RAPID COOLING CONTRACTURE WITH COLD CARDIOPLEGIA

Background. Cold cardioplegia can induce rapid cooling contracture. Th e relations of cardioplegia-induced cooling contracture to myocardial temperature or myocyte calcium are unknown. Methods. Twelve crystalloi d-perfused isovolumic rat hearts received three 2-minute cardioplegic infusions (1 mmol/L calcium) at 4 degrees, 20 degrees, and 37 degrees C in random order, each followed by 10 minutes of beating at 37 degree s C. Finally, warm induction of arrest by a 1-minute cardioplegic infu sion at 37 degrees C was followed by a 1-minute infusion at 4 degrees C Indo-1 was used to measure the intracellular Ca2+ concentration in 6 of these hearts. Additional hearts received hypoxic, glucose-free car dioplegia at 4 degrees or 37 degrees C. Results. After 1 minute of car dioplegia at 4 degrees, 20 degrees, and 37 degrees C, left ventricular developed pressure rose rapidly to 54% +/- 3%, 43% +/- 3%, and 18% +/ - 1% of its prearrest value, whereas the intracellular Ca2+ concentrat ion reached 166% +/- 23%, 94% +/- 4%, and 37% +/- 10% of its prearrest transient. Coronary flow was 5.7 +/- 0.2, 8.7 +/- 0.3, and 12.6 +/- 0 .6 mL/min, respectively. Warm cardioplegia induction at 37 degrees C r educed left ventricular developed pressure and [Ca2+](i) during subseq uent 4 degrees C cardioplegia by 16% (p = 0.001) and 34% (p = 0.03), r espectively. Adenosine triphosphate and phosphocreatine contents were lower after 4 degrees C than after 37 degrees C hypoxic, glucose-free cardioplegia. Conclusions. Rapid cooling during cardioplegia increases left ventricular pressure, [Ca2+](i), and coronary resistance, and is energy consuming. The absence of rapid cooling contracture may be a b enefit of warm heart operations and warm induction of cardioplegic arr est. (C) 1997 by The Society of Thoracic Surgeons.