Microcirculation: Microcirculation refers to the smallest blood vessels: arterioles, capillaries, venules, and lymphatics. Arterioles largely determine total peripheral resistance (TPR). They regulate how much blood enters the capillary beds by opening or closing the precapillary sphincters. Arterioles have sympathetic alpha 1 and alpha 2 receptors.
Capillaries are the main site for diffusion and osmosis. Lipid-soluble substances and gases cross the capillary wall easily by diffusion. Many capillaries also have aqueous clefts that allow water and water-soluble substances to pass.
Movement of fluid across the capillary wall is determined by Starling’s forces: the hydrostatic and oncotic pressures in the capillary and the interstitium.
Fluid movement across capillary wall is given by the Starling equation as follows -
Jv = K [(Pc - Pi) - σ (π c - π i)]
Starling’s equation states that fluid flux (J v ) depends on the balance between:
Where:
The reflection coefficient is inversely proportional to protein permeability. It is low in hepatic sinusoids and high in brain.
Forces favoring filtration out of the capillary are capillary hydrostatic pressure and interstitial oncotic pressure. Forces favoring absorption into the capillary are capillary oncotic pressure and interstitial hydrostatic pressure.
Plasma proteins (mainly albumin) determine capillary oncotic pressure, while arterial and venous pressures determine hydrostatic pressure. π c decreases in protein malnutrition, nephrotic syndrome, and liver failure. P c increases in heart failure. Conductance (K) increases when the vessel wall is damaged, such as in burns, inflammation, and trauma.
Regulation of local circulation: Local blood flow changes to match local tissue needs and metabolism. This is seen in autoregulation, active hyperemia, and reactive hyperemia.
Myogenic hypothesis: When arterial pressure increases, arterioles are stretched and respond by constricting. This helps maintain relatively constant blood flow despite increased pressure. When pressure decreases, the opposite response occurs (arteriolar dilation). This follows Laplace’s law: T = P X r, where T is tension on the vessel wall, P is pressure, and r is vessel radius. If P increases, r can decrease to keep T constant.
Metabolic hypothesis: Tissue metabolism increases the local concentration of vasoactive metabolites such as H+, K+, lactate, adenosine, and CO2. These metabolites cause arteriolar vasodilation and increase local blood flow. When pressure rises, these local vasodilator metabolites are washed out, leading to relative vasoconstriction.
Neurohormonal regulation of local blood flow: Peripheral blood vessels are innervated by the sympathetic nervous system. Skin and skeletal muscle vasculature have more sympathetic innervation than internal organs. Stimulation of alpha 1 receptors on cutaneous blood vessels causes vasoconstriction, which helps retain body heat.
Skeletal muscle vasculature shows:
Histamine released by mast cells causes vasodilation of arterioles but constriction of venules, which promotes fluid accumulation in the interstitium and edema. Bradykinin has similar effects and also stimulates production of nitric oxide and prostacyclins.
Serotonin and thromboxane A2 cause local vasoconstriction. Prostacyclins (prostaglandin I 2, stimulates Gs) and prostaglandin E 2 (stimulates Gs) are vasodilators, while prostaglandin F2 alpha (stimulates Gq) is a vasoconstrictor. Leukotriene LTC4 is a potent vasoconstrictor.
Regional circulations: Regional circulations differ in regulation based on organ function and metabolic needs.
Coronary circulation: Coronary blood flow is controlled mainly by local factors, especially adenosine and hypoxia, both of which cause vasodilation. The heart has the highest oxygen consumption per unit weight of any organ and a very high oxygen extraction rate.
Hypoxia decreases ATP production, which opens K -ATP channels. This hyperpolarizes vascular smooth muscle, reduces calcium entry, and causes vasodilation. Opening of K - ATP channels in endothelial cells increases nitric oxide formation, further promoting vasodilation.
Subendocardial tissue is the last to receive oxygenation. Increased myocardial contractility increases oxygen demand and produces active hyperemia. During systole, mechanical compression of intracardiac vessels temporarily obstructs blood flow, so it is followed by reactive hyperemia. In ischemic heart disease, even small reductions in perfusion pressure can significantly reduce flow across a stenosed vessel.
Pulmonary circulation: Pulmonary circulation is unique because it vasoconstricts in response to hypoxia. This shunts blood away from poorly ventilated regions toward well-ventilated areas. Pulmonary vessels are almost fully dilated even at rest. Nitric oxide and prostacyclin are important local vasodilators that help maintain low pulmonary vascular tone.
Cerebral circulation: The most important regulator of local cerebral blood flow is CO2 (H+). Increased cerebral Paco2 raises H+ (acidosis), causing vasodilation. A unique feature of cerebral circulation is that large extracranial and intracranial arteries contribute substantially to cerebral vascular resistance.
Renal circulation: Renal autoregulation occurs even in denervated kidneys. Myogenic mechanisms and tubuloglomerular feedback are key for maintaining renal blood flow.
Skeletal muscle: Skeletal muscle blood flow is regulated mainly by local metabolites during exercise and by sympathetic tone at rest. At rest, norepinephrine activates alpha 1 receptors on vascular smooth muscle, causing vasoconstriction. Epinephrine released from the adrenal medulla activates beta 2 receptors on vascular smooth muscle, causing vasodilation. During exercise, accumulation of lactate, adenosine, and K+ causes vasodilation.
Skin: Cutaneous circulation is regulated mainly by sympathetic innervation. When body temperature rises, sympathetic activity is inhibited, leading to vasodilation of cutaneous vessels and heat loss. The opposite response occurs in cold weather or hypothermia.
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