Lactate efflux from the ischaemic myocardium: The influence of pH

Dennis, Steven C.; McCarthy, James; Keding, B

doi:10.1016/s0022-2828(86)80835-5

Journal of Molecular and Cellular Cardiology

1986

DOI: 10.1016/s0022-2828(86)80835-5

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Lactate efflux from the ischaemic myocardium: The influence of pH

Steven C. Dennis¹,

James McCarthy²,

B Keding³

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1988

1993

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“…'4 For example, the hydrolysis of phosphocreatine (PCr) and accumulation of inorganic phosphate (Pi) will alter the buffering capacity of the heart,14'15 and the accumulation of CO2 and lactate may, when washed out during reperfusion, contribute to pHi recovery. [16][17][18][19][20] In this study, we report on the mechanisms of pHi recovery after global ischemia in the Langendorffperfused ferret heart and correlate the activity of these mechanisms with recovery of cardiac contraction. The role of H'-coupled lactate efflux has been estimated by assaying lactate in the myocardial effluent during reperfusion and by using 4,4'-dibenzamidostilbene-2,2'-disulfonate (DBDS) to inhibit lactate efflux.20 22 The contribution of the Na+-H antiport has been assessed using the high-affinity Na+-H+ antiport inhibitor 5-(N-ethyl-N-isopropyl)amiloride (EIPA).…”

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Mechanisms of pHi recovery after global ischemia in the perfused heart.

Vandenberg

Metcalfe

Grace

1993

Circulation Research

154

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A Na(+)-HCO3- coinflux carrier and the Na(+)-H+ antiport have both been shown to contribute to recovery from intracellular acidosis in cardiac tissue. We have investigated the participation of these mechanisms as well as metabolite (lactate and CO2) washout in the recovery of pHi after myocardial ischemia. Isovolumic ferret hearts were Langendorff-perfused with either HCO3(-)-buffered or nominally HCO3(-)-free (HEPES-buffered) medium at 30 degrees C. pHi was estimated from the chemical shift of the 31P-nuclear magnetic resonance signal of intracellular PO4-, and net H+ efflux rates were calculated at pHi 6.80. The H+ efflux rate during reperfusion, after 10 minutes of global ischemia, was 15.5 +/- 1.9 mmol.l-1 x min-1 (n = 10) in hearts perfused with HCO3(-)-buffered medium and 8.2 +/- 1.5 mmol.l-1 x min-1 (n = 9, p < 0.01) in hearts perfused with HEPES-buffered medium. HCO3- influx, assessed either by inhibition by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (20 microM) or by initially perfusing hearts with HEPES-buffered medium but reperfusing with HCO3(-)-buffered medium, accounted for 3.5-4.9 mmol.l-1 x min-1, and CO2 efflux accounted for 3.8-6.2 mmol.l-1 x min-1 of the additional H+ efflux in HCO3(-)-buffered medium. H(+)-coupled lactate efflux, measured by NAD(+)-linked spectrophotometric assay and inhibited by the sarcolemmal monocarboxylate transport inhibitor 4,4'-dibenzamidostilbene-2,2'-disulfonate (0.25 mM), contributed 3.7-6.2 mmol.l-1 x min-1. H+ efflux via the 5-(N-ethyl-N-isopropyl)amiloride-sensitive Na(+)-H+ antiport was 1.0-2.9 mmol.l-1 x min-1. pHi recovery after ischemia is therefore principally mediated by metabolite (lactate and CO2) washout. Na(+)-coupled acid extrusion contributed approximately 35% of total H+ efflux in this system. However, the associated Na+ entry (approximately 5 mmol.l-1 x min-1) may contribute to Ca2+ overload after reperfusion.

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confidence: 99%

Mechanisms of pHi recovery after global ischemia in the perfused heart.

Vandenberg

Metcalfe

Grace

1993

Circulation Research

154

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Aggravation of left ventricular dilatation and reduction of survival by a calcium channel blocker in rats with chronic myocardial infarction

Gaudron

Blumrich

Ertl

1993

American Heart Journal

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Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: A phosphorus-31 nuclear magnetic resonance study

Kirkels

Ruigrok

Echteld

et al. 1988

Journal of the American College of Cardiology

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To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total ischemia (37 degrees C), followed by 30 min of reperfusion. Pretreatment with anipamil altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of adenosine triphosphate (ATP) and creatine phosphate during ischemia. Intracellular acidification, however, was attenuated. On reperfusion, hearts from anipamil-pretreated animals recovered significantly better than untreated hearts with respect to replenishment of ATP and creatine phosphate stores, restitution of low levels of intracellular inorganic phosphate and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic phosphate peak indicated the existence of areas of different pH within the myocardium. It is concluded that anipamil pretreatment protects the heart against some of the deleterious effects of ischemia and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during ischemia. Therefore, alternative mechanisms of action are to be considered.

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Lactate efflux from the ischaemic myocardium: The influence of pH

Cited by 5 publications

References 0 publications

Mechanisms of pHi recovery after global ischemia in the perfused heart.

Mechanisms of pHi recovery after global ischemia in the perfused heart.

Aggravation of left ventricular dilatation and reduction of survival by a calcium channel blocker in rats with chronic myocardial infarction

Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: A phosphorus-31 nuclear magnetic resonance study

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