Acute:

-acts within seconds or minutes

-special phenomena: reactive and active hyperemia and autoregulation.

-based on metabolic rate or changes of oxygen availability

Chronic:

-acts in days or weeks.

-results in changes of physical sizes and numbers of blood vessels supplying the tissues.

-Based on the needs of the body as a whole.

-mainly through autonomic nervous system and other neural reflexes.

The local increase of the blood flow to a tissue  when the tissue becomes active (e.g. muscle contractions)

Mechanism:

Active tissue→ increase local metabolism→ use nutrients and release vasodilator substances (adenosine, NO, CO₂, K, Lactic Acid)→ increase blood flow.

-Increase in blood flow in reaction to a brief period of arterial occlusion(ischemia)

Mechanism:

Temporary blood occlusion→ oxygen deficiency and increase of vasodilators in local tissue→ vasodilation and increase blood flow

-similair to diastole and systoleof heart

The intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure.

Critical for BRAIN, HEART, KIDNEY, SKELETAL MUSCLE during exercise.

Metabolic theory

Myogenic theory

Metabolic:

-Vasodilator theory

-O₂ lack theory

Myogenic:

Stretch of vascular smooth muscle(high blood pressure)→ contraction of smooth muscle in small vessels

• Cerebral circulation(head)
• Coronary circulation(heart)
• Renal circulation(kidney)
• Skeletal muscle durig exercise

vasocontriction

VERY POTENT

released locally

Endothelin-1 is most common

Vasoconstriction in small arterioles

vasoconstriction in response to vessel damage(migraine)

vasoconstriction in small vessels

NO(Nitric Oxide) effect on blood flow;

Causes: Increased long-term metabolic demand (overactive tissues for a long period of time)

Effects: Formation of new blood vessels to keep up with the  metabolic demand.

Mechanisms: Deficiency of tissue oxygen and other nutrients → formation of angiogenic factors such as:

-Vascular Endothelial Growth Factor (VEGF)

-Fibroblast Growth Factor

-Angiogenin

Rest:(neural control) Sympathetic control. α1 and β2

Exercise:(local control) Lactic Acid and Autoregulation.

Adenosine: vasodilator

comes from ATP consumption

Local control

↑PCO₂= ↑blood flow

↓pH= ↑blood flow

Sympathetic stimulates sweat glands-bradykinin causes secondary vasodilation.

1. Thyroid hormones: thermogenic hormone. ↑metabolic rate, ↑heat production
2. SNS→ heat production in brown fat→ reduction in heat loss.
3. Shivering. Most Potent.

(temp is below set point)

(core temp is above set point)

1. decrease in sympathetic activity in skin blood vessels.
2. increase sympathetic cholinergic stimulation to sweat glands.

Increase environmental temperature→ dissipate heat mechanisms excess→ ↓ECF→ ↓blood volume→ ↓atrial pressure→ fainting

• Massive increase in the following in skeletal muscle: a)metabolic rate, b)O₂ consumption, c)heat production
• Heat-dissapating mechanisms can not keep up.
• Caused by inhalation anestetics.