Calcium-free cardioplegia--pro

Abstract

Preischaemic doubling of the myocardial buffer capacity optimizes the energy supply of the ischaemic heart by anaerobic glycolysis. 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. (1) delays the decay velocity of myocardial ATP by a factor of 7-8 in comparison with pure ischaemia; (2) leads to a good myocardial recovery with regard to metabolic, morphological, and functional criteria after an ischaemic stress of 300 min at 23 +/- 1 degrees C--especially after the addition of quinine; (3) is considerably reduced in its protective efficacy by adding 50 mumol l-1 Ca2+; (4) causes a calcium paradox if it is infused for 30 min at 35 degrees C; this does not happen if it is infused for 60 min at 25 degrees C or for 120 min at 15 degrees C; on adding 50 mumol l-1 Ca2+ to the solution the risk of a calcium paradox is significantly reduced, even after infusion for 35 min at 35 degrees C; (5) effects an evident delay of recovery, if a continuous ischaemic stress of 300 min at 23 degrees +/- 1 degree C is reduced to 3 X 100 min of ischaemia at 17 +/- 1 degrees C by intermittent cardioplegic reperfusion; (6) considerably improves the myocardial recovery even after intermittent cardioplegia if 50 mumol 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 effect' of [Ca2+]o can 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).

Intracellular sodium activity and Bretschneider's cardioplegia: Continuous measurement by ionselective microelectrodes at initial equilibration

“…The theoretical danger of inducing a "calcium paradox" -like injury associated with calcium-free cardioplegia remains a major controversy, despite its successful clinical application in the past decade (20,21,26). Although not investigated directly, our data touch on this problem.…”

Contribution of amino acids in protective solutions to postischemic functional recovery of canine kidneys

“…Renal perfusion with a nominally Ca++-free solution bears the risk of evoking a calcium paradox [50] if the solution has Ca + + complexing properties, especially with intermittent application [22]. It is not clear from the literature whether the reported potential nephrotoxicity or negative effects of amino acids such as aspartate [5,56,79] are related to calcium binding.…”

“…With a moderately increased Mg ++ only a part of the calcium-binding capacity of an aspartate solution can be saturated. On the other hand, in spite of beneficial effects on intracellular sites [2,10,22,32], an elevated Mg ++ under certain circumstances can intensify negative Ca ++ membrane effects [22].…”

Increased Primary Non-Function in Transplanted Deceased-Donor Kidneys Flushed with Histidine-Tryptophan-Ketoglutarate Solution

“…Originally introduced as a cardioplegic agent in the 1970s (1,2), Histidine‐Tryptophan‐Ketoglutarate (HTK) solution has increasingly replaced University of Wisconsin (UW) solution for allograft abdominal organ preservation, especially kidneys (3,4). Advantages claimed for HTK included better tissue perfusion due to lower viscosity, less potassium, additives are not required and no filtration is needed during perfusion (3,5).…”