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J Thorac Cardiovasc Surg 2000;120:528-537
© 2000 The American Association for Thoracic Surgery


Cardiopulmonary Support and Physiology

Experimental study of intermittent crossclamping with fibrillation and myocardial protection: Reduced injury from shorter cumulative ischemia or intrinsic protective effect?

Ryuzo Bessho, MD*, David J. Chambers, PhD

From Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute, Guy's and St Thomas' Hospital NHS Trust, St Thomas' Hospital, London, United Kingdom.

Address for reprints: David J. Chambers, PhD, Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute, Guy's and St Thomas' Hospital NHS Trust, St Thomas' Hospital, London SE1 7EH, United Kingdom (E-mail: david.chambers{at}kcl.ac.uk ).

Objective: During coronary artery revascularization, some surgeons favor intermittent crossclamping with ventricular fibrillation in preference to cardioplegic ischemic arrest for myocardial protection. It is unclear, however, whether intermittent crossclamping with fibrillation is equally protective or whether ischemic injury is reduced as a consequence of shorter cumulative ischemia.
Methods: We used isolated, Langendorff-perfused rat hearts, measured preischemic function (left ventricular developed pressure) with an intraventricular balloon, and then subjected the hearts to either (1) 40 minutes of global ischemia, (2) a 2-minute infusion of cardioplegic solution and 40 minutes of ischemia, (3) multidose (every 10 minutes) infusions of cardioplegic solution during 40 minutes of ischemia, (4) continuous ventricular fibrillation during 40 minutes of ischemia, (5) intermittent (4 x 10 minutes) ischemia with 10 minutes of reperfusion, (6) intermittent (4 x 10 minutes) ischemia preceded by intermittent cardioplegia, (7) intermittent (4 x 10 minutes) ischemia with ventricular fibrillation, (8) continuous (40 minutes) ventricular fibrillation during coronary perfusion, or (9) intermittent (4 x 10 minutes) ventricular fibrillation (with perfusion). All protocols were followed by 60 minutes of reperfusion.
Results: After 60 minutes of reperfusion, the percentage recovery of left ventricular developed pressure for groups 1 through 9 was as follows: 32% ± 2%, 57% ± 6%, 82% ± 3%, 19% ± 3%, 73% ± 3%, 70% ± 3%, 78% ± 4%, 55% ± 2%, and 57% ± 3%, respectively. No significant differences were identified among groups 3, 5, and 7, but the percentage recovery of developed pressure in group 3 was significantly higher than that in group 6; the degree of recovery in groups 3 and 5 to 7 was significantly (P < .05) higher than in groups 1, 2, 4, 8, and 9. Early recovery was significantly (P < .05) more rapid in groups 3 and 5 to 9, reaching a plateau (of 55%-80%) by 10 minutes of reperfusion; in groups 1, 2, and 4, the recovery plateau occurred after 50 minutes. Left ventricular end-diastolic pressure was elevated in groups 1, 2, and 4 but was almost unchanged from baseline in the other groups.
Conclusions: A similar level of myocardial protection was achieved with multidose (intermittent) cardioplegia or intermittent crossclamping (with or without fibrillation), indicating that intrinsic preservation by intermittent crossclamping with fibrillation does not exacerbate ischemic injury.




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