, Volume 76, Issue 4, pp 354-358

Can a single vasodilator be responsible for both coronary autoregulation and metabolic vasodilation?

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To test the hypothesis that both coronary autoregulation and metabolic vasodilation can be mediated by the same substance, we have analysed measured autoregulation curves with the aid of a simple mass balance model. In an open-chest dog preparation, increasing the heart rate by pacing results in a nearly parallel shift of the autoregulation curve to a higher flow (Q) level. We assume a unique relationship between vascular conductance and interstitial concentration of a vasodilating substance [A]. Applying a compartmental mass balance, it is possible to predict with a minimum of assumptions the increase of flow between two points with increased production but having the same vasodilator concentration. The simple result of this analysis is: ΔQ=Δproduction/[A]. If the vasodilator concentration varies by more than a factor 2 between low and high conductance points, the autoregulation curve cannot shift in a parallel fashion as a result of an increased production rate, but rather will become less and less steep. We conclude that a single vasodilator cannot be responsible for both autoregulation and metabolic vasodilation unless complex assumptions are made, for which there is as yet no experimental support.