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Ann Thorac Surg 1984;38:232-236
© 1984 The Society of Thoracic Surgeons

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Articles

Identification and Control of Noncoronary Collateral Blood Flow

Division of Cardiac Surgery, The Johns Hopkins Medical Institutions, Baltimore, MD

^* Address reprint requests to Dr. Bolling, Cardiac Surgical Service, Department of Surgery, The Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21205

To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 µm in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions: vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries.

Without effective LV venting, LV intracavitary pressure rose to 7.0 ± 0.1 mm Hg (mean ± standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 ± 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 ± 3.5 ml/min and myocardial blood flow fell to 0.3 ± 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent.

These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic–pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.

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