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Ann Thorac Surg 1997;63:1353-1360
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Rapid Cooling Contracture With Cold Cardioplegia

Cardiac Surgical Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts

Accepted for publication December 5, 1996.

Background. Cold cardioplegia can induce rapid cooling contracture. The relations of cardioplegia-induced cooling contracture to myocardial temperature or myocyte calcium are unknown.

Methods. Twelve crystalloid-perfused isovolumic rat hearts received three 2-minute cardioplegic infusions (1 mmol/L calcium) at 4°, 20°, and 37°C in random order, each followed by 10 minutes of beating at 37°C. Finally, warm induction of arrest by a 1-minute cardioplegic infusion at 37°C was followed by a 1-minute infusion at 4°C. Indo-1 was used to measure the intracellular Ca²⁺ concentration in 6 of these hearts. Additional hearts received hypoxic, glucose-free cardioplegia at 4° or 37°C.

Results. After 1 minute of cardioplegia at 4°, 20°, and 37°C, left ventricular developed pressure rose rapidly to 54% ± 3%, 43% ± 3%, and 18% ± 1% of its prearrest value, whereas the intracellular Ca²⁺ concentration 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°C reduced left ventricular developed pressure and [Ca²⁺]_i during subsequent 4°C cardioplegia by 16% (p = 0.001) and 34% (p = 0.03), respectively. Adenosine triphosphate and phosphocreatine contents were lower after 4°C than after 37°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 benefit of warm heart operations and warm induction of cardioplegic arrest.

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