Myocardial energy metabolism and ultrastructure with polarizing and depolarizing cardioplegia in a porcine model.
OBJECTIVE
This study investigated whether the novel St. Thomas' Hospital polarizing cardioplegic solution (STH-POL) with esmolol/adenosine/magnesium offers improved myocardial protection by reducing demands for high-energy phosphates during cardiac arrest compared to the depolarizing St. Thomas' Hospital cardioplegic solution No 2 (STH-2).


METHODS
Twenty anaesthetised pigs on tepid cardiopulmonary bypass were randomized to cardiac arrest for 60 min with antegrade freshly mixed, repeated, cold, oxygenated STH-POL or STH-2 blood cardioplegia every 20 min. Haemodynamic variables were continuously recorded. Left ventricular biopsies, snap-frozen in liquid nitrogen or fixed in glutaraldehyde, were obtained at Baseline, 58 min after cross-clamp and 20 and 180 min after weaning from bypass. Adenine nucleotides were evaluated by high-performance liquid chromatography, myocardial ultrastructure with morphometry.


RESULTS
With STH-POL myocardial creatine phosphate was increased compared to STH-2 at 58 min of cross-clamp [59.9 ± 6.4 (SEM) vs 44.5 ± 7.4 nmol/mg protein; P  <   0.025], and at 20 min after reperfusion (61.0 ± 6.7 vs 49.0 ± 5.5 nmol/mg protein; P  <   0.05), ATP levels were increased at 20 min of reperfusion with STH-POL (35.4 ± 1.1 vs 32.4 ± 1.2 nmol/mg protein; P  <   0.05). Mitochondrial surface-to-volume ratio was decreased with polarizing compared to depolarizing cardioplegia 20 min after reperfusion (6.74 ± 0.14 vs 7.46 ± 0.13 µm 2 /µm 3 ; P  =   0.047). None of these differences were present at 180 min of reperfusion. From 150 min of reperfusion and onwards, cardiac index was increased with STH-POL; 4.8 ± 0.2 compared to 4.0 ± 0.2 l/min/m 2 ( P  =   0.011) for STH-2 at 180 min.


CONCLUSIONS
Polarizing STH-POL cardioplegia improved energy status compared to standard STH-2 depolarizing blood cardioplegia during cardioplegic arrest and early after reperfusion.
Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.|Department of Clinical Science, University of Bergen, Bergen, Norway.
Terje
T
Aass
Department of Clinical Science, University of Bergen, Bergen, Norway.
Lodve
L
Stangeland
Cardiac Surgical Research, The Rayne Institute (King's College London), Guy's and St Thomas' NHS Foundation Trust, St Thomas' Hospital, London, UK.
David J
DJ
Chambers
Institute of Physiological Chemistry, Center of Physiological Medicine, Medical University Graz, Graz, Austria.
Seth
S
Hallström
Institute of Physiological Chemistry, Center of Physiological Medicine, Medical University Graz, Graz, Austria.
Christine
C
Rossmann
Department of Biomedical Research, Ludwig Boltzmann Cluster for Cardiovascular Research, Medical University of Vienna, Vienna, Austria.
Bruno K
BK
Podesser
Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
Malte
M
Urban
Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
Knut
K
Nesheim
Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.|Department of Clinical Science, University of Bergen, Bergen, Norway.
Rune
R
Haaverstad
Department of Clinical Science, University of Bergen, Bergen, Norway.
Knut
K
Matre
Department of Clinical Science, University of Bergen, Bergen, Norway.
Ketil
K
Grong
D000818:Animals; D001706:Biopsy; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003404:Creatinine / Q000378:metabolism; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006323:Heart Arrest / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D006324:Heart Arrest, Induced / Q000379:methods*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D010725:Phosphocreatine / Q000378:metabolism; D012372:ROC Curve; D013552:Swine
D002314:Cardioplegic Solutions; D010725:Phosphocreatine; D003404:Creatinine
Cardioplegia; Energy metabolism; Myocardial protection; Ultrastructure