Capillaries precapillary sphincter

The classical view of blood flow control involved the action of vasomotor influences on a set of vessels called the resistance vessels, generally arterioles and small arteries smaller than about 100 to 150 )u.m in diameter, which controlled flow to and within an organ [56]. The notion of precapillary sphincters that control flow in individual capillaries has been abandoned in favor of the current notion that the terminal arterioles control the flow in small capfllary networks that branch off of these arterioles. In recent years, it has become clear that the resistance to blood flow is distributed over a wider range of vessel branching orders with diameters up to 500 /um. There are mechanisms to be discussed in Section 59.4.2 that are available for coordinating the actions of local control processes over wider regions. 

The autoregulation response should ultimately arise from the action of multiple precapillary sphincters and resistance arterioles in the microcirculation. The control of flow in a microvascular model was analyzed by Mayrovitz et al. (1978). This model included muscular arterial and venous vasomotion, capillary filtration and reabsorption, and lymph flow. Tissue pressure was assumed to be regulated and was used to provide the control pathway for activation of the precapillary sphincter. Local flow was found to vary considerably with periodic sphincter activity. This model demonstrated that autoregulation of flow is likely to find its genesis at the microcirculatory level. 

Vasoconstriction cannot alone be responsible for hemostasis because in severe thrombocytopenia, vasoconstriction occurs, but hemorrhage is not prevented. It has been proposed that adhesion of the endothelial wall of the capillary causes hemostasis. The mechanism of this adhesive process is not clear it could result from collapse of the endothelial wall because of destruction of the surrounding connective tissue, compression of the capillary lumen by edema fluid, or collapse of the lumen because of reduced pressure due to activation of precapillary arteriolar sphincters. 

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