Microcirculation
Microcirculatio
Also known as: capillary bed, precapillary sphincter, arteriovenous anastomosis, autoregulation
The microcirculation is the working unit of the smallest vessels in an organ: terminal arterioles, metarterioles, capillaries, venules and arteriovenous anastomoses. Here blood flow is matched to local metabolic need, and exchange with the tissues takes place.
Overview
Organisation. A terminal arteriole leads into a metarteriole, which has only scattered smooth muscle. The metarteriole continues as a thoroughfare channel to a venule. True capillaries branch off this route, each guarded at its entrance by a precapillary sphincter. The sphincters and metarterioles open and close rhythmically every few seconds to minutes (vasomotion). At rest only a fraction of the capillaries in skeletal muscle carry blood at any moment. During exercise many more open (capillary recruitment), which enlarges the exchange area and shortens the distance oxygen must diffuse.
Arteriovenous anastomoses. These are direct connections between arterioles and venules, including coiled glomus bodies. They are found in the skin of the fingers, toes, ears and nose. Under sympathetic control, they shunt warm blood close to the skin surface to release heat, or close to conserve it.
Function
- Matches blood flow to tissue metabolic demand.
- Provides the site of exchange between blood and tissues.
- Contributes to thermoregulation through arteriovenous anastomoses.
- Physiology
Autoregulation. Several organs keep their blood flow nearly constant despite changes in perfusion pressure. The brain does so over a mean arterial pressure of about 60–150 mmHg, the kidney over about 80–180 mmHg, and the heart as well. Two mechanisms are responsible. In the myogenic response (Bayliss), arteriolar smooth muscle contracts when stretched. In the metabolic response, accumulating metabolites dilate arterioles. The main metabolite differs between organs: adenosine in the heart, CO₂ and H⁺ in the brain, and K⁺, lactate and low O₂ in skeletal muscle. The kidney also uses tubuloglomerular feedback.
Hyperaemia. Active hyperaemia is increased flow when tissue becomes more active. Reactive hyperaemia is the overshoot in flow after a temporary blockage is released.
Endothelial control. Shear stress releases nitric oxide, which causes flow-mediated dilation of upstream vessels.
Long-term control. Over weeks, chronic hypoxia increases the number of vessels through angiogenesis driven by VEGF.
Pulmonary exception. In the lungs, hypoxia causes constriction instead of dilation (hypoxic pulmonary vasoconstriction).
Clinical significance
Raynaud phenomenon
In Raynaud phenomenon, the digital arteries and arterioles constrict excessively in response to cold or emotion. The fingers turn white, then blue, then red as blood returns. It may occur alone (primary) or be secondary to systemic sclerosis or other connective tissue diseases.
Microcirculatory failure in shock
In septic shock, blood flow through the microcirculation becomes patchy and shunted, and the endothelium is damaged. Tissue hypoxia can continue even after blood pressure has been restored.
Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.