Abstract
Summary
LV pressure overload was created in adult male rats by abdominal aortic constriction. Three weeks following surgery, LV weight was increased by approximately 25% in aortic constricted animals. Aortic constriction produced a substantial pressure overload, as indicated by a 40 mmHg increase in peak LV pressure. Significant increases in heart rate and max dP/dt accompanied the pressure overload. The above hemodynamic factors would tend to reduce blood flow to the LV by (a) increasing vascular compression and (b) restricting the coronary inflow period. Alkaline phos-phatase specific activity was utilized as an index of vascular density in the EPI and ENDO portions of control and hypertro-phied LV. In control LV, the specific activity of the ENDO portion was significantly greater than the EPI portion, indicating a greater ENDO vascular density. The preferential ENDO vascular density gradient was eliminated in the LV which had enlarged in response to a pressure overload stimulus.
Both hemodynamic factors and alterations in vascular density were identified as being potentially capable of reducing blood flow to the hypertrophied LV.
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