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. 2018 Jan 2;150(1):145–168. doi: 10.1085/jgp.201711795

Figure 5.

Figure 5.

Effect of the time-average inlet perfusion pressure P¯in 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 (P¯in = 75 mmHg, A) under which all the vessels are maximally vasodilated with Fmterm = 1). It is completely suppressed at high perfusion pressure (P¯in = 165 mmHg) under which all the vessels are maximally vasoconstricted with Fmterm = 0).