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The Effects of Simultaneous Antegrade/Retrograde Cardioplegia on Cellular Volumes and Energy Metabolism
Author(s) -
Li Gang,
Tian Weichen,
Wang Jian,
Xiang Bo,
Wang Lei,
Deng Jixian,
Salerno Tomas A.,
Deslauriers Roxanne,
Tian Ganghong
Publication year - 2008
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.2008.00690.x
Subject(s) - phosphocreatine , retrograde perfusion , perfusion , medicine , extracellular , intracellular , homeostasis , energy metabolism , metabolism , adenosine triphosphate , extracellular fluid , high energy phosphate , cardiology , biochemistry , chemistry
Background and aim of the study: Simultaneous antegrade/retrograde cardioplegia (SARC) has been employed frequently during cardiac surgery to preserve the jeopardized myocardium. However, retrograde perfusion of SARC may interfere with myocardial drainage and disrupt myocardial fluid homeostasis, which may affect the myocardial energy metabolism and contractile function. The study was, therefore, designed to assess the effects of SARC on myocardial fluid homeostasis, cellular volumes, and energy metabolism. Methods: Eight isolated pig hearts were subjected to a protocol consisting of a 20‐minute control perfusion, 120‐minute SARC, and 20‐minute reperfusion. The myocardial water content was monitored using near‐infrared spectroscopy. Phosphorus‐31 magnetic resonance ( 31 P MR) spectroscopy was used to monitor the volumes of both intracellular and extracellular compartments and assess myocardial energy metabolism. Results: The near‐infrared spectra showed that the 120‐min SARC resulted in a 60 ± 12% increase in the myocardial water content. 31 P MR spectra showed a 36 ± 4% increase in the intracellular compartment and a 54 ± 8% increase in the extracellular compartment during SARC relative to their initial volumes measured during control perfusion (100%). However, the myocardial energy metabolites (adenosine triphosphate [ATP] and phosphocreatine [PCr]) remained unchanged during the 120‐minute SARC. Moreover, during reperfusion, the hearts showed an almost complete recovery in the left ventricular‐developed pressure. Conclusions: A prolonged SARC resulted in water accumulation in both extracellular and intracellular compartments in the normal myocardium. Although its detrimental effect on tissue fluid homeostasis did not jeopardize the myocardial energy metabolism, a prolonged use of SARC should be avoided, particularly in the diseased hearts.