Literature DB >> 6662128

Calcium-free cardioplegia--pro.

M M Gebhard, H J Bretschneider, E Gersing, C J Preusse, P A Schnabel, L J Ulbricht.   

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).

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Year:  1983        PMID: 6662128     DOI: 10.1093/eurheartj/4.suppl_h.151

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  7 in total

1.  Non-invasive assessment of perioperative myocardial cell damage by circulating cardiac troponin T.

Authors:  H A Katus; M Schoeppenthau; A Tanzeem; H G Bauer; W Saggau; K W Diederich; S Hagl; W Kuebler
Journal:  Br Heart J       Date:  1991-05

2.  Acronym aggravation.

Authors:  T O Cheng
Journal:  Br Heart J       Date:  1994-01

3.  Monitoring myocardial damage in cardiac surgery by troponin T detection.

Authors:  M Triggiani; A Dolci; F Donatelli; A Grossi
Journal:  Br Heart J       Date:  1994-01

4.  Effects of glucose in protected ischemic kidneys.

Authors:  M Kallerhoff; M Blech; G Kehrer; H Kleinert; M Langheinrich; W Siekmann; U Helmchen; H J Bretschneider
Journal:  Urol Res       Date:  1987

5.  Intracellular sodium activity and Bretschneider's cardioplegia: continuous measurement by ion-selective microelectrodes at initial equilibration.

Authors:  B Stinner; E Krohn; M M Gebhard; H J Bretschneider
Journal:  Basic Res Cardiol       Date:  1989 Mar-Apr       Impact factor: 17.165

6.  Metabolic, energetic and structural changes in protected and unprotected kidneys at temperatures of 1 degree C and 25 degrees C.

Authors:  M Kallerhoff; M Blech; F E Isemer; G Kehrer; H Kleinert; M Langheinrich; U Helmchen; H J Bretschneider
Journal:  Urol Res       Date:  1988

7.  The calcium paradox - what should we have to fear?

Authors:  Marcos Aurélio Barboza de Oliveira; Antônio Carlos Brandi; Carlos Alberto Dos Santos; Paulo Henrique Husseni Botelho; José Luís Lasso Cortez; Gilberto Goissis; Domingo Marcolino Braile
Journal:  Rev Bras Cir Cardiovasc       Date:  2014 Apr-Jun
  7 in total

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