrhage.

The relationship between blood pH and blood coagulability and alternations in the fibrinolytic system was studied using blood samples obtained from the umbilical artery of 178 cases. Further studies were performed on this relationship in 5 cases of intracranial hemorrhage detected by ultrasonography, and the following results were obtained: 1. A definitely significant correlation was noted between the hepaplastin value and blood pH and these values markedly decreased in the acidosis group. 2. Changes in FDPs and SFMC were not so obvious as changes in the hepaplastin values, but activation of the fibrinolytic system was noted in the acidosis group. 3. No consistent finding was obtained with respect to changes in At-III. 4. Among five cases of intracranial hemorrhage, abnormalities in the coagulation and fibrinolytic system were noted in cases of acidosis, indicating that presence of acidosis is associated with severe intracranial hemorrhage. 5. The necessity of future studies on biochemical changes during acidosis was discussed.

Acid-Base Equilibrium↗
PubMed2003

Lactic acidosis related to nucleoside therapy in HIV-infected patients.

The incidence of nucleoside analogue-related lactic acidosis has been estimated in 0.57 - 8.5 cases/1000 person years of antiretroviral therapy. The onset of lactic acidosis is usually insidious and patients complain of nausea, vomiting, abdominal pain, fatigue and weight loss. When lactate levels are high enough, a catastropic clinical situation develops, resulting in multiorgan failure. The mortality rate of patients with lactic acidosis related to nucleoside therapy is very high, 33 - 60%. Although all nucleoside analogues have been implicated in lactic acidosis, most cases are associated with stavudine. At present, there are no controlled trials to evaluate the treatment of nucleoside-induced lactic acidosis. Therapy is based on supportive measures and discontinuation of all antiretroviral drugs. Administration of essential vitamin coenzymes, electron acceptors and L-carnitine may be useful in some cases.

Acidosis, Lactic↗
PubMed2006

A dynamic model of excitation-contraction coupling during acidosis in cardiac ventricular myocytes.

Acidosis in cardiac myocytes is a major factor in the reduced inotropy that occurs in the ischemic heart. During acidosis, diastolic calcium concentration and the amplitude of the calcium transient increase, while the strength of contraction decreases. This has been attributed to the inhibition by protons of calcium uptake and release by the sarcoplasmic reticulum, to a rise of intracellular sodium caused by activation of sodium-hydrogen exchange, decreased calcium binding affinity to Troponin-C, and direct effects on the contractile machinery. The relative contributions and concerted action of these effects are, however, difficult to establish experimentally. We have developed a mathematical model to examine altered calcium-handling mechanisms during acidosis. Each of the alterations was incorporated into a dynamical model of pH regulation and excitation-contraction coupling to predict the time courses of key ionic species during acidosis, in particular intracellular pH, sodium and the calcium transient, and contraction. This modeling study suggests that the most significant effects are elevated sodium, inhibition of sodium-calcium exchange, and the direct interaction of protons with the contractile machinery; and shows how the experimental data on these contributions can be reconciled to understand the overall effects of acidosis in the beating heart.

Acidosis↗
PubMed1978

Effect of oral administration of calcium carbonate, aluminum hydroxide gel and dihydrotachysterol on renal acidosis.

The effects of oral administration of calcium carbonate, aluminum hydroxide gel, dihydrotachysterol (DHT) and sodium bicarbonate on metabolic acidosis and plasma calcium and phosphate were studied in 7 patients with chronic renal failure. Single administration of calcium carbonate alleviated the acidosis and increased the urinary bicarbonate excretion. These effects were potentiated when aluminum hydroxide gel was administered in combination with calcium carbonate. The plasma calcium was increased by this combination therapy. The effects of these two agents on acidosis and plasma calcium were further enhanced by the additional administration of DHT. Urinary bicarbonate excretion was less during the treatment with aluminum hydroxide gel and calcium carbonate than with aluminum hydroxide gel and sodium bicarbonate, when the excretions were compared at the similar concentrations of plasma bicarbonate. Aluminum hydroxide gel and DHT are likely to enhance the effect of calcium carbonate, which works as an alkalinizing salt on acidosis, probably through increasing calcium absorption in the intestine. And the three agents suppress the leak of bicarbonate into the urine contributing to the improvement of acidosis.

Acidosis↗
PubMed2001

Regulation of apoA1 gene expression with acidosis: requirement for a transcriptional repressor.

Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. Mutation of the nTRE/pH-RE abrogates protein binding and alters the activity of reporter genes controlled by this element. Repression by acidosis did not require de novo mRNA and protein synthesis. Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation.

Acidosis↗
PubMed2001

Upregulation of the secretory-type Na(+)/K(+)/2Cl(-)-cotransporter in the kidney by metabolic acidosis and dehydration in rats.

The functional role and mechanisms of regulation of the Na(+)/K(+)/2Cl(-)-cotransporter NKCC1 in the kidney have not yet been clarified. NKCC1 mRNA and protein expression in control rats, rats with dehydration (2 d), and rats with metabolic acidosis (NH(4)Cl in the food for 6 to 7 d) was examined using reverse transcription-PCR and Western blotting. In contrast to the abundant NKCC1 mRNA expression in the terminal inner medullary collecting ducts in mice, expression was found to be most abundant in the outer medullary collecting ducts (OMCD) in rats. Dehydration and metabolic acidosis increased NKCC1 mRNA expression three- to fivefold not only in the OMCD but also in the cortical collecting ducts and inner medullary collecting ducts. Dehydration and metabolic acidosis increased NKCC1 protein expression twofold in the membrane fraction from the outer medulla. NKCC1 protein expression was observed not in the microdissected medullary thick ascending limbs but in the OMCD, and it was stimulated twofold by dehydration and metabolic acidosis. Incubation of OMCD in low-pH medium increased NKCC1 mRNA expression. In summary, NKCC1 mRNA and protein expression is upregulated with dehydration and metabolic acidosis. NKCC1 may play an important role in adaptation to these physiologic conditions. Low pH and possibly hypertonicity stimulate NKCC1 mRNA expression in OMCD.

Acidosis↗
PubMed1997

Correction of acidosis in hemodialysis decreases whole-body protein degradation.

Correction of acidosis in hemodialysis (HD) decreases protein degradation. The effect of the correction of chronic metabolic acidosis in chronic renal failure patients treated with HD was determined from the kinetics of infused L-[1-(13)C]leucine. Six HD patients were studied before (acid) and after (bicarbonate) correction of acidosis (pH: acid 7.36 +/- 0.01, bicarbonate 7.40 +/- 0.01, P < 0.005). Leucine appearance from body protein (PD) and leucine disappearance into body protein (PS) decreased significantly with correction of acidosis (PD: acid 180.6 +/- 7.3, bicarbonate 130.9 +/- 7.2 mumol.kg-1.h-1, P < 0.005; PS: acid 172.3 +/- 6.8, bicarbonate 122.0 +/- 6.8 mumol.kg-1.h-1, P < 0.005). There was no significant change in leucine oxidation or plasma amino acid concentrations. These results demonstrate that optimal correction of acidosis in HD is beneficial in terms of protein turnover and may improve long-term nutritional status in HD.

Acidosis↗
PubMed1985

Lactic acidosis and hypoglycemia associated with acute leukemia.

A 42-year-old man was admitted because of episodic attack of general malaise. He was lethargic and had a severe lactic acidosis and hypoglycemia. Blood chemistry and endocrinological data were normal. Glucose administration led to an improvement in the hypoglycemia but not the lactic acidosis. At autopsy, there was a massive infiltration of leukemic cells in both kidneys and in liver. Phosphoenolpyruvate carboxykinase, pyruvate carboxylase and glucose-6-phosphatase activities in patient's liver were much the same as in the control liver, but fructose-1, 6-diphosphatase activity was slightly reduced. Since circulatory failure was absent, type B lactic acidosis has to be considered. Since hypoglycemia was associated with acidosis, the severe lactic acidosis in our patient may have been due to an overproduction of lactic acid as well as to an impaired hepatic gluconeogenesis in the presence of leukemic cells.

Acidosis↗
PubMed2005

[Distal renal tubular acidosis as a cause of osteomalacia in a patient with primary Sjögren's syndrome].

BACKGROUND: One half of the patients with primary Sjögren's syndrome has extraglandular manifestations, including renal involvement. The most frequent renal lesion is tubulo-interstitial nephritis, which manifests clinically as distal tubular acidosis and may result in the development of osteomalacia. CASE REPORT: In a 29-year-old female patient, with bilateral nephrolithiasis, the diagnosis of primary Sjögren's syndrome, tubulo-interstitial nephritis, distal renal tubular acidosis, and hypokalemia were established. She was treated for hypokalemia. Two years later she developed bone pains and muscle weakness, she wasn't able to walk, her proximal muscles and pelvic bones were painful, with radiological signs of pelvic bones osteopenia and pubic bones fractures. The diagnosis of osteomalacia was established and the treatment started with Schol's solution, vitamin D and calcium. In the following two months, acidosis was corrected, and the patient started walking. CONCLUSION: In our patient with primary Sjögren's syndrome and interstitial nephritis, osteomalacia was a result of the long time decompensate acidosis, so the correction of acidosis, and the supplementation of vitamin D and calcium were the integral part of the therapy.

Acidosis, Renal Tubular↗
PubMed2006

Effect of changes in ionized calcium concentration in arterial blood and metabolic acidosis on the arterial partial pressure of oxygen in dogs.

OBJECTIVE: To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca2+) concentration on PaO2 in dogs. ANIMALS: 33 anesthetized dogs receiving assisted ventilation. PROCEDURE: Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO2, Ca2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. RESULTS: In group II, PaO2 increased from baseline value (96 +/- 2 mm Hg) within 10 minutes (pHa, 7.33 +/- 0.001); at 60 minutes (pHa, 7.21 +/- 0.02), PaO2 was 108 +/- 2 mm Hg. For the same pHa decrease, the PaO2 increase was less in group III. In group I, hypocalcemia caused PaO2 to progressively increase (from 95 +/- 2 mm Hg to 104 +/- 3 mm Hg), which correlated (r = -0.66) significantly with a decrease in systolic blood pressure (from 156 +/- 9 mm Hg to 118 +/- 10 mm Hg). Parathyroidectomy did not alter PaO2 values. CONCLUSIONS AND CLINICAL RELEVANCE: Induction of hypocalcemia and metabolic acidosis each increased PaO2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.

Acidosis↗
PubMed1995

The effects of ruminal acidosis on volatile fatty acid absorption and plasma activities of pancreatic enzymes in lambs.

Twenty crossbred wethers (41.9 +/- 4.0 kg BW), each fitted with a ruminal cannula and a jugular catheter, were used in a completely randomized design to examine the effects of ruminal acidosis on plasma activities of pancreatic enzymes and fractional rates of VFA absorption. Lambs had ad libitum access to a 50% concentrate diet. Acidosis was induced by an intraruminal dose of glucose at 0, 6, 12, or 18 g/kg BW via the ruminal cannula. Ruminal fluid and plasma were collected 0, 4, 8, 12, 18, 24, 36, 48, and 72 h after dosing. Ruminal fluid pH was reduced (linear, P < .001) with increasing ruminal glucose. Total ruminal VFA concentration decreased (linear, P < .01) and D(-)-lactate (linear, P < .01) and L(+)- lactate (linear, P = .07) concentrations increased with increasing ruminal glucose. Activities of amylase and lipase in plasma were not affected by ruminal glucose (P > .10). Ten days after the acidosis insult, rumens were evacuated and contents were replaced with an isotonic Cr:VFA solution to measure ruminal VFA absorption. Ruminal fluid was collected hourly from 0 to 6 h. Fractional rate of acetate absorption was 13% lower for lambs receiving 18 g/kg BW glucose than for control lambs. In addition, fractional liquid passage rate was lower (P < .05) in lambs receiving 18 g/kg BW glucose 6 mo after the insult of acidosis. These data suggest that a short-term, severe insult of acute acidosis does not result in pancreatic tissue damage but may result in reduced ruminal VFA absorption for an extended period of time.

Absorption↗
PubMed1995

Efficacy of laidlomycin propionate to reduce ruminal acidosis in cattle.

Three trials were conducted to evaluate the efficacy of laidlomycin propionate (LP) to reduce the incidence and severity of ruminal acidosis in cattle fed high-grain finishing diets. In each trial, LP was fed at 0, 6, or 12 mg/kg of diet DM. In two acidosis-challenge trials, ruminally fistulated steers were fed (DM basis) a 50% concentrate diet and then fed a 95% concentrate diet at a specific intake (2.75% BW) or steers were dosed intraruminally with a 100% concentrate diet. Laidlomycin propionate did not alter ruminal pH or total acid concentrations, but in Trial 1 the 6 mg/kg level altered (P < .10) the molar proportions of the acids, increasing total ruminal VFA and decreasing ruminal lactate. In Trial 3, a finishing trial, LP reduced (P < .10) intake day-to-day variation of individually fed steers during a 13-d adaptation period from a 65 to a 100% concentrate diet, suggesting reduced incidence of subacute acidosis. Feed intake was lower (P < .05) during the first 13 d of the trial due to LP but was not affected over the entire trial. Laidlomycin propionate improved feed efficiency (gain/feed) when calculated on a live weight basis (linear, P = .05) or carcass weight basis (linear, P = .20). Laidlomycin propionate does not prevent ruminal acidosis, but it may reduce the severity of ruminal acidosis during adaptation to a 100% concentrate diet.

Acidosis↗
PubMed1999

Effect of chronic metabolic acidosis on renal growth and renal sodium handling in uninephrectomized rats.

Paucity studies have indicated that a systemic metabolic acidosis cause a decrease in salt and water reabsorption in the kidney. The following study was undertaken on male Wistar-Hannover rats (200-250 g) to investigate the effects of a chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in sham-operated and uninephrectomized rats, by lithium clearance. The present study shows that chronic acidosis (blood pH, 7.16 +/- 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 +/- 36.4%), accompanied by a rise in the fractional proximal (113.3 +/- 3.6%) and post-proximal (179.7 +/- 20.2%) Na+ and fractional K+ (163.4 +/- 5.6%) excretions when compared to pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. On the other hand, a body growth impairment was observed in the acidotic (control, 258 +/- 3.7 g versus acidotic, 232 +/- 4.6 g) and pair-fed rats (225 +/- 3.6 g), whereas there was significant enhance in the kidney weights in acidotic rats (1.73 +/- 0.05 g) compared to other experimental groups (control, 1.46 +/- 0.05 g; pair-fed, 1.4 +/- 0.05 g). The renal growth indexes after metabolic acidosis NH4Cl-induced did not shown statistical difference at 1.5, 3.0 and 12 hours after uninephrectomy when were compared with pair-fed groups. However, from the fifth to tenth day after unilateral nephrectomy the renal growth index of acidotic group was significantly greater than pair-fed groups. Unilateral nephrectomy in acidotic animals caused a striking additional but transient increase in fractional renal sodium (FENa+) and potassium (FEK+) excretion from 1.5 to 3 hours post-surgery meanly associated with an enhanced post-proximal sodium excretion when compared to pair-fed uninephrectomized rats. By the fifth postoperative day the all functional values returned to baseline levels. This altered renal Na+ handling and K+ excretion may result from a reciprocal relationship between tubular metabolic pathway stimuli and ion transport. Further studies are required to investigate the acidosis involvement on functional kidney response.

Acidosis, Renal Tubular↗
PubMed1978

Effect of acidosis on heart cAMP-dependent protein kinase.

The effect of acidosis on cAMP-dependent protein kinase activity in perfused hearts from normal and reserpinized rats has been investigated. The results were compared to the effect of acidosis on myocardial contractility under the same conditions. The results showed that acidosis increases the cAMP-dependent protein kinase activity in normal hearts. This increase was abolished when the hearts were depleted of norepinephrine by previous treatment with reserpine. As regards myocardial contractility, there was a similar decrease by acidosis either in normal hearts with increased cAMP-dependent protein kinase activity or in reserpinized hearts in which the increase in protein kinase activity was prevented. Two alternative hypotheses are suggested: (1) a dissociation between contractility and cAMP levels, or (2) a "blockade" by acidosis of the mechanical effect of increasing cAMP-dependent protein kinase activity.

Acidosis↗
PubMed1997

Bovine acidosis: implications on laminitis.

Bovine lactic acidosis syndrome is associated with large increases of lactic acid in the rumen, which result from diets that are high in ruminally available carbohydrates, or forage that is low in effective fiber, or both. The syndrome involves two separate anatomical areas, the gastrointestinal tract and body fluids, and is related to the rate and extent of lactic acid production, utilization, and absorption. Clinical manifestations range from loss of appetite to death. Lactic acid accumulates in the rumen when the bacteria that synthesize lactic acid outnumber those that utilize lactic acid. The systemic impact of acidosis may have several physiological implications, including laminitis, a diffuse aseptic inflammation of the laminae (corium). Although a nutritional basis for the disease exists, etiology includes a multitude of interactive factors, such as metabolic and digestive disorders, postpartum stress, and localized trauma, which lead to the release of vasoactive substances that trigger mechanisms that cause degenerative changes in the foot. The severity of laminitis is related to the frequency, intensity, and duration of systemic acidotic insults on the mechanisms responsible for the release of vasoactive substance. The critical link between acidosis and laminitis appears to be associated with a persistent hypoperfusion, which results in ischemia in the digit. Management of acidosis is critical in preventing laminitis. High producing dairy herds attempting to maximize energy intake are continually confronted with subclinical acidosis and laminitis. Management of feeding and husbandry practices can be implemented to reduce incidence of disease.

Acidosis, Lactic↗
PubMed2001

Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion.

The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's Glasgow Coma Scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.

Acidosis↗
PubMed1987

Morphological changes in the skin of Rana pipiens in response to metabolic acidosis.

The skin of Rana pipiens excretes H+ and this excretion is increased by metabolic acidosis. The mitochondria-rich (MR) cells of the skin have been found to mediate this H+ transport. The purpose of this study was to determine if there is a change in the MR cells of the skin during metabolic acidosis and if the isolated split epithelia of frog skin maintains its capacity to excrete H+. Metabolic acidosis was induced by injecting 120 mM NH4Cl (0.025 ml/g body wt) into the dorsal lymph sac three times a day for 2 days. The frogs were sacrificed and collagenase-split skins from the abdomen of normal and metabolic acidotic frogs were mounted between 2-ml chambers. H+ fluxes into both the mucosal and serosal media were measured and reported in units of (nmol) (cm2)-1 (min)-1. An increase in H+ flux was seen on both the mucosal and serosal sides of the acidotic split skins. The isolated epithelia were fixed, postosmicated, and dehydrated in the chamber. They were then embedded in Spurr's resin and 1-micron sections were cut and stained with Paragon multiple stain. Coded slides were used to count various cell types. Sections were randomly selected and approximately 40,000 cells were counted. Four basic cell types were noted and confirmed by TEM photomicrographs; basal (B) cells, granular (G) cells, keratinized cells, and MR cells. The ratio of G + B cells:MR cells in the normal skins was 1.0:0.021. The ratio in acidotic skins was 1.0:0.34. The average percentage of cell population of MR cells in the normal skins was 2.08 + 0.18 and in acidotic skins 3.20 + 0.36 (P less than 0.005). We conclude that the split skin maintains the capacity to acidify the mucosal fluid. Additionally, during metabolic acidosis there is an increased number of MR cells in the skin and this increase may be an adaptive mechanism of the skin to excrete excess H+ during acidosis.

Acidosis↗