Effects of vasoconstriction and vasodilatation on LV and segmental circulatory energetics.
Although the hydraulic work generated by the left ventricle (LV) is not disputed, how the work was dissipated through the systemic circulation is still subject to interpretation. Recently, we proposed that the systemic circulation should be considered as waves and a reservoir system (Wk). By combining the arterial and venous reservoirs, the systemic vascular resistance can be viewed as a series of resistors, which in sequence are the large-artery resistance, arterial reservoir resistance, the microcirculatory resistance, venous reservoir resistance, and large-vein resistance, and propelling blood through these resistance elements represents resistive losses. We then studied the changes in the fraction of the work consumed by each element when infusing methoxamine (MTX), a vasoconstrictor, and sodium nitroprusside (NP), a vasodilator. Results show that, under control condition, approximately 50% of the LV stroke work was dissipated through arterial reservoir resistance (NP, approximately 36%; MTX, approximately 27%), another approximately 25% was dissipated by the microcirculation (NP, approximately 20%; MTX, approximately 66%), and approximately 20% of work by the large-artery resistances (NP, approximately 37%; MTX, approximately 6%). The energy dissipated by the venous resistances was small and had limited variation with NP and MTX, where the large-vein and venous reservoir resistances shared approximately 1 and approximately 3% of LV stroke work, respectively. Approximately 60% of LV stroke work is stored as the potential energy during systole under control, and the ratio decreases to approximately 45% with NP and approximately 80% with MTX.
Wang
Jiun-Jr
JJ
Libin Cardiovascular Institute of Alberta, Department of Cardiac Sciences, University of Calgary, Calgary, AL, Canada T2N 4N1.
Shrive
Nigel G
NG
Parker
Kim H
KH
Tyberg
John V
JV
D000465:Algorithms; D000818:Animals; D001775:Blood Circulation / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008729:Methoxamine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D008729:Methoxamine