Local control of blood flow

Local control of blood flow

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   Introduction  Regulation Acute control  Autoregulation  Active hyperaemia  Reactive hyperaemia  Longterm control  Humoral regulation  Role of Ions
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  Introduction  Tissues andorgans within the body are able to intrinsically regulate, to varying degree their own blood supply in order to meet their metabolic and functional needs. This is called local or intrinsic regulation of blood flow.  Blood flow is regulated locally in the arterioles and capillaries using smooth muscle contraction, hormones, oxygen, and changes in pH.
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  Regulation Organ blood flowis determined by perfusion pressure and vasomotor tone in the resistance vessels of the organ. Divides into 2 phases: 1. Acute control 2. Long term control
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  Acute control It occursin seconds to minutes through constriction or dilation of arterioles, metarterioles, and precapillary sphincters. Reasons: 1. Increased tissue metabolic rate raises local blood flow 2. Decreased oxygen availability increases local blood flow 3. Increased demand for oxygen and nutrients increases local blood flow 4. Accumulation of vasodilator metabolites increases local blood flow 5. A lack of other nutrients may also cause vasodilation
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  Autoregulation  The intrinsicability of an organ to maintain a constant blood flow despite changes in perfusion pressure. it occurs in the absence of neural and hormonal influences.  The renal, cerebral, and coronary circulations show excellent autoregulation  Skeletal muscle, and splanchnic circulations show moderate autoregulation  Cutaneous circulation show little or no autoregulation.
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   A changein systemic arterial pressure can lead to autoregulatory responses in certain organs.  Whenever a distributing artery to an organ becomes narrowed, this can result in an autoregulatory response.  This autoregulation is particularly important in organs such as the brain and heart.
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  Theories of autoregulation 1.Metabolic theory 2. Myognic theory 3. In kidneys – tubulo-glomerular feedback 4. In brain – concentration of carbon dioxide and hydrogen
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  Active hyperemia  AHis the increase in organ blood flow that is associated with increased metabolic activity of an organ or tissue.  It occurs when the tissue metabolic rate increases.  E.g.  increase in that accompanies muscle contraction, called exercise or functional hyperemia in skeletal muscle.  Increase in GIT blood flow during digestion of food  Increase in coronary blood flow with increase in heart rate  Increase in cerebral blood flow with increased neuronal activity of the brain
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   AH canresult in up to a 50 – fold increase in muscle blood flow with maximal exercise, whereas cerebral blood flow may only increase 2 fold with increased neuronal activity.  AH may be due to a combination of tissue hypoxia and the generation of vasodilator metabolites such as potassium ion, carbon dioxide, nitric oxide, and adenosine.
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  Reactive hyperemia  RHis the transient increase in organ blood flow that occurs following a brief period of ischemia.  It occurs after the blood supply to a tissue is blocked for a short period.  It occurs following the removal of tourniquet, unclamping an artery during surgery, or restoring flow to a coronary artery after recanalization  Hyperemia occurs because during the period of occlusion, tissue hypoxia and build up of vasodilator metabolites dilate arterioles and decrease vascular resistance.
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  Long term control Occurs over a period of days, weeks, or even months. It is due to increases or decreases in the physical size and numbers of blood vessels supplying the tissues.  Factors: 1. Change in tissue vascularity 2. Angiogenic factors a. Vascular endothelial growth factor b. Fibroblast growth factor c. Angiogenin 3. Development of collateral blood vessels when artery or vein is blocked.
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  Humoral regulation  Vasoconstrictors: E & NE  Angio II  Vasopressin  Endothelin  Prostaglandins – thromboxane A2, PGF  Vasodilators:  Bradykinin  Histamine  Prostaglandins – prostacyclin, PGE.
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  Ions and otherchemicals  Increased calcium – vasoconstriction  Increased potassium – vasodilation  Increased magnesium – vasodilation  Increased sodium – vasodialtion  Increased hydrogen – vasodilation  Increased carbon dioxide – vadodilation  Increased osmolarity of blood - vasodilation