Diameter control in the arteriolar tree by changes in post-capillary resistance. A theoretical study.

Abstract

Presently, the mechanisms underlying local adjustment of organ perfusion to the metabolic needs of the tissue are not well understood. Even though a large number of vasoactive substances is known to be released upon variations in tissue metabolism,24,28 the exact mechanisms of their action are unclear: Because diffusion is a slow and inefficient transport process for covering long distances, arterioles can only sense those changes in concentration and hence in release rate of these mediators with acceptable spatial and temporal resolution that originate from their immediate vicinity. On the other hand, perfusion needs to be regulated such that also the worst supplied tissue regions located remote from the arterioles (“lethal corners”) receive sufficient supply of oxygen and nutrients. Thus, the question arises: how can the information about the metabolic status of these tissue regions be transmitted to the arteriolar tree in order to adjust blood flow to their needs? A number of suggestions has been advanced on how this gap in the signal chain might be bridged9,13,26,29 all of which, however, fail to furnish satisfactory explanations: Tissue diffusion of vasoactive substances has been ruled out before. Upstream conduction of dilator signals along the capillary wall appears to be effective in controlling the feeding arteriole only if signals are generated within the proximal one third of the capillary29 which excludes the “lethal corners”. Diffusion of vasodilator substances from venules to their accompanying arterioles, despite being the best supported one of all presently proposed explanations,9,13,26 is not adequate because venular-arteriolar distances are highly variable,7 the smallest branches of the vascular tree are not arranged as such pairs at all, and in the larger vessel pairs, an arteriole often supplies a tissue microregion different from the one drained by its accompanying venule.22