scholarly journals Control of red blood cell metabolism in rainbow trout after exhaustive exercise

1990 ◽  
Vol 154 (1) ◽  
pp. 491-507 ◽  
Author(s):  
C. M. Wood ◽  
P. J. Walsh ◽  
S. Thomas ◽  
S. F. Perry
Keyword(s):  
Cell Metabolism ◽  
Red Cell ◽  
O2 Consumption ◽  
Plasma Lactate ◽  
Acid Base ◽  
Lactate Oxidation ◽  
Post Exercise ◽  
Acid Base Status ◽  
Catecholamine Levels

Metabolic responses (rates of CO2 production from 14C-labelled glucose or lactate, and total O2 consumption) of red blood cells were monitored in rainbow trout (Oncorhynchus mykiss) at rest and during 12 h of recovery from exhaustive exercise. Extracellular acid-base status, red blood cell intracellular pH (pHi), and plasma metabolite and catecholamine levels were recorded simultaneously. Despite a post-exercise rise in plasma glucose level, glucose oxidation was depressed, at least partly because of a rise in plasma lactate level. However, lactate oxidation was stimulated markedly, especially at 0–2 h post-exercise. Subsequent multifactorial experiments in vitro demonstrated that augmentation of lactate oxidation was due partly to increased plasma lactate, and partly to separate stimulatory effects of elevated PCO2 and catecholamine levels. Changes in pH and HCO3- level were not directly involved, but the stimulatory effects of catecholamines occurred only under acidotic conditions. Total red cell O2 consumption (MO2) remained generally stable after exercise. Similar multifactorial experiments in vitro demonstrated that respiratory, metabolic and mixed acidoses all inhibited MO2, an effect largely attributable to the lowered pH. This inhibition was reversed by typical post-exercise levels of epinephrine and norepinephrine; again, catecholamines had no effect under control conditions. Red cell pHi regulation was achieved without an increase in MO2 above resting levels. Our results indicate a complex sensitivity of red cell metabolism to acid-base status and a shift in substrate preference for oxidation after strenuous exercise. The mobilization of catecholamines plays an important coordinating role and helps sustain normal rates of oxidative metabolism by red cells in the face of post-exercise blood acidosis.

scholarly journals Effect of oxalate and malonate on red cell metabolism

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1389-1393
Author(s):  
E Beutler ◽  
L Forman ◽  
C West
Keyword(s):  
Pyruvate Kinase ◽  
Cell Metabolism ◽  
Inhibitory Effect ◽  
Red Cells ◽  
Red Cell ◽  
Acid Analogue ◽  
2,3 Dpg

The addition of oxalate to blood stored in Citrate-phosphate-dextrose (CPD) produces a marked improvement in 2,3-diphosphoglycerate (2,3-DPG) preservation; an increase in 2,3-DPG levels can also be documented in short-term incubation studies. Oxalate is a potent in vitro inhibitor of red cell lactate dehydrogenase, monophosphoglycerate mutase, and pyruvate kinase (PK). In the presence of fructose 1,6-diphosphate the latter inhibitory effect is competitive with phospho(enol)pyruvate (PEP). Determination of the levels of intermediate compounds in red cells incubated with oxalate suggest the presence of inhibition at the PK step, indicating that this is the site of oxalate action. Apparent inhibition at the glyceraldehyde phosphate dehydrogenase step is apparently due to an increase in the NADH/NAD ratio. Oxalate had no effect on the in vivo viability of rabbit red cells stored in CPD preservatives for 21 days. Greater understanding of the toxicity of oxalate is required before it can be considered suitable as a component of preservative media, but appreciation of the mechanism by which it affects 2,3-DPG levels may be important in design of other blood additives. Malonate, the 3-carbon dicarboxylic acid analogue of oxalate late did not inhibit pyruvate kinase nor affect 2,3-DPG levels.

The Effect of Long-Term Aerial Exposure on Heart Rate, Ventilation, Respiratory Gas Exchange and Acid-Base Status in the Crayfish Austropotamobius Pallipes

1981 ◽  
Vol 92 (1) ◽  
pp. 109-124
Author(s):  
E. W. TAYLOR ◽  
MICHÈLE G. WHEATLY
Keyword(s):  
Heart Rate ◽  
Lactic Acid ◽  
O2 Consumption ◽  
Aerial Exposure ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Content Difference ◽  
Acid Base Status ◽  
Lactate Levels

1. When first removed into air, crayfish showed transient increases in heart rate (fH) and scaphognathite rate (fR) which rapidly recovered to submerged levels and were unchanged for 24 h. The rate of O2 consumption(Moo2) increased from an initially low level and was then maintained for 24 h in air at the same level as in settled submerged animals. 2. There was an initial acidosis in the haemolymph which was both respiratory and metabolic due to the accumulation of CO2 and lactate. Progressive compensation by elevation of the levels of bicarbonate buffer in the haemolymph and reduction of circulating lactate levels returned pH towards submerged levels after 24 h in air. 3. Exposure to air resulted in a marked internal hypoxia with haemolymph O2, tensions, both postbranchial Pa, oo2 and prebranchial Pv, oo2, remaining low throughout the period of exposure. The oxygen content or the haemolymph was initially reduced, with a - vOO2 content difference close to zero. Within 24 h both Ca, oo2 and Cv, OO2 had returned towards their levels in submerged animals. These changes are explained by the Bohr shift on the haemocyanin consequent upon the measured pH changes. 4. After 48 h in air, MO2 and fH were significantly reduced and ventilation became intermittent. There was a slight secondary acidosis, increase in lactic acid levels and reduction in a - vO2 content difference in the haemolymph. 5. When crayfish were returned to water after 24 h in air, MOO2, fHfR were initially elevated by disturbance and there was a period of hyperventilation. In the haemolymph there was an initial slight alkalosis, and an increase in Ca, OO2 lactic acid. All variables returned to their settled submerged levels within 8 h.

White Muscle Intracellular Acid-Base and Lactate Status Following Exhaustive Exercise: A Comparison between Freshwater- and Sea Water- Adapted Rainbow Trout

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
White Muscle ◽  
Sea Water ◽  
Ph Regulation ◽  
Recovery Period ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Acid Base Status ◽  
Intracellular Acid

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.

The Role of β-Adrenoreceptors in the Recovery from Exhaustive Exercise of Freshwater-Adapted Rainbow Trout

1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Nacl Concentration ◽  
Adrenergic Mechanism ◽  
Acid Base Status ◽  
Isoproterenol Infusion ◽  
Net Fluxes

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.

scholarly journals Effect of oxalate and malonate on red cell metabolism

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1389-1393 ◽  
Author(s):  
E Beutler ◽  
L Forman ◽  
C West
Keyword(s):  
Pyruvate Kinase ◽  
Cell Metabolism ◽  
Inhibitory Effect ◽  
Red Cells ◽  
Red Cell ◽  
Acid Analogue ◽  
2,3 Dpg

Abstract The addition of oxalate to blood stored in Citrate-phosphate-dextrose (CPD) produces a marked improvement in 2,3-diphosphoglycerate (2,3-DPG) preservation; an increase in 2,3-DPG levels can also be documented in short-term incubation studies. Oxalate is a potent in vitro inhibitor of red cell lactate dehydrogenase, monophosphoglycerate mutase, and pyruvate kinase (PK). In the presence of fructose 1,6-diphosphate the latter inhibitory effect is competitive with phospho(enol)pyruvate (PEP). Determination of the levels of intermediate compounds in red cells incubated with oxalate suggest the presence of inhibition at the PK step, indicating that this is the site of oxalate action. Apparent inhibition at the glyceraldehyde phosphate dehydrogenase step is apparently due to an increase in the NADH/NAD ratio. Oxalate had no effect on the in vivo viability of rabbit red cells stored in CPD preservatives for 21 days. Greater understanding of the toxicity of oxalate is required before it can be considered suitable as a component of preservative media, but appreciation of the mechanism by which it affects 2,3-DPG levels may be important in design of other blood additives. Malonate, the 3-carbon dicarboxylic acid analogue of oxalate late did not inhibit pyruvate kinase nor affect 2,3-DPG levels.

scholarly journals Host-Derived Metabolites Modulate Transcription ofSalmonellaGenes Involved in L-Lactate Utilization during Gut Colonization

2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Caroline C. Gillis ◽  
Maria G. Winter ◽  
Rachael B. Chanin ◽  
Wenhan Zhu ◽  
Luisella Spiga ◽  
...  
Keyword(s):  
Cell Metabolism ◽  
Regulatory Protein ◽  
Transcriptional Level ◽  
Lactate Oxidation ◽  
Terminal Electron Acceptor ◽  
Content Type ◽  
Gut Colonization ◽  
Serovar Typhimurium ◽  
Lactate Utilization

ABSTRACTDuringSalmonella entericaserovar Typhimurium infection, host inflammation alters the metabolic environment of the gut lumen to favor the outgrowth of the pathogen at the expense of the microbiota. Inflammation-driven changes in host cell metabolism lead to the release ofl-lactate and molecular oxygen from the tissue into the gut lumen.Salmonellautilizes lactate as an electron donor in conjunction with oxygen as the terminal electron acceptor to support gut colonization. Here, we investigated transcriptional regulation of the respiratoryl-lactate dehydrogenase LldDin vitroand in mouse models ofSalmonellainfection. The two-component system ArcAB repressed transcription ofl-lactate utilization genes under anaerobic conditionsin vitro. The ArcAB-mediated repression oflldDtranscription was relieved under microaerobic conditions. Transcription oflldDwas induced byl-lactate but notd-lactate. A mutant lacking the regulatory protein LldR failed to inducelldDtranscription in response tol-lactate. Furthermore, thelldRmutant exhibited reduced transcription ofl-lactate utilization genes and impaired fitness in murine models of infection. These data provide evidence that the host-derived metabolites oxygen andl-lactate serve as cues forSalmonellato regulate lactate oxidation metabolism on a transcriptional level.

Changes in uterine fluid composition and acid-base status during shell formation in the chicken

1989 ◽  
Vol 257 (4) ◽  
pp. R732-R737 ◽  
Author(s):  
Z. Arad ◽  
U. Eylath ◽  
M. Ginsburg ◽  
H. Eyal-Giladi
Keyword(s):  
Sharp Increase ◽  
Blood Gases ◽  
Future Application ◽  
Epithelial Tissue ◽  
Fluid Composition ◽  
Acid Base ◽  
Co2 Partial Pressure ◽  
Uterine Fluid ◽  
Acid Base Status

The aim of this study was to characterize the dynamic changes in uterine fluid composition and acid-base status during shell calcification in the chicken. Uterine eggs at timed intervals were manually aborted and the accompanying fluid collected and analyzed for composition of osmolytes, enzymes, and acid-base parameters. Blood samples were analyzed for comparison. No considerable change in blood gases took place in relation to residence time of the calcifying egg in the uterus. A significant acidosis occurred at latter stages. Only minor changes were revealed in plasma osmotic and biochemical composition throughout egg calcification. In contrast, major changes were revealed in uterine fluid composition and acid-base status during calcification. The most prominent phenomenon was the sharp increase in CO2 partial pressure, from 82.2 Torr at 0 h to 132.8 Torr at 10 h. As bicarbonate concentration remained almost stable, fluid pH dropped from 7.412 to 7.250 within this stage. Uterine fluid sodium and chloride concentrations and osmolality dropped significantly in the course of calcification, whereas potassium concentration significantly increased. A sharp increase in glucose, calcium, and magnesium concentrations was measured in the early stages of calcification. These findings are discussed in relation to existing models for transport mechanisms of the uterine epithelial tissue. The comprehensive picture that emerges from the present study should enable future application in establishing a self-contained culturing system in vitro for studies of embryonic development.

Cellular actions of cAMP on HCO3(-)-secreting cells of rabbit CCD: dependence on in vivo acid-base status

1994 ◽  
Vol 266 (4) ◽  
pp. F528-F535 ◽  
Author(s):  
C. Emmons ◽  
J. B. Stokes
Keyword(s):  
Anion Exchanger ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Acid Base Status

HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pHi) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 microM isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pHi. Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (approximately 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na(+)-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits.

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