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Paradoxical Intracellular Acidosis

Disturbances Of Acidbase Homeostasis

Disturbances Of Acidbase Homeostasis

Metabolic disorders - Disturbances of acidbase homeostasis - technical Principles of treatment of acidbase disorders Despite a daily load of protons, derived mainly from metabolism, the hydrogen ion concentration of arterial blood in health is tightly maintained within a slightly alkaline range (pH 7.367.42); concentrations of intracellular hydrogen ions are also controlled. Failure adequately to excrete or neutralize protons causes acidic conditions to prevail (decreased pH): undue intake of base, uncompensated loss of protonsor the substrates from which they are derivedinduces an alkaline milieu (raised pH). The term acidosis refers to the pathological reduction of pH, also to the circumstance when pH would have been decreased were it not for the occurrence of compensatory mechanisms; an equivalent but reciprocal definition applies to alkalosis. In health, the principal source of protons is CO2, which originates from aerobic metabolism, is volatile and thus eliminated readily by the lungs. Lesser contributions come from urea synthesis and the generation of lactate and other organic anions such as 3-hydroxybutyrate and acetoacetate, which are eliminated by metabolism in the liver, kidneys and other tissues. Less than 1% of the proton burden is derived from the breakdown of sulphur- and phosphorus-containing molecules; these are ultimately converted to non-volatile sulphuric and phosphoric acids, which are excreted exclusively by the kidneys. The body has limited capacity to offset rapid changes in pH by using extracellular and intracellular buffers, which are chiefly proteins (e.g. haemoglobin) or bicarbonate and phosphate ions. Acidbase buffering allows decompensation to be avoided transiently, but the proton burden must in the end be eliminated. When the primary aci Continue reading >>

Response To 100mmol Of Sodium Bicarbonate

Response To 100mmol Of Sodium Bicarbonate

Response to 100mmol of Sodium Bicarbonate These are the physiological effects of infusing 100mmol of concentrated (8.4%) sodium bicarbonate into a patient. A 1 molar solution of sodium bicarbonate is what you are giving. The osmolality is 2000mosm/L. Let us unfocus from the movements of water and sodium, as they are predictable, and their patterns already well rehearsed. Let us instead observe the traffic of the HCO3- anion. Let us pretend that suddenly 100mmol of this anion is dumped into the extracellular fluid (and being easily water soluble, it frolics merrily through the extracellular fluid compartments, distributing evenly among them). This means 25mmol of HCO3- is now in the vascular compartment and 75 mmol is in the interstitial fluid. The extracellular concentration of bicarbonate pre-infusion in our model is 24mmol/L, which gives us 336 mmol overall. A sudden increase by 100mmol (to a total content of 436 mmol) would cause the concentration to rise to 31.1mmol/L. The change in extracellular bicarbonate concentration following a bicarbonate infusion From the above calculations, it would seem that the volume of distribution for bicarbonate is the same as the extracellular fluid, 14L or about 0.2L/Kg. Experimental findings demonstrate that this is not the case. Simplistic fluid-filled cylinder models of distribution do not do justice to the complexity of bicarbonate distribution. The major source of complexity, is the tendency of the bicarbonate to buffer hydrogen ions and become "lost" in the process, converting to water and carbon dioxide. This tendency, as one might imagine, is dependent on the presence of acidosis or alkalosis. An excellent article has examined this relationship, and I will clumsily paraphrase Figure 5 from it below. The figure describes the Continue reading >>

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

0.25-0.50 mmol/kg/hour. Continuous IV infusion. Doses needs to be individualised and titrated according to response and to adverse effects (e.g. hypernatraemia) Not recommended for hypercapnia or hypernatraemic states. Caution in infants with renal impairment. Caution in preterm infants. Rapid infusion of hypertonic NaHCO3 has been incriminated in the pathogenesis of intraventricular haemorrhage in preterm infants. Sodium bicarbonate is the alkali most frequently employed for correction of metabolic acidosis. The drug is well absorbed from the gastrointestinal tract. Between 20-50% of an orally administered dose can be recovered in the form of expired carbon dioxide. The apparent bicarbonate space has been estimated to be 74% of body weight (range of 37-134%). Thus calculations of bicarbonate dosage are based on an apparent volume of distribution of 0.3 to 0.6 L/kg. Bicarbonate is rapidly metabolised to carbonic acid which rapidly dissociates into water and carbon dioxide. The carbon dioxide is excreted via the lungs. Venous irritation, soft tissue injury at the site of IV injection. Increased vascular volume, serum osmolarity, serum sodium. Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Kimmoun et al.; licensee BioMed Central.2015 The Erratum to this article has been published in Critical Care 2017 21:40 Lactic acidosis is a very common biological issue for shock patients. Experimental data clearly demonstrate that metabolic acidosis, including lactic acidosis, participates in the reduction of cardiac contractility and in the vascular hyporesponsiveness to vasopressors through various mechanisms. However, the contributions of each mechanism responsible for these deleterious effects have not been fully determined and their respective consequences on organ failure are still poorly defined, particularly in humans. Despite some convincing experimental data, no clinical trial has established the level at which pH becomes deleterious for hemodynamics. Consequently, the essential treatment for lactic acidosis in shock patients is to correct the cause. It is unknown, however, whether symptomatic pH correction is beneficial in shock patients. The latest Surviving Sepsis Campaign guidelines recommend against the use of buffer therapy with pH 7.15 and issue no recommendation for pH levels <7.15. Furthermore, based on strong experimental and clinical evidence, sodium bicarbonate infusion alone is not recommended for restoring pH. Indeed, bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. This review addresses the principal hemodynamic consequences of shock-associated lactic acidosis. Despite the lack of formal evidence, this review also highlights the various adapted supportive therapy options that could be putatively added to causal treatment in attempting to reverse the hemodynamic consequences of shock-associated lactic Continue reading >>

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Volume 49, Issue 5 , May 1996, Pages 1262-1267 Effect of sodium bicarbonate on intracellular pH under different buffering conditions Author links open overlay panel JacquesLevrautDr. Effect of sodium bicarbonate on intracellular pH under different buffering conditions. Previous in vitro studies have reported a paradoxical exacerbation of intracellular acidosis following bicarbonate therapy due to the generated CO2 entering the cytoplasm. However, these studies were conducted in nonphysiological Hepes-buffered media. We compared the effect of a sodium bicarbonate load on the intracellular pH (pHi) of hepatocytes placed in nonbicarbonate (NBBS) or bicarbonate (BBS) buffering systems. The pHi of isolated rat hepatocytes was measured using the fluorescent pH sensitive dye BCECF and a single-cell imaging technique. Cells were placed in medium buffered with or Hepes. All media were adjusted to pH 7 with L-lactic acid or HCl. An acute 45mM sodium bicarbonate load was added to each medium and the changes in pHi were measured every three seconds for 90 seconds. The sodium bicarbonate load caused rapid cytoplasmic acidification of cells in NBBS (N = 50, P < 0.001). In contrast, hepatocytes in BBS underwent a marked increase in pHi (N = 50, P < 0.001) without any initial decrease in pHi. These differences were highly significant for the buffer (P < 0.01), but not for the acid used. We conclude that sodium bicarbonate exacerbates intracellular acidosis only in a NBBS. Hence, in vitro studies reporting a paradoxical intracellular acidosis following bicarbonate therapy cannot be extrapolated to the in vivo buffering conditions, and should not be used to argue against bicarbonate therapy. Continue reading >>

Sodium Bicarbonate

Sodium Bicarbonate

Indications Metabolic Acidosis Diabetic Ketoacidosis (DKA) (see Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State) Indications: pH <6.9-7.0 (however, evidence for this recommendation is lacking) Patients with Hemodynamic Compromise (Due to Impaired Myocardial Contractility and Vasodilation) or Life-Threatening Hyperkalemia May Particularly Benefit from Bicarbonate Administration to Correct the pH Lactic Acidosis (see Lactic Acidosis) Adverse Effects of Acidemia: these (selected adverse effects) provide a rationale for administering bicarbonate with pH <7.1 Arrhythmias Arterial Vasodilation and Venoconstriction Decreased Left Ventricular Contractility Impaired Responsiveness to Catecholamine Vasopressors (Nat Rev Nephrol, 2012) [MEDLINE] Indications: pH <7.1 (however, evidence for this recommendation is lacking) This is due to the fact that at pH <7.1, small changes in pCO2 and serum bicarbonate result in large changes in the serum pH Clinical Efficacy: neither of these trials demonstrated clinical benefit with bicarbonate administration in patients with pH >7.1 Trial of Sodium Bicarbonate in Critically Ill Patients with Lactic Acidosis (Ann Intern Med, 1990) [MEDLINE] Sodium Bicarbonate Did Not Improve Hemodynamics in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Did Not Increase the Cardiovascular Response to Infused Catecholamines in in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Decreased Plasma Ionized Calcium and Increased the pCO2 Trial of Sodium Bicarbonate in Lactic Acidosis (Crit Care Med, 1991) [MEDLINE] Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation Non-Anion Gap Metabo Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis.

Bicarbonate Therapy And Intracellular Acidosis.

1. Clin Sci (Lond). 1997 Dec;93(6):593-8. Bicarbonate therapy and intracellular acidosis. (1)Renal Laboratory, St Thomas' Hospital, London, U.K. 1. The correction of metabolic acidosis with sodium bicarbonate remainscontroversial. Experiments in vitro have suggested possible deleterious effectsafter alkalinization of the extracellular fluid. Disequilibrium of carbon dioxideand bicarbonate across cell membranes after alkali administration, leading to thephenomenon of 'paradoxical' intracellular acidosis, has been held responsible forsome of these adverse effects. 2. Changes in intracellular pH in suspensions ofleucocytes from healthy volunteers were monitored using a fluorescentintracellular dye. The effect in vitro of increasing extracellular pH with sodiumbicarbonate was studied at different sodium bicarbonate concentrations. Lacticacid and propionic acid were added to the extracellular buffer to mimicconditions of metabolic acidosis. 3. The addition of a large bolus of sodiumbicarbonate caused intracellular acidification as has been observed previously.The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate wasadded as a series of small boluses the reduction in intracellular pH was small.Under conditions of initial acidosis this was rapidly followed by intracellularalkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect isminimal when the conditions approximate those seen in clinical practice. Wesuggest that the observed small and transient lowering of intracellular pH isinsufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis

Bicarbonate Therapy And Intracellular Acidosis

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of 'paradoxical' intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Do you want to read the rest of this article? ... However, an experimental study by Benjamin et al. on dogs subjected to hemorrhagic shoc Continue reading >>

Metabolic Acidosis In Childhood: Why, When And How To Treat

Metabolic Acidosis In Childhood: Why, When And How To Treat

Metabolic acidosis in childhood: why, when and how to treat Olberes V. B. AndradeI; Flvio O. IharaII; Eduardo J. TrosterIII IProfessor assistente, Faculdade de Cincias Mdicas, Irmandade da Santa Casa de Misericrdia de So Paulo, So Paulo, SP, Brasil. Mestre, Universidade Federal de So Paulo (UNIFESP), So Paulo, SP, Brasil. Doutor, Irmandade da Santa Casa de Misericrdia de So Paulo, So Paulo, SP, Brasil. Mdico, Centro de Terapia Intensiva Peditrico, Hospital Israelita Albert Einstein, So Paulo, SP, Brasil IIMdico pediatra. Aluno, Curso de Aperfeioamento em Nefrologia Peditrica, Nvel R4, Irmandade da Santa Casa de Misericrdia de So Paulo, So Paulo, SP, Brasil IIIProfessor livre-docente, Departamento de Pediatria, Faculdade de Medicina, Universidade de So Paulo (USP), So Paulo, SP, Brasil. Coordenador, CTI Peditrico, Instituto da Criana, Hospital das Clnicas, Faculdade de Medicina, USP, So Paulo, SP, Brasil. Coordenador, Centro de Terapia Intensiva Peditrico, Hospital Israelita Albert Einstein, So Paulo, SP, Brasil OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resul Continue reading >>

Sodium Bicarb For Treatment Of Acidosis?

Sodium Bicarb For Treatment Of Acidosis?

SDN members see fewer ads and full resolution images. Join our non-profit community! Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? except, when a sudden intolerable decrease in pH is expected (ie release of a clamp or tourniquet), or when all else is failing (ie during a code when i want the pressors to work long enough to gain a foothold - little evidence for this). Agreed. Bicarb is only masking the acidosis and it is better to treat the cause rather than correct the pH. However, if things are beginning to go south in a hurry and you can't correct the problem rapidly enough then bicarb can be a benefit. Mostly by increasing the effectiveness of your inotropes, as Slavin said. Remember, some of the criticism of bicarb came from codes where removal of CO2 was impaired. We don't usually have that issue so some say it won't harm anything to give bicarb. I disagree, CO2 will Continue reading >>

Md51 - Anaesthesia_mcq

Md51 - Anaesthesia_mcq

MD51 [Jul01] An intravenous infusion of 8.4% sodium bicarbonate to a healthy adult maycause:A. HypotonicityB. Intracellular AcidosisC. Ionized HypercalcaemiaD.?Respiratory AlkalosisE. Rebound Metabolic AcidosisMD51b [Feb04] BicarbonateA. Complications include intracellular acidosisB. 100ml of 8.4% NaCO3 has 200 milliosmolesC.? Aug15 108. Side effect 8.4% NaHCO3 administration A. Intracellular acidosisB. Rebound metabolic acidosisC. ... Other options were easy to rule out =============================================================================================================== Brandis p38 - almost word for word (is that allowed?) 8.4% NaHCO3 is a one molar solution because the molecular weight of NaHCO3 is 84 = 84g/L = 8.4g/100mls.But each molecule of NaHCO3 dissociates into 2 particles in solution so the osmolality is double the molality. ie 2 osmoles/kg = 2000mOsm/kg = about 7 times the plasma osmolality. 100mls of the solution would then have 200 mOsm. The ECF HCO3 will cause decrease in H+ concentration. I think this then causes H+ to move out of the cells and K+ to move in. If this is true, B would also be incorrect. Don't know about C,D,E can some smart person help me? Rebound alkalosis is a complication so E would be incorrect. Also read somewhere that hypocalcaemia is a complication (but could be a trick q - ionised or total?) The dissociation of HCO3 would form CO2, which then diffuses into cell to cause intracellular acidosis (from P Kam's lecture notes). This intracellular acidosis has been mentioned before. Keeping in mind that the "neutral pH" intracellularly is thought to be anywhere from 6.8-7.0 where [H+]=[OH-]. See off-the-record discussions at queensland part one course. Lots of sources mention a paradoxical intracellular acidosis occuring followi Continue reading >>

Lactic Acidosis Triggers Starvation Response With Paradoxical Induction Of Txnip Through Mondoa

Lactic Acidosis Triggers Starvation Response With Paradoxical Induction Of Txnip Through Mondoa

Lactic Acidosis Triggers Starvation Response with Paradoxical Induction of TXNIP through MondoA Affiliations Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliation Department of Statistical Science, Duke University, Durham, North Carolina, United States of America Affiliation Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah, Salt Lake City, Utah, United States of America Affiliations Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America Affiliations Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, United States of America, Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, United States of America, Department of Medicine, National Yang-Ming University, Taipei, Taiwan Affiliation Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah, Salt Lake City, Utah, United States of America Affiliation Sarah W. Stedman Nutrition and Metabolism Center, Department of Pharmacology and Cancer Biology and Department of Medicine, Duke University Medical Center, Durham, North Carolina, United States of America Affiliation Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah, Salt Lake City, Utah, United States of America Affiliation Department of Statistical Science, Duke University, Durham, North Carolina, United States of America Affiliations Institute for Genome Sciences and Continue reading >>

Pyruvate In The Correction Of Intracellular Acidosis: A Metabolic Basis As A Novel Superior Buffer

Pyruvate In The Correction Of Intracellular Acidosis: A Metabolic Basis As A Novel Superior Buffer

Pyruvate in the Correction of Intracellular Acidosis: A Metabolic Basis as a Novel Superior Buffer Tel. +1 847 394 6250, Fax +1 847 394 4621, E-Mail [email protected] The review focuses on biochemical metabolisms of conventional buffers and emphasizes advantages of sodium pyruvate (Pyr) in the correction of intracellular acidosis. Exogenous lactate (Lac) as an alternative of natural buffer, bicarbonate, consumes intracellular protons on an equimolar basis, regenerating bicarbonate anions in plasma while the completion of gluconeogenesis and/or oxidation occurs via tricarboxylic-acid cycle in mitochondria mainly in liver and kidney, or heart. The general assumption that Lac is metabolized to bicarbonate in liver to serve as a buffer has been questioned. Pyr as a novel buffer would be superior to conventional ones in the correction of metabolic acidosis. Several likely biochemical mechanisms of Pyr action are discussed. Experimental evidence, in vivo, strongly suggested that Pyr would be particularly efficient in the correction of severe acidemia: type A lactic acidosis, hypercapnia with cardiac arrest, and diabetic and alcoholic ketoacidosis in animal experiments and clinic settings. Because of its multi-cytoprotection, Pyrs not only correct acidosis, but also benefit theunderlying dysfunction of vital organs. In addition, Pyr is also a potential buffer component of dialysis solutions. However, the instability of Pyr in aqueous solutions restricts its clinical applications as a therapeutic agent. Attempts to create a stable Pyr preparation are needed. Since 1970s, pyruvate (Pyr) has become increasingly attractive in the protection of dysfunctional vital organs, particularly in myocardial ischemia and reperfusion injury, pointing to a potential therapeutic value for the dy Continue reading >>

Effect Of Acidic Reperfusion On Prolongation Of Intracellular Acidosis And Myocardial Salvage

Effect Of Acidic Reperfusion On Prolongation Of Intracellular Acidosis And Myocardial Salvage

Effect of acidic reperfusion on prolongation of intracellular acidosis and myocardial salvage Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Pg. Vall d Hebron 119129, Barcelona 08035 Corresponding author. Tel: +34 93 489 4038; fax: Cardiovascular Research, Volume 77, Issue 4, 1 March 2008, Pages 782790, Javier Inserte, Ignasi Barba, Vctor Hernando, Arancha Abelln, Marisol Ruiz-Meana, Antonio Rodrguez-Sinovas, David Garcia-Dorado; Effect of acidic reperfusion on prolongation of intracellular acidosis and myocardial salvage, Cardiovascular Research, Volume 77, Issue 4, 1 March 2008, Pages 782790, It has been proposed that intracellular acidosis may be the basis of the cardioprotection of different interventions, including postconditioning. However, contradictory reports exist on the effects of acidic reperfusion on myocardial salvage. Here we characterized the effect of lowering the pH of the reperfusion media (pHo) on intracellular pH (pHi) and cell death. The effect of acidic perfusion on reperfusion injury was studied in isolated rat hearts submitted to 40 min of ischaemia and 30 min of reperfusion, and its effect on the Na+/Ca2+-exchanger (NCX) was analysed in isolated myocytes. pHi and phosphocreatine (PCr) were monitored by nuclear magnetic resonance spectroscopy. Lowering pHo to 6.4 during the initial 3 min of reperfusion delayed pHi normalization, improved PCr recovery, and markedly reduced (P < 0.001) lactate dehydrogenase release and infarct size (tetrazolium reaction). This cardioprotection was attenuated as pHo was increased, and was lost at pH0 7.0. Extendi Continue reading >>

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