Y Wainai1. 1. Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Abstract
STUDY OBJECTIVE: Compensatory mechanisms of the left ventricle for volume overloading caused by acute aortic regurgitation and associated changes in physiological properties of the aorta were studied in rabbits. DESIGN: Aortic regurgitation was produced by aortic valve perforation, and haemodynamic measurements were performed before, 1 h and 4 weeks afterwards. Characteristic impedance of the distensibility of the aorta were calculated. EXPERIMENTAL ANIMALS: 42 Japanese white rabbits were used. The animals were anaesthetised with intravenous urethane. MEASUREMENTS AND MAIN RESULTS: Total systemic vascular resistance did not change significantly during the 4 weeks. When aortic regurgitation was produced, an immediate increase in circumferential distensibility was followed by the gradual dilatation of the aorta. An increase in circumferential distensibility resulted in decreased characteristic impedance, and the reduction in cardiac output caused by aortic regurgitation was compensated by increased systolic shortening of left ventricular dimensions at 1 h. After 4 weeks, however, decreased characteristic impedance was associated with increased aortic diameters during both systole and diastole, and dilatation and hypertrophy of the left ventricle were responsible for compensation of left ventricular performance. CONCLUSIONS: Volume overloading of the left ventricle by aortic regurgitation gave rise to a two stage compensatory process over a 4 week period and the aorta interacted with chronological changes in left ventricular performance.
STUDY OBJECTIVE: Compensatory mechanisms of the left ventricle for volume overloading caused by acute aortic regurgitation and associated changes in physiological properties of the aorta were studied in rabbits. DESIGN:Aortic regurgitation was produced by aortic valve perforation, and haemodynamic measurements were performed before, 1 h and 4 weeks afterwards. Characteristic impedance of the distensibility of the aorta were calculated. EXPERIMENTAL ANIMALS: 42 Japanese white rabbits were used. The animals were anaesthetised with intravenous urethane. MEASUREMENTS AND MAIN RESULTS: Total systemic vascular resistance did not change significantly during the 4 weeks. When aortic regurgitation was produced, an immediate increase in circumferential distensibility was followed by the gradual dilatation of the aorta. An increase in circumferential distensibility resulted in decreased characteristic impedance, and the reduction in cardiac output caused by aortic regurgitation was compensated by increased systolic shortening of left ventricular dimensions at 1 h. After 4 weeks, however, decreased characteristic impedance was associated with increased aortic diameters during both systole and diastole, and dilatation and hypertrophy of the left ventricle were responsible for compensation of left ventricular performance. CONCLUSIONS: Volume overloading of the left ventricle by aortic regurgitation gave rise to a two stage compensatory process over a 4 week period and the aorta interacted with chronological changes in left ventricular performance.