Effects of vasoconstriction and vasodilatation on LV and segmental circulatory energetics

Abstract

Wang J-J, Shrive NG, Parker KH, Tyberg JV. Effects of vasoconstriction and vasodilatation on LV and segmental circulatory energetics. Am J Physiol Heart Circ Physiol 294: H1216-H1225, 2008. First published January 4, 2008 doi:10.1152/ajpheart.00983.2007.-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, ϳ50% of the LV stroke work was dissipated through arterial reservoir resistance (NP, ϳ36%; MTX, ϳ27%), another ϳ25% was dissipated by the microcirculation (NP, ϳ20%; MTX, ϳ66%), and ϳ20% of work by the large-artery resistances (NP, ϳ37%; MTX, ϳ6%). 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 ϳ1 and ϳ3% 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 ϳ45% with NP and ϳ80% with MTX. left ventricle circulatory coupling; systemic vascular resistance; arterial and venous reservoirs THE HYDRAULIC WORK GENERATED by the left ventricle (LV) pushes blood into the systemic circulation to provide the metabolic requirements of the organs. Although the amount of LV hydraulic work (i.e., the area of the pressure-volume loop) is not disputed, how this work is dissipated in the systemic circulation is still subject to interpretation. Thus far, the analysis of arterial hemodynamics has been dominated by the Fourier-based impedance method, in which aortic pressure and flow have been treated as the sum of sinusoidal wave trains oscillating about mean values; this construct led to the separation of LV hydraulic work into oscillatory work and work related to mean pressure and flow. However, it is difficult to directly relate either to the energy dissipated by the individual components of the serial resistive network.We recently proposed a new approach to the systemic circulation, using the principle of Otto Frank's windkessel (8, 9), in which arterial reservoir pressure (P A-Res ) is proportional to the instantaneous blood volume. Viewed in the time domain, the arterial reservoir is a hydraulic integrator; the reservoir is charged when inflow exceeds outflow (during systole) and vice ...

Wave intensity analysis and the development of the reservoir–wave approach

“…When they compared their results to those previously reported [24], they found that the energy of the backward decompression wave responsible for diastolic suction was 2.6-fold greater than previously reported. The numerical correction may be of only limited interest but the extension of the principle-reservoir-related pressure changes should be discounted before analyzing wave motion-is very important.…”

“…Recently, we studied the effects of vasodilatation (sodium nitroprusside, NP) and vasoconstriction (methoxamine, Mtx) on this system and found that *50% of the LV stroke work is normally dissipated by the arterial reservoir resistance (NP, *36%; Mtx, *27%) and *20% normally by the large-artery resistance (NP, *37%; Mtx, *6%) [24]. Figure 3 defines the relation of the series resistances but the relation of the compliances has not been defined.…”

“…9. In the bottom panel, by integrating the area under the wave intensity vs. time curves, we calculated the energy associated with waveinduced acceleration and deceleration and found it to be *1% of the total hydraulic work (i.e., the integral of the P wave 9 Q in product; the third panel), which we interpret to be done in overcoming the proximal resistance [24]. To further evaluate the magnitude of viscous resistance, we recently performed bench-top experiments using plastic tubing with a diameter similar to the canine ascending aorta [21].…”

Aortic Reservoir Pressure Corresponds to Cyclic Changes in Aortic Volume

“…26 However, when compliance is reduced (ie, when reservoir function is impaired), some of the pressure buffering capacity is diminished and aortic BP may become elevated because of a more rapid increase in reservoir pressure for a similar rise in aortic volume. 17,25 This hemodynamic consequence has been demonstrated in animal studies whereby application of noncompliant grafts around (or in replacement of) the proximal aorta acutely yields more pathological central BP waveforms (augmented BP) and increased myocardial load resulting in LV hypertrophy. [27][28][29] It is, therefore, not surprising that as the large arteries become stiff with age, 30 the altered aortic reservoir function largely accounts for the augmentation of the central BP waveform.…”

“…Importantly, however, a large proportion of the pressure from the column of blood ejected into the arterial network during systole is dampened within the ascending aorta via the reservoir function (≤37%). 25 This buffer role in mitigating cyclic pulsatile fluctuations in BP ensures a more steady flow of blood at the peripheral tissue level and maintains outflow in diastole. After closure of the aortic valve, the aorta recoils (releasing the stored energy) as blood discharges from the proximal aorta into the distal vasculature throughout diastole.…”