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Ann Thorac Surg 1997;64:1360-1367
© 1997 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Comparative Effects of Continuous Warm Blood and Intermittent Cold Blood Cardioplegia on Coronary Reactivity

Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel–Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts

Accepted for publication June 2, 1997.

Background. Cardioplegia is known to affect coronary vascular reactivity. We examined the effects of intermittent cold and continuous warm blood cardioplegia on ß-adrenoceptor–mediated, adenosine triphosphate–sensitive K⁺ (K⁺_ATP)–channel–mediated, and endothelium-dependent relaxation and on the myogenic tone of coronary arterioles.

Methods. Pigs were placed on cardiopulmonary bypass. Hearts were arrested for 1 hour with a cold blood cardioplegic solution administered intermittently (n = 12; iCB-CP) or with a warm blood cardioplegic solution delivered continuously (n = 12; cWB-CP). Selected hearts (n = 6 in each group) were then reperfused for 1 hour. In vitro relaxation responses of precontracted microvessels (50 to 160 µm) were studied in a pressurized no-flow state.

Results. Relaxation in response to isoproterenol (ß-adrenergic agonist) was similar after iCB-CP and cWB-CP, whereas forskolin (adenylate cyclase activator)–induced relaxation was impaired more after iCB-CP than after cWB-CP. After reperfusion the respective responses were similar. Both iCB-CP and cWB-CP preserved receptor-mediated, endothelium-dependent relaxation in response to adenosine, 5`-diphosphate; non–receptor-mediated endothelium-dependent relaxation in response to A23187; endothelium-independent cyclic guanosine monophosphate–mediated relaxation in response to sodium nitroprusside, and K⁺_ATP-channel–mediated relaxation. Relaxations in response to 8-bromo-cyclic guanosine monophosphate (a cyclic guanosine monophosphate–dependent protein kinase activator) and to 8-bromo-cyclic adenosine monophosphate (a cyclic adenosine monophosphate–dependent protein kinase activator) were impaired after iCB-CP alone and after reperfusion, whereas the respective responses were not affected after cWB-CP. Myogenic tone was decreased similarly after iCB-CP and cWB-CP but was not further altered after reperfusion. Cardiac function was similar after iCB-CP and cWB-CP.

Conclusions. These results suggest that cWB-CP is similar to iCB-CP in its ability to preserve endothelium-dependent relaxation and K⁺_ATP-channel function. The superior preservation of ß-adrenergic-cyclic adenosine monophosphate–mediated coronary responses after cWB-CP is brief and associated with minimal improvement of myocardial function and myogenic tone.

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