Mechanism of preconditioning. Ionic alterations.
Identifieur interne : 000C32 ( Ncbi/Merge ); précédent : 000C31; suivant : 000C33Mechanism of preconditioning. Ionic alterations.
Auteurs : C. Steenbergen [États-Unis] ; M E Perlman ; R E London ; E. MurphySource :
- Circulation research [ 0009-7330 ] ; 1993.
Descripteurs français
- KwdFr :
- Adaptation physiologique, Adénosine triphosphate (métabolisme), Animaux, Calcium (métabolisme), Cochons d'Inde, Ischémie myocardique (physiopathologie), Lésion d'ischémie-reperfusion (), Lésion d'ischémie-reperfusion (métabolisme), Modèles animaux de maladie humaine, Mâle, Phosphates (métabolisme), Protons, Rat Sprague-Dawley, Rats, Sodium (métabolisme).
- MESH :
- métabolisme : Adénosine triphosphate, Calcium, Lésion d'ischémie-reperfusion, Phosphates, Sodium.
- physiopathologie : Ischémie myocardique.
- Adaptation physiologique, Animaux, Cochons d'Inde, Lésion d'ischémie-reperfusion, Modèles animaux de maladie humaine, Mâle, Protons, Rat Sprague-Dawley, Rats.
English descriptors
- KwdEn :
- Adaptation, Physiological, Adenosine Triphosphate (metabolism), Animals, Calcium (metabolism), Disease Models, Animal, Guinea Pigs, Male, Myocardial Ischemia (physiopathology), Phosphates (metabolism), Protons, Rats, Rats, Sprague-Dawley, Reperfusion Injury (metabolism), Reperfusion Injury (prevention & control), Sodium (metabolism).
- MESH :
- chemical , metabolism : Adenosine Triphosphate, Calcium, Phosphates, Sodium.
- metabolism : Reperfusion Injury.
- physiopathology : Myocardial Ischemia.
- prevention & control : Reperfusion Injury.
- Adaptation, Physiological, Animals, Disease Models, Animal, Guinea Pigs, Male, Protons, Rats, Rats, Sprague-Dawley.
Abstract
The mechanism by which preconditioning (brief intermittent periods of ischemia and reflow) improves recovery of function and reduces enzyme release after a subsequent 30-minute period of ischemia was investigated in perfused rat hearts. Specifically, it was hypothesized that ischemia after preconditioning would result in a decreased production of H+ and therefore a smaller rise in [Na+]i and [Ca2+]i via Na(+)-H+ and Na(+)-Ca2+ exchange. To test this hypothesis we measured pHi, [Na+]i, [Ca2+]i, and cell high-energy phosphates during ischemia and reflow, and we correlated this with recovery of contractile function and release of creatine kinase during reflow. 31P nuclear magnetic resonance (NMR) was used to measure pHi and cell phosphates. [Na+]i was measured by 23Na NMR using the shift reagent thulium 1,4,7,10-tetraazacyclododecane-N,N,'N",N"'-tetramethylenephosph onate to distinguish intracellular from extracellular sodium. [Ca2+]i was measured by 19F NMR using hearts loaded with 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid, termed 5F-BAPTA. Basal time-averaged levels of pHi, [Na+]i, and [Ca2+]i were 7.07 +/- 0.08, 9.4 +/- 0.8 mM, and 715 +/- 31 nM, respectively. After 30 minutes of ischemia, in preconditioned hearts, pHi was 6.5 +/- 0.06, [Na+]i was 2.09 +/- 4.4 mM, [Ca2+]i was 2.1 +/- 0.4 microM, and ATP was negligible. In untreated hearts, after 30 minutes of ischemia, pHi was 6.3 +/- 0.08, [Na+]i was 26.7 +/- 3.8 mM, [Ca2+]i was 3.2 +/- 0.6 microM, and ATP was undetectable. During reperfusion after 30 minutes of ischemia, preconditioned hearts had significantly better recovery of contractile function than untreated hearts (71 +/- 9% versus 36 +/- 8% initial left ventricular developed pressure), and after 60 minutes of ischemia, preconditioned hearts had significantly less release of the intracellular enzyme creatine kinase (102 +/- 12 versus 164 +/- 17 IU/g dry wt). We also found that unpreconditioned hearts arrested with 16 mM MgCl2 (to inhibit calcium entry via calcium channels and Na(+)-Ca2+ exchange) before 30 minutes of ischemia recover function on reflow to the same extent as preconditioned hearts with or without magnesium arrest. Thus, preconditioning has no additional benefit in addition to magnesium arrest. In addition, in hearts that received 16 mM MgCl2 just before the 30-minute period of ischemia, preconditioning had no effect on the rise in [Ca2+]i during the 30-minute period of ischemia. These data support the hypothesis that preconditioning attenuates the increase in [Ca2+]i, [Na+]i, and [H+]i during ischemia, most likely because of reduced stimulation of Na(+)-H+ and Na(+)-Ca2+ exchange.(ABSTRACT TRUNCATED AT 400 WORDS)
PubMed: 8380259
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pubmed:8380259Le document en format XML
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<term>Animals</term>
<term>Calcium (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Guinea Pigs</term>
<term>Male</term>
<term>Myocardial Ischemia (physiopathology)</term>
<term>Phosphates (metabolism)</term>
<term>Protons</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Reperfusion Injury (metabolism)</term>
<term>Reperfusion Injury (prevention & control)</term>
<term>Sodium (metabolism)</term>
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<term>Adénosine triphosphate (métabolisme)</term>
<term>Animaux</term>
<term>Calcium (métabolisme)</term>
<term>Cochons d'Inde</term>
<term>Ischémie myocardique (physiopathologie)</term>
<term>Lésion d'ischémie-reperfusion ()</term>
<term>Lésion d'ischémie-reperfusion (métabolisme)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Phosphates (métabolisme)</term>
<term>Protons</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Sodium (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine Triphosphate</term>
<term>Calcium</term>
<term>Phosphates</term>
<term>Sodium</term>
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<term>Calcium</term>
<term>Lésion d'ischémie-reperfusion</term>
<term>Phosphates</term>
<term>Sodium</term>
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<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Ischémie myocardique</term>
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<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Myocardial Ischemia</term>
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<term>Modèles animaux de maladie humaine</term>
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<front><div type="abstract" xml:lang="en">The mechanism by which preconditioning (brief intermittent periods of ischemia and reflow) improves recovery of function and reduces enzyme release after a subsequent 30-minute period of ischemia was investigated in perfused rat hearts. Specifically, it was hypothesized that ischemia after preconditioning would result in a decreased production of H+ and therefore a smaller rise in [Na+]i and [Ca2+]i via Na(+)-H+ and Na(+)-Ca2+ exchange. To test this hypothesis we measured pHi, [Na+]i, [Ca2+]i, and cell high-energy phosphates during ischemia and reflow, and we correlated this with recovery of contractile function and release of creatine kinase during reflow. 31P nuclear magnetic resonance (NMR) was used to measure pHi and cell phosphates. [Na+]i was measured by 23Na NMR using the shift reagent thulium 1,4,7,10-tetraazacyclododecane-N,N,'N",N"'-tetramethylenephosph onate to distinguish intracellular from extracellular sodium. [Ca2+]i was measured by 19F NMR using hearts loaded with 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid, termed 5F-BAPTA. Basal time-averaged levels of pHi, [Na+]i, and [Ca2+]i were 7.07 +/- 0.08, 9.4 +/- 0.8 mM, and 715 +/- 31 nM, respectively. After 30 minutes of ischemia, in preconditioned hearts, pHi was 6.5 +/- 0.06, [Na+]i was 2.09 +/- 4.4 mM, [Ca2+]i was 2.1 +/- 0.4 microM, and ATP was negligible. In untreated hearts, after 30 minutes of ischemia, pHi was 6.3 +/- 0.08, [Na+]i was 26.7 +/- 3.8 mM, [Ca2+]i was 3.2 +/- 0.6 microM, and ATP was undetectable. During reperfusion after 30 minutes of ischemia, preconditioned hearts had significantly better recovery of contractile function than untreated hearts (71 +/- 9% versus 36 +/- 8% initial left ventricular developed pressure), and after 60 minutes of ischemia, preconditioned hearts had significantly less release of the intracellular enzyme creatine kinase (102 +/- 12 versus 164 +/- 17 IU/g dry wt). We also found that unpreconditioned hearts arrested with 16 mM MgCl2 (to inhibit calcium entry via calcium channels and Na(+)-Ca2+ exchange) before 30 minutes of ischemia recover function on reflow to the same extent as preconditioned hearts with or without magnesium arrest. Thus, preconditioning has no additional benefit in addition to magnesium arrest. In addition, in hearts that received 16 mM MgCl2 just before the 30-minute period of ischemia, preconditioning had no effect on the rise in [Ca2+]i during the 30-minute period of ischemia. These data support the hypothesis that preconditioning attenuates the increase in [Ca2+]i, [Na+]i, and [H+]i during ischemia, most likely because of reduced stimulation of Na(+)-H+ and Na(+)-Ca2+ exchange.(ABSTRACT TRUNCATED AT 400 WORDS)</div>
</front>
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<Abstract><AbstractText>The mechanism by which preconditioning (brief intermittent periods of ischemia and reflow) improves recovery of function and reduces enzyme release after a subsequent 30-minute period of ischemia was investigated in perfused rat hearts. Specifically, it was hypothesized that ischemia after preconditioning would result in a decreased production of H+ and therefore a smaller rise in [Na+]i and [Ca2+]i via Na(+)-H+ and Na(+)-Ca2+ exchange. To test this hypothesis we measured pHi, [Na+]i, [Ca2+]i, and cell high-energy phosphates during ischemia and reflow, and we correlated this with recovery of contractile function and release of creatine kinase during reflow. 31P nuclear magnetic resonance (NMR) was used to measure pHi and cell phosphates. [Na+]i was measured by 23Na NMR using the shift reagent thulium 1,4,7,10-tetraazacyclododecane-N,N,'N",N"'-tetramethylenephosph onate to distinguish intracellular from extracellular sodium. [Ca2+]i was measured by 19F NMR using hearts loaded with 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid, termed 5F-BAPTA. Basal time-averaged levels of pHi, [Na+]i, and [Ca2+]i were 7.07 +/- 0.08, 9.4 +/- 0.8 mM, and 715 +/- 31 nM, respectively. After 30 minutes of ischemia, in preconditioned hearts, pHi was 6.5 +/- 0.06, [Na+]i was 2.09 +/- 4.4 mM, [Ca2+]i was 2.1 +/- 0.4 microM, and ATP was negligible. In untreated hearts, after 30 minutes of ischemia, pHi was 6.3 +/- 0.08, [Na+]i was 26.7 +/- 3.8 mM, [Ca2+]i was 3.2 +/- 0.6 microM, and ATP was undetectable. During reperfusion after 30 minutes of ischemia, preconditioned hearts had significantly better recovery of contractile function than untreated hearts (71 +/- 9% versus 36 +/- 8% initial left ventricular developed pressure), and after 60 minutes of ischemia, preconditioned hearts had significantly less release of the intracellular enzyme creatine kinase (102 +/- 12 versus 164 +/- 17 IU/g dry wt). We also found that unpreconditioned hearts arrested with 16 mM MgCl2 (to inhibit calcium entry via calcium channels and Na(+)-Ca2+ exchange) before 30 minutes of ischemia recover function on reflow to the same extent as preconditioned hearts with or without magnesium arrest. Thus, preconditioning has no additional benefit in addition to magnesium arrest. In addition, in hearts that received 16 mM MgCl2 just before the 30-minute period of ischemia, preconditioning had no effect on the rise in [Ca2+]i during the 30-minute period of ischemia. These data support the hypothesis that preconditioning attenuates the increase in [Ca2+]i, [Na+]i, and [H+]i during ischemia, most likely because of reduced stimulation of Na(+)-H+ and Na(+)-Ca2+ exchange.(ABSTRACT TRUNCATED AT 400 WORDS)</AbstractText>
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