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PubMed2001

Histologic and dynamic changes induced by chronic metabolic acidosis in the rat growth plate.

To understand better the pathophysiology of growth impairment in persistent metabolic acidosis, the morphology and dynamics of the growth plate were studied in young rats grouped as follows: rats that were made acidotic by oral administration of ammonium chloride for 14 d (AC), nonacidotic rats that were fed ad libitum (control [C]), and nonacidotic rats that were pair-fed with the AC group (PF). AC rats became markedly acidotic and growth retarded. The volume of newly formed bone per day (mean +/- SEM) was significantly lowered (P < 0.05) in AC rats (AC, 3.4 +/- 0.4; C, 8.4 +/- 0.6; PF, 6.4 +/- 0.5 mm(3)/d). Growth plate height was lower in AC rats (303.8 +/- 12.7 microm) than in either C (478.0 +/- 16.0 microm) or PF rats (439.0 +/- 21.4 microm). The processes of chondrocyte proliferation (assessed by bromodeoxyuridine labeling) and maturation (assessed by stereologic estimators of size and shape of chondrocytes and the volume of matrix per cell) were not impaired by acidosis. By contrast, the dynamics of hypertrophic chondrocytes were altered significantly: both cell turnover per column per day (AC, 4.4 +/- 0.4; C, 8.0 +/- 0.8; PF, 6.2 +/- 0.6) and linear velocity of advance of chondrocytes (AC, 5.7 +/- 0.5; C, 11.2 +/- 0.9; PF, 9.4 +/- 0.8 microm/h) were lowered significantly. The study presented here shows the inhibitory effect of metabolic acidosis on cartilage cell progression and endochondral bone formation. Finally, the data show that metabolic acidosis caused a marked shortening of the growth plate because chondrocyte turnover was affected to a greater extent than bone tissue formation.

Acidosis↗
PubMed2002

Acidosis mediates the upregulation of UT-A protein in livers from uremic rats.

Liver expresses a 49-kD UT-A protein whose abundance is increased by uremia. Chronic renal failure causes acidosis; therefore, the role of acidosis in increasing UT-A abundance was tested. Rats underwent 5/6 nephrectomy, and half were given bicarbonate mixed in their food. Bicarbonate administration significantly increased blood pH. Compared with sham-operated rats, UT-A protein abundance was significantly increased by 50% in livers from uremic, acidotic rats; bicarbonate administration prevented the increase in UT-A protein. To determine whether acidosis alone would increase UT-A protein in liver, rats were made acidotic, but not uremic, by feeding them HCl. HCl-feeding significantly lowered blood pH, increased urea excretion, and increased the abundance of the 49-kD liver UT-A protein by 36% compared with pair-fed nonacidotic rats. HCl-feeding significantly increased the abundance of the 117-kD UT-A1 protein in kidney inner medulla but did not change aquaporin-2 protein. Next, rats were fed urea to determine whether elevated blood urea would increase UT-A protein. However, urea feeding had no effect on UT-A in liver or kidney inner medulla. It was, therefore, concluded that acidosis, either directly or through a change in ammonium concentration, rather than other dietary components, stimulates the upregulation of UT-A protein in liver and kidney inner medulla.

Acidosis↗
PubMed1991

Cellular electrolyte and volume changes induced by acidosis in the rabbit proximal straight tubule.

Cellular acidosis induced either by high Pco2 or by low HCO3- concentrations has been shown to cause cell swelling in isolated, lumen-collapsed, S2 segments of the rabbit proximal tubule (Sullivan et al., Am J Physiol 1990; 258: F831-F839). The swelling is not followed by a volume regulatory response. The ionic basis of the swelling has been investigated by measurement of the cellular K+, Na+, and Cl- content (electron probe) and HCO3- concentration (pH-sensitive fluorescent dye). Cell content of K+, Na+, and Cl- was expressed as a ratio to P content. Exposure to 15% CO2 increased K/P from 0.98 to 1.16, Cl/P from 0.14 to 0.20, and Na/P from 0.09 to 0.11. Cell (HCO3-) increased from 22 to 32 mM. Reduction in bath (HCO3-) from 25 to 5 mM reduced cell (HCO3-) from 24 to 8 mM and increased K/P from 0.75 to 0.90. Na/P fell from 0.13 to 0.09, and Cl/P fell from 0.15 to 0.12. Thus, swelling resulting from acidosis induced by high CO2 was accompanied by an accumulation of K+, Cl-, and HCO3-; that resulting from acidosis induced by a fall in (HCO3-) was combined with an accumulation of K+ and an unidentified anion. To determine if the swelling induced by a fall in pH might be coupled with depolarization of the basolateral membrane, the effect of 1 mM barium was tested. Barium caused cell volume to increase 10.2%. Cell pH rose from 7.38 to 7.56, K/P increased from 0.63 to 0.73, Na/P did not change, and Cl/P rose from 0.17 to 0.20. Cell (HCO3-) increased 10.4 mM. When the pH of the barium-treated tissue was reduced to 7.02 by raising Pco2, additional cell swelling and accumulation of K+ occurred. The effect on cell volume of a reduction of bath (HCO3-) from 25 to 5 mM at constant bath pH was determined. Cell pH was not altered. Cell volume decreased 3% initially and then returned to the control level. When the bath (HCO3-) was restored to 25 mM, cell volume increased 3.9% and then returned to the baseline. Thus, volume regulation was not impaired. It was concluded that a fall in cell pH induces swelling, and this is coupled with an accumulation of K+. This is probably the result of a pH effect on barium-sensitive and barium-insensitive K+ conductance pathways. The nature of the anions that balance the gain in K+ depends on the means used to induce acidosis.

Acidosis, Renal Tubular↗
PubMed1992

On the mechanism of impaired distal acidification in hyperkalemic renal tubular acidosis: evaluation with amiloride and bumetanide.

It has been postulated that a distinctive type of hyperkalemic distal renal tubular acidosis (DRTA), referred to as voltage-dependent DRTA, results from diminished potassium and hydrogen ion secretion in the distal nephron, which is due to a suboptimal voltage (lumen negative) as a result of impaired sodium reabsorption. To test for the presence of a voltage-dependent DRTA, we used amiloride (20 mg oral, single dose) and bumetanide (2 mg oral, single dose) to inhibit and to stimulate voltage-dependent potassium and hydrogen ion secretion, respectively. Eighteen patients with hyperkalemic DRTA and seven controls with a comparable degree of renal impairment were studied. Patients were subdivided in two groups on the basis of their ability to lower their urine pH during spontaneous acidosis. Patients in Group I lowered their urine pH to the level of controls (5.29 +/- 0.06 and 5.37 +/- 0.11, respectively) whereas patients in Group II could not lower their urine pH below 5.5 (6.38 +/- 0.11). Patients in Group I and Group II had a similar degree of metabolic acidosis and hyperkalemia whereas controls had neither acidosis or hyperkalemia. Most patients in Group II and all patients in Group I had low plasma aldosterone levels. The administration of amiloride resulted in an increase in urine pH and a decrease in potassium excretion in all three groups. The finding that amiloride, presumably by obliterating the transtubular voltage as a result of blockade of sodium transport, inhibited potassium excretion to about the same extent in both groups of patients and in controls argues against the existence of a voltage-dependent defect. Bumetanide produced a fall in urine pH below 5.5 and an increase in potassium excretion in controls and Group I patients. In Group II patients, bumetanide failed to elicit a fall in urine pH below 5.5 but resulted in an increase in potassium excretion similar to that seen in controls and Group I patients. These findings suggest that a derangement other than a voltage-dependent defect is responsible for the inability, characteristic of Group II patients, to lower their urine pH. It was concluded that the impairment in urinary acidification observed in patients with this subtype of hyperkalemic DRTA is due to a defect in collecting tubule hydrogen secretion that results from H+ ATPase dysfunction rather than from a voltage-dependent defect.

Acidosis, Renal Tubular↗
PubMed1995

Correcting acidosis in hemodialysis: effect on phosphate clearance and calcification risk.

Control of uremic acidosis by hemodialysis carries the potential risks of reducing phosphate clearance and worsening metastatic calcification; modeling bicarbonate delivery has been proposed to adequately correct acidosis without impairing phosphate removal. To test the efficacy and safety of different methods for controlling acidosis, nine stable adults received in random order standard (S; dialysate HCO3- 30 to 34 mmol/L), high (H; 40 mmol/L) or modeled (M; 28 mmol/L, rising exponentially to 35 mmol/L at 3 h, 40 mmol/L at 4 h) bicarbonate dialysis for 4 wk each, and were tested during the last two dialyses of each treatment. More oral bicarbonate capsules were required with M than H (2.8 +/- 0.4 versus 1.4 +/- 0.4/day, P = 0.04) to maintain predialysis HCO3- at 24 to 26 mmol/L. Plasma HCO3- was significantly higher with H than M during dialysis, and than S before, during, and after dialysis. Plasma inorganic phosphate, phosphate rebound, clearance of phosphate from plasma (80 to 90 mL/min) and mass transfer of phosphate into dialysate (12 to 13 mmol/4 h dialysis) were no different among the three treatments. Similarly, there were no differences in plasma concentration of urea, total calcium, estimated ionized calcium, lipids, and potassium, clearance and mass transfer of urea, blood pressure, and symptoms with the three treatments. Estimated levels of tribasic inorganic phosphate, the phosphate component of hydroxyapatite, were very similar before and after each treatment. Plasma calcium x phosphate product was less than 3.5 mmol2/L2 at all times with each treatment. A risk factor for metastatic calcification was calculated from the relative saturation ratio of its principle component, hydroxyapatite (Ca5 (PO4)3 OH); this was no different among each of the treatments, and was not altered significantly by dialysis. Uremic acidosis can be fully corrected by high or modeled bicarbonate dialysis without any reduction of phosphate clearance or increased risk of metastatic calcification. The added cost of modeling technology is not justified by the criterion of phosphate clearance alone.

Acidosis↗
PubMedDate not supplied

Renal tubular acidosis in horses (1980-1999).

Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.

Acidosis, Renal Tubular↗
PubMed1999

Lactic acidosis in metformin-treated patients. Prognostic value of arterial lactate levels and plasma metformin concentrations.

OBJECTIVE: The antidiabetic drug metformin has been associated in a small number of patients with lactic acidosis, a serious condition with a poor prognosis. However, because of lack of data, the prognostic significance of hyperlactataemia in metformin-treated patients is not known. METHODS: Data were collected from 49 metformin-treated patients with lactic acidosis (arterial lactate level > or = 5 mmol/L and blood pH < or = 7.35) and available plasma metformin concentration data to investigate the association of arterial lactate levels and plasma metformin concentrations with mortality. RESULTS: The overall mortality rate in this patients sample was 45% and the median arterial lactate level was 13.1 mmol/L. Median lactate levels were similar in patients who survived (13 mmol/L) and those who died (14.3 mmol/L), whereas the median plasma metformin concentration was 3 times higher in patients who survived (20.6 mg/L versus 6.3 mg/L). CONCLUSION: In this, the largest series of metformin-treated patients with lactic acidosis yet reported, 55% of patients survived and these patients had a median arterial lactate level of 13.1 mmol/L. Neither arterial lactate levels nor plasma metformin concentrations were of prognostic significance in relation to mortality in this sample of metformin-treated patients with lactic acidosis. Death in these patients appeared instead to be associated with other hypoxic disease or underlying ill health. These observations suggest that accumulation of metformin may not be as significant with respect to high arterial levels of lactate and their effects as has been traditionally thought.

Acidosis, Lactic↗
PubMed1976

Phenformin-associated metabolic acidosis.

We report 18 consecutive phenformin-treated diabetic patients admitted to this Medical Service acutely ill with metabolic acidosis. Lactic acidosis was anticipated, and documented, in all. Also, however, though most of the patients had only weakly positive, or even negative, serum reactions with the nitroprusside reagent, all were found to have coexisting ketoacidosis, plasma 3-hydroxybutyrate averaging 7.1 mmol/L. +/- 3.9 (S.D.). This finding suggest that treatment of these patients should include insulin, and often also glucose, because most do not have marked hyperglycemia and some have hypoglycemia. The lactic acidosis in the nine patients who survivied was, on average, less severe than in the nine who died, but the difference was not statistically significant. Surivival correlated closely with the absence of shock on arrival. Only eight patients had a identifiable acute illness other than the metabolic acidosis. The other 10 patients had no discernible cause for the acute illness apart from their treatment with phenoformin. This finding raises serious doubts about whether phenformin should be used to treat patients with diabetes.

Acidosis↗
PubMed1989

Effects of acute metabolic acidosis and alkalosis on leucine metabolism in conscious dogs.

To determine the effects of acute metabolic acidosis and alkalosis on leucine metabolism in vivo, mongrel dogs were infused with [1-14C]leucine for 8 h, along with NaCl, HCI, or NaHCO3 over the last 4 h. Arterial pH did not change from the basal value during NaCl infusion but decreased (P less than .01) and increased (P less than .01) during HCl and NaHCO3 infusions, respectively. Total leucine carbon entry did not change from the basal value during saline infusion but increased (P less than .01) with acidosis and decreased (P less than .05) with alkalosis. Compared with saline controls, acidosis increased (P less than .01) leucine oxidation. During alkalosis decreased (P less than .01) leucine oxidation. During acidosis, total plasma essential and nonessential amino acid concentrations increased (P less than .05), whereas during alkalosis, total plasma essential and nonessential amino acid concentrations decreased (P less than .05). These studies suggest that acute alterations in arterial pH may affect the regulation of protein metabolism in vivo and must be considered in the interpretation of results from experiments in which alterations of acid-base homeostasis may have occurred.

3-Hydroxybutyric Acid↗
PubMed1995

Role of metformin accumulation in metformin-associated lactic acidosis.

OBJECTIVE: To investigate the role of metformin accumulation in the pathophysiology of metformin-associated lactic acidosis. RESEARCH DESIGN AND METHODS: We used high-performance liquid chromatography to measure plasma metformin concentrations in 14 patients who experienced lactic acidosis (pH < 7.35 and lactate concentration 5 > mmol/l) while receiving chronic metformin treatment. Their treatment was generally based on alkalinization and dialysis therapy. RESULTS: Clinical shock and/or evidence of tissue hypoxia was found in all patients with the exception of one who had a nonsteroidal anti-inflammatory drug-induced anuria. Ten patients had significant metformin accumulation (plasma metformin concentrations 4.1-84.9 mg/l, normal value 0.6 +/- 0.5 mg/l before drug intake), generally because of failure to withdraw metformin despite intercurrent pathological conditions affecting its renal elimination (serum creatinine concentrations ranging from 269 to 1,091 mumol/l). There was no metformin accumulation (plasma metformin 0.03-0.7 mg/l) in the four other patients, who had less severe renal failure (serum creatinine 140-349 mumol/l). The severity of the patient's general condition did not predict early hospital mortality (death before discharge from the intensive care unit) even in patients in shock. Whereas it was high in those without metformin accumulation (only 1 of 4 patients recovered), early hospital mortality was low in the 10 patients with metformin accumulation and was not related to its extent (3 patients died with end-stage hepatic failure or cardiac failure). Correlation studies showed a positive correlation between serum creatinine and plasma metformin and between plasma metformin and arterial lactate but, for the latter correlation, only in patients with metformin accumulation. CONCLUSION: Metformin-associated lactic acidosis is not necessarily due to metformin accumulation; true type B (aerobic) lactic acidosis, i.e., without an apparent associated hypoxic factor, seems exceptional. Neither the severity of the clinical picture nor the degree of metformin accumulation predicted survival; rather, the prognosis was dependent upon the severity of the associated pathological conditions.

Acidosis, Lactic↗
PubMed1999

Effects of imposed feed intake variation on acidosis and performance of finishing steers.

Four metabolism and two finishing trials were conducted to determine the effects of imposed feed intake variation on acidosis and performance of finishing steers. In Metabolism Trial 1, four ruminally fistulated steers were limit-fed and subjected to either a constant amount of feed per day (C) or low intake variation of .7 kg/d (LV). No treatment differences were found for intake or measures of acidosis. Metabolism Trial 2 was conducted similarly to Metabolism Trial 1 with treatments of C and high intake variation of 1.4 kg/d (HV). Treatment HV increased (P < .05) acidosis, as indicated by the area of ruminal pH below 5.6. In Metabolism Trial 3, four steers were fed at ad libitum levels of intake and subjected to three levels of intake variation: ad libitum intake with no imposed intake variation (AL), LV of .7 kg/d, and HV of 1.4 kg/d. No treatment differences were found. In Metabolism Trial 4, six ruminally fistulated steers were fed at ad libitum levels and subjected to three levels of intake variation: AL, LV of .9 kg/d, and HV of 1.8 kg/d. Average ruminal pH increased (P < .05) and area of ruminal pH below 5.6 decreased (P < .05) as level of intake variation was increased. In Finishing Trial 1, 75 steers were assigned to eight pens and two treatments: AL or HV of 1.8 kg/d. Dry matter intake increased (P < .05) from AL to HV. Daily gain and gain/feed were not affected by treatment. In Finishing Trial 2, 94 steers were assigned to 12 pens and two treatments: AL or HV of 1.8 kg/d. No treatment differences were noted in DMI, daily gain, or gain/ feed. Therefore, results of these trials indicate that intake variation of up to 1.8 kg/d does not increase acidosis or decrease performance of finishing steers fed at ad libitum levels of intake.

Acidosis↗
PubMed2005

Effect of rapid or gradual grain adaptation on subacute acidosis and feed intake by feedlot cattle.

The effects of grain adaptation protocol on subacute acidosis and feed intake by cattle were studied in a completely randomized experiment using 12 crossbred heifers (384 +/- 25 kg BW). The dietary proportion of concentrate was increased from 40 to 90% (DM basis) either by rapid adaptation (65% concentrate diet fed for 3 d) or by gradual adaptation (five intermediate diets containing 48.3, 56.7, 65.0, 73.3, and 81.7% concentrate, fed for 3 d each). Feed intake and ruminal pH (by indwelling ruminal electrodes) were monitored over 20 d. Mean daily pH variables did not differ (P > or = 0.10) between treatments on any of the 3 or 4 d that 65 or 90% concentrate was fed. Variances of a number of pH variables were greater (P < 0.05) for rapidly adapted heifers than for those on the gradual adaptation protocol during adaptation to 65 and 90% concentrate. Mean hourly pH did not differ over the first 24 h of adaptation to 65% concentrate, but variance of hourly pH tended (P < 0.10) to be greater for rapidly adapted than for gradually adapted heifers for eight of the first 24 h. On the first day of feeding 90% concentrate, ruminal pH tended (P = 0.07) to be less at 11 and 12 h after feeding with rapid adaptation than with gradual adaptation. Variance of hourly pH increased steadily in rapidly adapted heifers from 6 h after feeding onward. Ruminal VFA concentration and osmolality did not differ between treatments. Ruminal lactate concentration was < 1 mM, except in two rapidly adapted heifers and one gradually adapted heifer after introduction to 90% concentrate. Adaptation method did not affect DMI or day-to-day variation in DMI. Detection of acidosis was associated with increased variance in ruminal pH variables. A range of individual responses to grain challenge was observed, but current management strategies for preventing acidosis in pens of cattle are based on responses of the most susceptible individuals. A better understanding of factors governing individual responses to acidotic challenge may allow for the development of more effective acidosis prevention practices.

Acidosis↗
PubMed1994

Role of angiotensin II in renal vasoconstriction with acute hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate the role of renin-angiotensin in the renal vasoconstriction with combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied eight conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 mEq/24 h x 4 days). The animals were studied during combined acute hypoxemia and hypercapnic acidosis (PaO2 34 +/- 1 mm Hg, PaCo2 57 +/- 1 mm Hg, pH 7.20 +/- 0.01) preceded by 80 min of acute hypoxemia (PaO2 34 +/- 1 mm Hg) during: (a) intrarenal infusion of vehicle (n = 8); or (b) intrarenal administration of the angiotensin II antagonist [Sar1,Ala8]-AII, 70 ng kg-1 min-1 (n = 8). The combination of acute hypoxemia and hypercapnic acidosis resulted in diminished effective renal plasma flow and increased renal vascular resistance during intrarenal vehicle infusion. Intrarenal [Sar1,Ala8]-AII did not abolish the renal vasoconstriction in the initial 20 min of this combined blood gas derangement but resulted in a more prompt return of the renal vascular variables toward control levels with continuation of the blood gas derangement for an additional 20 min, suggesting a role for angiotensin in renal vasoconstriction. These observations suggest that while renin-angiotensin may not mediate the initial renal vasoconstriction in the first 20 min of combined acute hypoxemia and hypercapnic acidosis, in uninephrectomized conscious dogs, it attenuates the spontaneous recovery of renal hemodynamic variables to baseline as the blood gas derangement continues.

Acidosis, Respiratory↗
PubMed1984

Association of beta hydroxybutyric acidosis with isoniazid intoxication.

Acute metabolic acidosis associated with accumulation of lactate has been previously reported in isoniazid (INH) intoxication. To our knowledge, association of INH toxicity with beta-hydroxybutyric acidosis has not been demonstrated previously. The present report documents the occurrence of beta-hydroxybutyric acidosis in patients with INH intoxication. The reason for the lack of previous reports of this association is not clear, although failure to measure plasma beta-hydroxybutyrate levels in previous studies is a likely possibility. Our patients received intravenous sodium bicarbonate, anticonvulsants and dialysis which resulted in complete reversal of metabolic acidosis and other manifestations of INH toxicity.

3-Hydroxybutyric Acid↗
PubMed1991

[The characteristics of metabolic acidosis in aged patients with chronic renal failure].

The present study was designed to clarify the characteristics of metabolic acidosis in aged patients with chronic renal failure. The subjects consisted of ambulatory cooperative patients (19 males and 18 females). Their values of creatinine clearance (Ccr) varied from 6.8 to 107.5 ml/min/1.73 m2. The relationship of Ccr to acid-base and electrolyte disturbances was investigated. The estimations of normal values in acid-base and electrolyte composition were based on the method of Hoffmann. The results are summarized as follows: 1. A high incidence of metabolic acidosis was demonstrated in patients whose Ccr values were below 20 ml/min/1.73 m2. 2. A significant positive correlation of Ccr values and plasma levels of bicarbonate (p less than 0.001) and a significant inverse correlation of Ccr values and serum levels of chloride (p less than 0.01) were observed. 3. The values of the anion gap did not change, irrespective of Ccr values. 4. Serum concentrations of potassium were inversely correlated with plasma levels of bicarbonate (p less than 0.01). Hyperchloremic normal anion gap acidosis with hyperpotassemia was the characteristic feature of metabolic acidosis in aged patients with chronic renal failure. The normal anion gap could be explained by normophosphatemia or mild hyperphosphatemia, even in the patients with advanced renal failure.

Acid-Base Equilibrium↗
PubMed1997

Comparison of oral sodium compounds for the correction of acidosis.

Three Na compounds were tested to determine which was best able to treat metabolic acidosis in dairy cows. Metabolic acidosis was induced in test cows by feeding a diet that was high in anions for 7 d before the administration of treatment on d 8. The orally administered treatments were equivalent amounts of Na in the form of NaCl (208.6 g), NaHCO3 (300 g), or Na propionate (343 g). The initiation of oral treatment was designated as time 0, and blood samples were taken 15 min before treatment, immediately before treatment, and 15, 30, 45, 60, 90, 120, 180, 240, 300, and 360 min after treatment. Before treatment, all cows were in a state of metabolic acidosis as was evidenced by low blood pH, low HCO3 concentrations, and high plasma Cl concentrations. After treatment, blood pH and HCO3 were markedly higher for cows receiving NaHCO3 and Na propionate but not for cows receiving NaCl. We concluded that orally administered NaHCO3 and Na propionate were equally effective in correcting the acid-base balance of blood, as was predicted by the strong ion difference theory of acid-base physiology. Sodium propionate may be considered a more effective treatment of metabolic acidosis in diseases such as ketosis because the added propionate can serve as a source of glucose for the cow.

Acidosis↗
PubMed1998

Thiamine-deficient lactic acidosis with brain tumor treatment. Report of three cases.

Lactic acidosis due to thiamine deficiency is known to complicate chemotherapy and radiotherapy treatment of malignant extracranial tumors, but to the authors' knowledge, this complication has not been reported in patients treated for malignant brain tumors. They report three such cases, demonstrating that this complication can occur during treatment of brain tumors. In all patients, consciousness levels deteriorated within 1 to 2 days. Serum lactic acid levels increased to concentrations between 62 and 96.7 mg/dl, resulting in severe metabolic acidosis. A low blood thiamine level (9 ng/ml) was demonstrated at the onset in one case, and high-dose thiamine infusions dramatically improved lactic acidemia as well as impairment of consciousness in two cases. In the other case, hydrocephalus was suspected initially, resulting in a delay in thiamine supplementation. Clinical differentiation of this form of lactic acidosis from hydrocephalus or tumor progression can be very difficult in a patient undergoing treatment for a malignant brain tumor. Demand for thiamine is thought to be increased in patients with malignant brain tumors, and supplemental thiamine during treatment is necessary to prevent lactic acidosis. When this complication occurs, immediate treatment with sufficient thiamine is essential, together with normalization of pH by using sodium bicarbonate. With timely intervention, the level of consciousness can recover to the preacidotic state with no new neurological deficits.

Acidosis, Lactic↗
PubMed2002

Lactic acidosis associated with the usual theophylline dose in a patient with asthma.

Metabolic and electrolyte abnormalities, including hypokalemia, hyperglycemia and lactic acidosis, are associated with theophylline overdose. However, we report an unusual case of sinus tachycardia, lactic acidosis, hypokalemia and hyperglycemia associated with the usual theophylline dose in a patient with asthma. The theophylline dose was 200 mg orally twice daily. Three hours after administration of the third dose, the patient experienced palpitation. An electrocardiogram showed a sinus tachycardia. Arterial blood gas analysis revealed a mixed metabolic acidosis and respiratory alkalosis. Serum lactate level was 51 mmol/L (normal 0.7-2.1 mmol/L). Biochemistry results were sodium 136 mEq/L, chloride 99 mEq/L, potassium 1.9 mEq/L and glucose 204 mg/dL. Our case suggests that a possibility of theophylline-associated metabolic abnormalities should be considered when an asthmatic patient given the usual theophylline dose presents with lactic acidosis, hypokalemia and hyperglycemia of unknown etiology.

Acidosis, Lactic↗