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Calcium-free cardioplegia—pro

Preischaemic doubling of the myocardial buffer capacity optimizes the energy supply of the ischaemic heart by anaerobic glyeolysis. For osmotic reasons this method of improving ischaemia tolerance can only be realized in combination with cardioplegia by extracellular Na+ and Ca2+ reduction. The card...

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Published in:European heart journal 1983-12, Vol.4 (suppl-H), p.151-160
Main Authors: Gebhard, M. M., Bretschneider, H. J., Gersing, E., Preusse, C. J., Schnabel, Ph. A., Ulbricht, L. J.
Format: Article
Language:English
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Summary:Preischaemic doubling of the myocardial buffer capacity optimizes the energy supply of the ischaemic heart by anaerobic glyeolysis. For osmotic reasons this method of improving ischaemia tolerance can only be realized in combination with cardioplegia by extracellular Na+ and Ca2+ reduction. The cardioplegic solution ‘HTK’ which has been developed according to these considerations delays the decay velocity of myocardial ATP by a factor of 7–8 in comparison with pure ischaemia: leads to a good myocardial recovery with regard to metabolic, morphological, and functional criteria after an ischaemic stress of 300 min at 23±1ΰC—especially after the addition of quinine: is considerably reduced in its protective efficacy by adding 50 μmol l−1 Ca2+ causes a calcium paradox if it is infused for 30 min at 35ΰC: this does not happen if it is infused for 60 min at 25ΰC or for 120 min at 15ΰC: on adding 50 μmol l−1 Ca2+ to the solution the risk of a calcium paradox is significantly reduced, even after infusion for 35 min at 35ΰC: effects an evident delay of recovery, if a continuous ischaemic stress of 300 min at 23±1ΰC is reduced to 3×100 min of ischaemia at 17±1ΰC by intermittent cardioplegic reperfusion: considerably improves the myocardial recovery even after intermittent cardioplegia if 50 μmol l−1 Ca2+ are added or Mg2+ is reduced from 9 to 4 mmol l−12 The metabolic, morphological, and functional results are equivalent to those after 300 min of continuous ischaemia. Further investigations must show to what extent the ‘membrane stabilizing eftect’ of [Ca2+]ocan be achieved by taking advantage of mutual ionic interaction on the level of plasmalemma (e.g. H+-Mg2+-Ca2+) or by adding membrane effective substances (quinine).
ISSN:0195-668X
1522-9645
DOI:10.1093/eurheartj/4.suppl_H.151