Figure 5.
Effect of the time-average inlet perfusion pressure and MVI on the distribution of metabolic activation across the terminal vessels, Fmterm, for a terminal target flow, qtarget, of 1.5 × 10−3 mm3/s. (A–L) With MVI (A–F) and without MVI (G–L). The capacity of metabolic regulation to maintain flow homogeneity is exhausted at low perfusion pressure ( = 75 mmHg, A) under which all the vessels are maximally vasodilated with Fmterm = 1). It is completely suppressed at high perfusion pressure ( = 165 mmHg) under which all the vessels are maximally vasoconstricted with Fmterm = 0).