Chemical blockade of the reticuloendothelial system results in arteriolar spasms: possible role of endothelial cells.

Scattered qualitative studies in the literature suggest that the reticuloendothelial system (RES) interacts with the microcirculation to effect host defense and that chemical or pharmacologic blockade of the RES might compromise the microcirculation. With this possibility in mind, we designed experiments in rats to determine whether colloid and pharmacologic blockade of the RES could alter microvascular tone and reactivity. The effects of colloidal carbon, thorium dioxide, tripalmitin and tetracycline on reticuloendothelial system phagocytic function, mesenteric terminal arteriolar tone and arteriolar reactivity to noradrenaline and acetylcholine were examined in situ at magnifications up to 5000x. Colloidal carbon and thorium dioxide, in the doses utilized, produced complete blockade of the RES. Treatment with tripalmitin and tetracycline produced pronounced RES depression. RES blockade and depression were associated with marked reductions in terminal arteriolar lumen sizes, curtailment of capillary inflow and outflow, hyper-reactivity to the constrictor, noradrenaline, and hypo-reactivity to the dilator, acetylcholine. Close examination of the endothelial linings of the capillaries, postcapillary venules and terminal arterioles of the experimentally-treated animals indicated pronounced uptake of carbon particles in the endothelial cells, different degrees of endothelial cell swelling and often bulging into the microvessel lumens. Our findings suggest that RES-induced alterations in microvascular tone and arteriolar reactivity may be related to injury of the microvascular endothelial cells.