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Intrinsic Blood Flow Regulation
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Intrinsic Blood Flow Regulation

Intrinsic Blood Flow Regulation
Intrinsic, aka, local, regulation ensures that blood flow and nutrient supply matches the needs of target tissues.
Intrinsic mechanisms respond to local changes in metabolic products and/or transmural pressure via changes in vascular resistance.
  • Autoregulation
  • Active hyperemia
  • Re-active hyperemia
Autoregulation
Maintains constant local blood flow despite fluctuations in systemic mean arterial pressure.
Autoregulation Is particularly important for the brain, which requires a constant supply of oxygen and other nutrients.
As long as mean arterial pressure remains between 60-160mmHg, autoregulation of vessel diameter maintains a nearly constant cerebral blood flow of 50 ml/100 g/min.
However, there are limits to what autoregulation alone can achieve: outside of the ideal pressure range, cerebral blood flow will increase and decrease depending on mean arterial pressure.
In stroke or brain hemorrhage, there is often dysfunction of cerebral autoregulation.
Active Hyperemia
Reflects the positive correlation between blood flow and tissue metabolic requirements:
Skeletal muscle oxygen consumption drives blood local blood flow.
  • As skeletal muscle activity increases, so does its oxygen consumption.
  • In response, vasodilation increases local blood flow and oxygen supply to meet increased demand.
  • During periods of vigorous exercise, there will be vasodilation to increase blood flow to the skeletal muscles.
Re-active Hyperemia
Occurs in response to a period of decreased blood flow.
Typically, baseline blood flow is constant over time.
When blood flow is obstructed, oxygen debt accumulates in the tissues of the hand.
  • Removal of the obstruction enables blood flow to resume, even above baseline levels to make up for oxygen debt.
  • As an unintended consequence, hyperemia can occur when clinicians mechanically unclog a clotted vessel and this phenomenon can have deleterious effects.
Myogenic Hypothesis
Assumes that the goal is to maintain vascular wall tone despite changes in blood flow.
Increased blood flow raises the transmural pressure, which stretches the vascular smooth muscle cells of the smooth muscle layer.
In response, the vascular smooth muscle cells initiate vasoconstriction: Contraction of the smooth muscle maintains the vascular wall tone and reduces blood flow.
The Myogenic hypothesis can explain autoregulation, in which the vasculature responds to changes in mean arterial pressures, and, therefore, transmural pressure. But it does not explain active nor re-active hyperemia, which are responses to changes in local oxygen needs.
Metabolic Hypothesis
Assumes that the goal is to match oxygen supply and demand.
Increased skeletal muscle tissue activity results in the production of vasodilator metabolites that induce vasodilation of nearby vessels.
Thus, blood flow and oxygen supply increases.
Eventually, increased blood flow washes away the vasodilator metabolites and blood flow returns to baseline.
The metabolic hypothesis explains autoregulation and active and re-active hyperemia.