Chao-Yu Miao1, Ding-Feng Su. 1. Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai, China. cymiao@citiz.net
Abstract
OBJECTIVE: The main objective was to examine the role of hemodynamics in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation (SAD). DESIGN AND METHODS: Rats were examined at different times after SAD or sham operation (Sham). Hemodynamics were recorded continuously in conscious unrestrained rats. The time course of hemodynamic changes and cardiovascular hypertrophy was observed and linear regression analysis was performed to study the role of hemodynamics in SAD-induced aortic and left ventricular hypertrophy. Long-term mortality, water and food intake, and body weight were also determined after operation. RESULTS: High mortality (40%), dramatic reduction of water and food intake, and weight loss occurred within 1 week after SAD. Chronic SAD rats exhibited a marked increase in blood pressure variability (BPV), with no change in the average level of blood pressure (BP), as compared with the Sham control rats. Increased BPV was higher at 2 weeks (about threefold) than 16 weeks (about twofold) after SAD. Aortic hypertrophy existed in all three kinds of examined rats: 2-, 10- and 16-week SAD rats. Left ventricular hypertrophy was found only in 10- and 16-week SAD rats. Both aortic hypertrophy and left ventricular hypertrophy were significantly and positively correlated with BPV, but not with BP level. CONCLUSION: Persistent high BPV following SAD can lead to aortic and left ventricular hypertrophy. The aorta is more sensitive to increased BPV than the heart.
OBJECTIVE: The main objective was to examine the role of hemodynamics in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation (SAD). DESIGN AND METHODS: Rats were examined at different times after SAD or sham operation (Sham). Hemodynamics were recorded continuously in conscious unrestrained rats. The time course of hemodynamic changes and cardiovascular hypertrophy was observed and linear regression analysis was performed to study the role of hemodynamics in SAD-induced aortic and left ventricular hypertrophy. Long-term mortality, water and food intake, and body weight were also determined after operation. RESULTS: High mortality (40%), dramatic reduction of water and food intake, and weight loss occurred within 1 week after SAD. Chronic SAD rats exhibited a marked increase in blood pressure variability (BPV), with no change in the average level of blood pressure (BP), as compared with the Sham control rats. Increased BPV was higher at 2 weeks (about threefold) than 16 weeks (about twofold) after SAD. Aortic hypertrophy existed in all three kinds of examined rats: 2-, 10- and 16-week SAD rats. Left ventricular hypertrophy was found only in 10- and 16-week SAD rats. Both aortic hypertrophy and left ventricular hypertrophy were significantly and positively correlated with BPV, but not with BP level. CONCLUSION: Persistent high BPV following SAD can lead to aortic and left ventricular hypertrophy. The aorta is more sensitive to increased BPV than the heart.
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