Abstract
Reduced cardiac output during cross-clamping of the aorta has been attributed to the increased afterload. A second mechanism involves reperfusion of the ischemic lower torso. The author studied cardiac contractility during and following one hour of infrarenal aortic cross-clamping. Methods: Ultrasonic crystals were implanted on the anterior and posterior aspects of the left ventricle in 11 anesthetized dogs to measure the external minor diameter. A pressure transducer was placed in the left ventricular, and aortic and Swan-Ganz catheters were introduced. The animals were divided into two groups: A Clamp group (n=6) sustaining one hour of infrarenal aortic cross-clamping, and a Control group (n=5) who underwent a sham operator. Hemodynamic data were collected during the one hour of cross-clamping and for the next two hours.
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