The response of the kidney of the freshwater rainbow trout to true metabolic acidosis

1980 ◽  
Vol 84 (1) ◽  
pp. 227-244 ◽  
Author(s):  
K. A. Kobayashi ◽  
C. M. Wood

Infusion of lactic acid into the bloodstream of trout produced a short-lived depression of blood pH and a long-lasting elevation of blood lactate. The lactate injected was distributed in a volume of 198 ml/kg. Renal excretion of lactate anion and total acid increased by approximately equal amounts during the period of high blood lactate levels, but total renal loss over 72 h accounted for only 2% of the lactate load and 6% of the proton load. Comparable differences in the time courses of blood lactate and pH changes occurred when lactacidosis was induced endogenously by normocapnic hypoxia. The immediate response of the kidney was similar to that with lactic acid infusion, but there was a long-lasting (12–72 + h) elevation of urinary acid efflux that was not associated with lactate excretion. Following hypoxia, renal excretion over 72 h accounted for 1% of the estimated lactate load and 12–25% of the proton load. A renal lactate threshold of 4–10 muequiv/ml prevents significant urinary lactate excretion. The response of the trout kidney to true metabolic acidosis is similar to that of the mammalian kidney.

1986 ◽  
Vol 250 (4) ◽  
pp. F702-F709 ◽  
Author(s):  
S. Abu Romeh ◽  
R. L. Tannen

Recent studies have shown that ketoacid production is exquisitely sensitive to changes in systemic pH, with a decrease inhibiting and an increase stimulating the production rate. To determine whether inhibition of net endogenous acid production is a widely applicable mechanism for the defense of acid-base homeostasis, we examined the effect of superimposed acidosis on lactic acid production by hypoxic rats. Anesthetized paralyzed mechanically ventilated rats with normocapnia increased blood lactate progressively in response to a fractional inspired O2 (FIO2) of 8% (PaO2, 35-38 mmHg) and achieved a level of 7.0 +/- 1.2 mM at 3 h. Superimposition of either mild respiratory acidosis (PCO2, 59 mmHg) or exogenous inorganic metabolic acidosis (intra-arterial HCl sufficient to decrease pH from 7.33 to 7.23) after 1 h of hypoxia dramatically diminished the rise in blood lactate. At the end of the third hour, blood lactate levels averaged 1.7 +/- 0.6 mM with superimposed respiratory acidosis and 2.7 +/- 0.4 mM with superimposed metabolic acidosis, both values being significantly less than the hypoxic controls. Termination of the superimposed respiratory acidosis resulted in a rapid increase in blood lactate levels, demonstrating the reversibility of the pH modulation of lactic acid production. Thus systemic acidosis appears to feed back in a protective fashion to inhibit net lactic acid production in rats with hypoxia-induced lactic acidosis. These findings suggest that finely tuned feedback control mechanisms that keep systemic pH within a narrow range operate under both major conditions of enhanced endogenous acid production (i.e., keto- and lactic acidosis).


1964 ◽  
Vol 207 (6) ◽  
pp. 1226-1230 ◽  
Author(s):  
H. I. Miller ◽  
B. Issekutz ◽  
P. Paul ◽  
K. Rodahl

Sodium lactate infusions into unanesthetized pancreatectomized dogs, with indwelling arterial and venous catheters, markedly decreased the plasma free fatty acid (FFA) level. Infusions of palmitate-1-C14 at constant rates showed that the rate of release of FFA was considerably reduced by the lactate. There was an inverse correlation between the logarithm of the plasma FFA concentrations and the logarithm of the blood lactate levels. Glucose infusion alone had no significant effect on the plasma FFA of the pancreatectomized dog. When both lactate and glucose were infused into the pancreatectomized dog, the plasma FFA was inversely correlated with the blood lactate level but not with the blood sugar. When the plasma FFA was elevated in normal dogs by norepinephrine infusion, the FFA-lowering effect of sodium lactate was not prevented. Neither acetylcholine nor nitroglycerine infusions had any marked effect on the plasma FFA. It is concluded that lactic acid has a direct effect on the release of FFA which does not require the presence of insulin and is independent of the blood glucose concentration.


1975 ◽  
Vol 48 (2) ◽  
pp. 121-131 ◽  
Author(s):  
J. Yudkin ◽  
R. D. Cohen

1. The rate of removal from the circulation of an intravenous lactic acid load has been studied in conscious rats, previously subjected either to bilateral nephrectomy or to a sham operation. 2. In rats with normal blood pH, the apparent contribution of the kidneys to removal of the lactic acid load is 30%; less than 12% of the renal contribution is attributable to urinary excretion. 3. In bilaterally nephrectomized rats made acidotic by administration of ammonium chloride, the rate of removal of a half-neutralized lactic acid load is progressively decreased with increasing severity of acidosis. No such effect is seen in sham-operated animals. 4. An increase in the ability of the kidney to remove lactate during acidosis compensates for approximately half of the simultaneous fall in the capacity of the remainder of the body for lactate assimilation. 5. Basal blood lactate concentrations fall in the presence of metabolic acidosis.


1978 ◽  
Vol 77 (1) ◽  
pp. 141-155 ◽  
Author(s):  
C. S. WARDLE

1. Plaice caught by trawl net and plaice exercised in laboratory tanks all show high levels of lactic acid (33–44 mmol/kg) in the anaerobic swimming muscle. During exhausting exercise 2 moles of lactate are formed from 1 mole of glycogen glucose. After an 8 h rest 50–80% of the muscle glycogen is restored. 2. Blood lactate levels remain low (0.5-2 mmol/1) in the majority of plaice caught by trawl. In a small number of plaice, peak levels over 5 mmol/1 are reached 2-4 h after capture. Low blood lactate levels could be guaranteed in all fish exercised 24 h after the stress of capture and in tank-adapted fish exercised and injected with the β-adrenergic stimulating drug, isoxsuprine hydrochloride. The blood lactate in plaice, tank-adapted for more than 8 days and then exercised, may reach peak levels up to 5 mmol/l 2-4 h later. 3. High blood lactate levels were obtained by injecting the β-adrenergic block propranolol to stressed exercised fish. The α-adrenergic block did not have this effect. All plaice with blood lactate levels reaching 5–12 mmol/l died. 4. The results indicate that the muscle cells regulate the release or nonrelease of their lactate load to the blood stream and increases in the blood circulating to the muscle do not influence this release. The non-release mechanism may be actived by a catecholamine circulated in the blood stream following a stress.


2021 ◽  
Author(s):  
Megumi Hoshiai ◽  
Kaori Ochiai ◽  
Yuma Tamura ◽  
Tomoki Tsurumi ◽  
Masato Terashima ◽  
...  

AbstractNeuromuscular electrical stimulation has been used to treat cardiovascular diseases and other types of muscular dysfunction. A novel whole-body neuromuscular electrical stimulation (WB-NMES) wearable device may be beneficial when combined with voluntary exercises. This study aimed to investigate the safety and effects of the WB-NMES on hemodynamics, arrhythmia, and sublingual microcirculation. The study included 19 healthy Japanese volunteers, aged 22–33 years, who were not using any medication. Electrocardiogram (ECG), echocardiography, and blood sampling were conducted before a 20-min WB-NMES session and at 0 and 10 min after termination of WB-NMES. Their tolerable maximum intensity was recorded using numeric rating scale. Arrhythmia was not detected during neuromuscular electrical stimulation or during 10 min of recovery. Blood pressure, heart rate, left ventricular ejection fraction, and diastolic function remained unchanged; however, mild mitral regurgitation was transiently observed during WB-NMES in a single male participant. A decrease in blood glucose and an increase in blood lactate levels were observed, but no changes in blood fluidity, sublingual microcirculation, blood levels of noradrenaline, or oxidative stress were shown. WB-NMES is safe and effective for decreasing blood glucose and increasing blood lactate levels without changing the blood fluidity or microcirculation in healthy people.


2014 ◽  
Vol 685 ◽  
pp. 486-489 ◽  
Author(s):  
Yan Yan Wu ◽  
Gang You ◽  
Lai Hao Li ◽  
Xian Qing Yang ◽  
Ya Wei

Inoculation with compound lactobacillus in the low-salt pickled fish, fermented and dried to produce cured fish. The paper studied the effects of inoculating compound lactobacillus on the pH, total volatile basic nitrogen (TVB-N), amino acid nitrogen content (AA-N) and total acid content of salted fish quality. The results showed that, compared with the non-vaccinated groups (CK), The cured fish inoculated lactobacillus had a lower pH and TVB-N content, higher the amino acid nitrogen content and total acid content. Inoculated compound lactic acid bacteria into salted fish, to a certain extent, could improve the nutritional value and edible value, which had positive effects on the fish quality.


Author(s):  
Giovanni Carpenè ◽  
Diletta Onorato ◽  
Riccardo Nocini ◽  
Gianmarco Fortunato ◽  
John G. Rizk ◽  
...  

Abstract Coronavirus disease 2019 (COVID-19) is an infectious respiratory condition sustained by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which manifests prevalently as mild to moderate respiratory tract infection. Nevertheless, in a number of cases the clinical course may deteriorate, with onset of end organ injury, systemic dysfunction, thrombosis and ischemia. Given the clinical picture, baseline assessment and serial monitoring of blood lactate concentration may be conceivably useful in COVID-19. We hence performed a systematic literature review to explore the possible association between increased blood lactate levels, disease severity and mortality in COVID-19 patients, including comparison of lactate values between COVID-19 and non-COVID-19 patients. We carried out an electronic search in Medline and Scopus, using the keywords “COVID-19” OR “SARS-CoV-2” AND “lactate” OR “lactic acid” OR “hyperlactatemia”, between 2019 and present time (i.e. October 10, 2021), which allowed to identify 19 studies, totalling 6,459 patients. Overall, we found that COVID-19 patients with worse outcome tend to display higher lactate values than those with better outcome, although most COVID-19 patients in the studies included in our analysis did not have sustained baseline hyperlactatemia. Substantially elevated lactate values were neither consistently present in all COVID-19 patients who developed unfavourable clinical outcomes. These findings suggest that blood lactate monitoring upon admission and throughout hospitalization may be useful for early identification of higher risk of unfavourable COVID-19 illness progression, though therapeutic decisions based on using conventional hyperlactatemia cut-off values (i.e., 2.0 mmol/L) upon first evaluation may be inappropriate in patients with SARS-CoV-2 infection.


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