Circulatory Control and Special Circulations Flashcards
(23 cards)
Acute blood flow control
Rapid changes in local vasodilation and vasoconstriction of arterioles. Occurs within seconds to minutes to provide very rapid maintenance of appropriate local tissue blood flow
Long term blood flow control
slow, controlled changes in flow over a period of days, weeks, or months. Changes come about as an increase or decrease in the physical sizes and numbers of actual blood vessels supplying the tissues
Increase in tissue metabolism increases tissue blood flow, how?
Whenever the availability of oxygen to the tissues is decreased (high metabolism), the blood flow through the tissues increases
Examples:
1. high altitude
2. pneumonia
3. carbon monoxide poisoning (decreases ability of hemoglobin to transport O2)
4. cyanide poisoning (decreased capability of tissues to use oxygen)
Vasodilator Theory for acute local blood flow control
Vasodilator substances released from the tissue mainly in response to oxygen deficiency
Examples:
Adenosine
Carbon Dioxide
Lactic Acid
Histamine
Potassium ions
Hydrogen ions
Role of Adenosine
Decreased availability of oxygen can cause both adenosine and lactic acid (containing hydrogen ions) to be released into the spaces between the tissue cells
- Minute quantities of adenosine are released from heart muscle cells when coronary blood flow decreases. This causes enough local vasodilation in the heart to return coronary blood flow back to normal
What is the most important local vasodilator for controlling local blood flow?
Adenosine
Oxygen Lack theory/Oxygen Demand theory for local blood flow control
Oxygen is required as one of the metabolic nutrients to cause vascular muscle contraction. In the absence of adequate oxygen, the blood vessels would relax and naturally dilate.
Increased utilization of oxygen in the tissues as a result of increased metabolism could also decrease the availability of oxygen to the smooth muscle fibres in the local blood vessels and this would cause local vasodilation
Tissue vasodilation could also occur due to:
- lack of glucose
- lack of amino acids
- lack of fatty acids
- deficiency of vitamin B substances thiamine, niacin and riboflavin
Reactive Hyperaemia
An increase in blood flow to an organ that occurs following a period of arterial occlusion (sudden increase in blood flow after occlusion removed)
Active Hyperaemia
Blood flow to the tissue will increase proportionately to meet the increased metabolic demands.
For example, during muscle stimulation during exercise the skeletal muscles can increase local muscle blood flow as much as 20-fold during intensive exercise
The Metabolic Theory (Autoregulation)
When arterial pressure becomes too great, the excess flow provides too much oxygen and too many other nutrients to the tissues. These nutrients (especially oxygen) then cause the precapillary sphincters and arterioles to constrict and the flow to return nearly to normal despite increased pressure
The Myogenic Theory (Autoregulation)
Sudden stretch of small blood vessels causes the smooth muscle of the vessel wall to contract
Myogenic Contraction is initiated by stretch induced vascular depolarization, which rapidly increases calcium ion entry from the extracellular fluid into the cells, causing them to contract.
At low pressures, the degree of stretch of the vessel is less, so that the smooth muscle relaxes and allows increased flow
Mechanism of Long term regulation of blood flow
If a tissue becomes chronically overactive and requires chronic increased quantities of oxygen and other nutrients, the arteriole and capillary vessels usually increase both in number and size (increased vascularity) within a few weeks to match the needs of the tissue
**oxygen is an important stimulus for regulating tissue vascularity: when there is low O2, cells release growth factors like VEGF which stimulate capillaries to grow and branch out (tumours, wound healing, COPD, high altitudes). Hypoxia will signal an increase in blood supply so we get vasodilation and angiogenesis
Angiogenesis
- Growth of new blood vessels
Angiogenesis occurs in response to angiogenic factors released from:
1. ischemic tissue
2. rapidly growing tissue
3, tissue with high metabolic rates
What are angiogenic factors?
Small peptides such as vascular endothelial cell growth factor (VEGF), fibroblast growth factor (FGF) and angiogenin
Development of Collateral Circulation
When an artery or vein is blocked in any tissue, new vascular channels develop around the blockage and allows at least partial resupply of blood to the affected tissue
** Most important example of development of collateral blood vessels occur after thrombosis of one of the coronary arteries, most people over 60 don’t know they have a coronary vessel close due to this to prevent myocardial damage
Vasoconstrictor Agents
- norepinephrine and epinephrine
- angiotensin II
- Vasopressin/ADH
- Endothelin (released from damaged endothelium)
Vasodilator Agents
- Bradykinin: powerful arteriolar dilation and increased capillary permeability
- Histamine: can increase capillary porosity like bradykinin allowing leakage of both fluid and plasma protein into the tissues
- Endothelium Derived Relaxing Factors (Nitric Oxide): endothelial cells lining the blood vessel causes relaxation of blood vessels
- Prostacyclin (PG12): inhibits platelet adhesion to vascular endothelium
Ions related to Vascular control
Vasoconstriction:
1. Calcium: stimulate smooth muscle contraction
2. decrease in hydrogen ion concentration
Vasodilation:
1. Potassium: inhibits smooth muscle contraction
2. Magnesium: inhibits smooth muscle contraction
3. Acetate and Citrate
4. Carbon dioxide: moderate vasodilation in tissues but marked vasodilation in brain
What is the most important Endothelium derived relaxing factor?
Nitric Oxide (NO)
cGTP —–> cGMP (relaxation) from soluble guanylate cyclase
Coronary Circulation
Coronary circulation is controlled almost entirely by local metabolites (hypoxia and adenosine released by the cells)
Increase in Myocardial contractility will cause:
- increased O2 demand by the cardiac muscle
- increased O2 consumption, causing local hypoxia
- local hypoxia causes vasodilation of the coronary arterioles which then produces a compensatory increase in coronary blood flow and O2 delivery
Hypoxia causes coronary vasodilation directly but also releases adenosine and opens ATP-sensitive potassium channels (remember potassium is a vasodilator and lack of oxygen also vasodialates).
Pre-capillary sphincters are relaxed and more capillaries are recruited, this will meet the demand of the cardiac muscle (ACTIVE HYPERAEMIA)
What is an unusual feature of coronary circulation?
There is the effect of mechanical compression of the blood vessels
During systole, muscle compression causes a brief period of occlusion and reduction of blood flow. When the period of occlusion is over (systole), reactive hyperaemia occurs to increase blood flow and O2 delivery
What are the most important vasodilators for cerebral circulation?
CO2 and H+ = a decrease in pH causes increased vasodilation so CO2 can go away easier
Vasodilation of cerebral arterioles results in increased blood flow to assist in the removal of excess CO2.
Blood-Brain barrier plays a major role in the metabolites of the brain
Describe Pulmonary Circulation and its control by Oxygen
Hypoxia causes vasoconstriction, the OPPOSITE of its effect in other places.
Regions of hypoxia in the lung cause local vasoconstriction which will shunt blood away from the poorly ventilated areas (where blood flow would be wasted) towards the well ventilated areas so gas exchange can occur.
