Related Experiment Videos
Right coronary pressure modulates right ventricular systolic stiffness and oxygen consumption
1Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth 76107-2699, USA.
Objective:
The low transmural pressure of the thin right ventricular (RV) wall may render it responsive to right coronary (RC) pressure-induced changes in systolic stiffness and account for the dependence of RV MVO2 on RC pressure (RCP).
Methods:
In eight dogs anesthetized with pentobarbital and fentanyl, RCP was lowered from the baseline to 30 mmHg in 10 mmHg steps by adjusting an occluder on the proximal RC. Myocardial segment length and isometric developed force were measured, and the slope of the force-length curve during ejection period (delta F/ delta SL) was used as an index of systolic myocardial stiffness. MVO2 was calculated from RC flow and arteriovenous O2 difference.
Results:
As RCP was varied from 120 to 40 mmHg with positive lactate uptake, RC flow, maximum developed force (Fmax), delta F, and MVO2 decreased linearly, whereas end-diastolic length, delta SL, and other hemodynamic variables stayed constant. Thus, RV systolic stiffness fell linearly with RC pressure. When RCP was further lowered from 40 to 30 mmHg, Fmax and delta F continued to fall, end-diastolic segment length and right atrial pressure increased significantly, delta SL and RV dp/dtmax fell significantly, and delta F/delta SL reached its lowest value. RV systolic stiffness was 22% of previously reported left ventricular systolic stiffness for coronary perfusion pressure at 100 mmHg, and varied less steeply with coronary pressure.
Conclusions:
(1) Reductions in RV systolic stiffness preserve delta SL as coronary pressure is reduced over a wide range. (2) The resulting increase in RV efficiency reduces oxygen demand as oxygen supply is reduced, so ischemia is avoided. (3) RV systolic stiffness is much less than left ventricular stiffness, consistent with their anatomical and functional differences.