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Ann Thorac Surg 1998;65:1065-1070
© 1998 The Society of Thoracic Surgeons

Calcium Preconditioning in Human Myocardium

^a Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado, USA

Accepted for publication November 18, 1997.

Address reprint requests to Dr Cain, Department of Surgery, University of Colorado Health Sciences Center, C-320, 4200 East Ninth Ave, Denver, CO 80262

Background. Ischemic stress and other protein kinase C (PKC)–linked receptor stimuli can induce rapid cardiac protection against ischemia-reperfusion injury. We and others have demonstrated that exogenous calcium (Ca²⁺) pretreatment confers PKC-mediated cardiac functional and infarct protection in animal models, but it remains unknown whether Ca²⁺ preconditioning confers similar postischemic functional protection in human myocardium, and, if so, whether the mechanism is mediated by PKC. We postulated that Ca²⁺ preconditioning confers ischemic tolerance to human myocardium by a PKC-dependent mechanism.

Methods. Human atrial trabeculae were suspended in organ baths and paced at 1 Hz, and force development was recorded. After 90 minutes of equilibration, all trabeculae were subjected to ischemia (45 minutes) and reperfusion (120 minutes). Exogenous CaCl₂ (3.0 mmol/L for 5 minutes) or vehicle (saline solution) was administered before simulated ischemia, with or without concurrent PKC inhibition (bisindolylmaleimide I, 150 nmol/L).

Results. Ischemia-reperfusion resulted in decreased postischemic developed force, Ca²⁺ preconditioning protected human myocardium against ischemia-reperfusion injury (p < 0.05 versus control ischemia-reperfusion), and concurrent PKC inhibition abolished the salutary effect of Ca²⁺ preconditioning in human myocardium (p < 0.05 versus Ca²⁺ preconditioning).

Conclusions. Preconditioning with Ca²⁺ represents a potent means of accessing PKC-mediated protection of the human myocardium against ischemia-reperfusion injury.

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