The document discusses the regulation of blood flow to tissues and organs. It describes acute control which occurs rapidly through vasoconstriction or vasodilation and long term control which involves changes to blood vessel structure over days or weeks. Key mechanisms of acute control include autoregulation to maintain constant blood flow despite pressure changes, active hyperemia to increase flow during increased activity, and reactive hyperemia providing a temporary surge in flow after ischemia. Long term control involves angiogenesis and developing collateral blood vessels. Regulation also occurs through vasoactive hormones, ions, and other chemicals that cause vasoconstriction or vasodilation.

2.  Introduction
 Regulation
 Acute control
 Autoregulation
 Active hyperaemia
 Reactive hyperaemia
 Longterm control
 Humoral regulation
 Role of Ions

3. Introduction
 Tissues and organs 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.

4. Regulation
Organ blood flow is 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

5. Acute control
It occurs in 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

6. Autoregulation
 The intrinsic ability 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.

7.  A change in 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.

8. Theories of autoregulation
1. Metabolic theory
2. Myognic theory
3. In kidneys – tubulo-glomerular feedback
4. In brain – concentration of carbon dioxide and
hydrogen

9. Active hyperemia
 AH is 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

10.  AH can result 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.

11. Reactive hyperemia
 RH is 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.

12. 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.

13. Humoral regulation
 Vasoconstrictors:
 E & NE
 Angio II
 Vasopressin
 Endothelin
 Prostaglandins – thromboxane A2, PGF
 Vasodilators:
 Bradykinin
 Histamine
 Prostaglandins – prostacyclin, PGE.

14. Ions and other chemicals
 Increased calcium – vasoconstriction
 Increased potassium – vasodilation
 Increased magnesium – vasodilation
 Increased sodium – vasodialtion
 Increased hydrogen – vasodilation
 Increased carbon dioxide – vadodilation
 Increased osmolarity of blood - vasodilation