Guyton Kap. 17- Local Control Of Blood Flow

Front 1

Blood flow in liver:

Back 1

1350 ml/min or 95 ml/100 g of liver tissue

Front 2

Blood flow in kidneys:

Back 2

1100 ml/ min (360 ml/min/100g of tissue)

Front 3

Blood flow in muscles:

Back 3

750 ml/ min or only 4 ml/100g of muscle tissue
(Can increase to 80 ml/min/100g of tissue in heavy exercise)

Front 4

Why regulate local blood flow to a minimum of needed to supply tissues with O2 and nutrients:

Back 4

To keep workload of the heart at a minimum level

Front 5

Mechanism of blood flow control:

Back 5

1. Acute control: Vessel tonus
2. Long term control: Growing number and size of vessels

Front 6

Blood flow in adrenal glands:

Back 6

25 ml/ min or 300 ml/min/100g of tissue

Front 7

Blood flow in skin:

Back 7

300 ml/min but only 3 ml/min/100g of tissue

Front 8

8 times increase in metabolism gives how many times increase in local blood flow:

Back 8

4 times increase in local blood flow

Front 9

Two basic theories for regulation of local blood flow when either the rate of tissue metabolism changes or the availability of oxygen changes:

Back 9

1. The vasodilatory theory
2. The oxygen lack theory

Front 10

Vasodilator theory for regulation of local blood flow:

Back 10

Increased rate of metabolism and decreased oxygen level releases vasodilator substances that relaxes smooth mm. in arterioles, metarterioles and precapillary sphincters. (Adenosine, CO2, histamine, K+, H+)

Front 11

Adenosine as a vasodilator in coronary arteries:

Back 11

More active heart then usual increases metabolism--> decreases O2 concentration + increased degradation of ATP--> increased release of adenosine which diffuses out of cell===> vasodilatation.

Front 12

Oxygen lack theory of local blood flow control:

Back 12

Decreased O2 will cause vasodilatation because muscles need O2/ nutrients to contract, deprivation of O2 will subsequently lead to relaxation of mm. and vasodilatation.

Front 13

Reactive hyperemia:
(Specialized way of acute local blood flow control)

Back 13

If you block a vessel, and then unblock it, blood flow will increase 4 to 7 times for seconds to hours depending on the duration of the blockage to "repay" the oxygen deficit during the blocked period.

Front 14

Active hyperemia:

Back 14

Active metabolism in tissue deprives nutrients and releases vasodilators to ensure adequate blood flow and nutrient delivery.

Front 15

Production of nitric oxide (NO):

Back 15

Nitric oxide synthase enzymes in endothelial cells synthesize NO from arginine and oxygen and by reduction of inorganic nitrate.

Front 16

Mechanism of how NO works as a local vasodilator:

Back 16

NO activates soluble guanylate cyclases in vascular smooth muscle cells resulting in conversion of cGTP to cGMP---> activation of cGMP- dependent protein kinase==> vasodilatation

Front 17

Stimulation of NO release:

Back 17

1. Increased blood flow (stress on blood vessels)
2. Angiotensin II

Front 18

Arteriosclerosis and its effect on NO:

Back 18

NO synthesis is impaired leading to excessive vasoconstriction---> worsening of hypertension and endothelial damage

Front 19

Endothelin:

Back 19

Substance released for endothelium after injury causing vasoconstriction. Drugs inhibiting endothelin can be used against pulmonary hypertension.

Front 20

Mechanism of long term regulation of blood flow:

Back 20

1. Change in tissue vascularity (angiogenesis). Chronic increase in metabolism in tissue leads to increased growth of number of vessels and size of vessels. (Within days in neonate, up to months in old aged people)
2. Development of collateral circulation

Front 21

Oxygen`s effect on long term regulation of local blood flow:

Back 21

High PO2 in newborns in oxygen tents leads to degeneration of vessels. Removal from oxygen tent with subsequent large drop in PO2 leads to proliferation of vessels to make up for the low O2 pressure.

Front 22

Retrolental fibroplasia:

Back 22

Neonates exposed to high oxygen pressure which is then removed from the high O2 pressure have an overgrowth of retinal vessels where the vessels grow out from the retina in to the eye´s vitreous humor and eventually cause blindness.

Front 23

Vascular endothelial growth factors: (Small peptides)

Back 23

Vascular endothelial growth factor VEGF
Fibroblast growth factor
Angiogenin

Front 24

Mechanism of vascular endothelin growth factors:

Back 24

1.Decreased O2 leads to increase in growth factors
2. Dissolution of basement mebrane of a small vessel
3. Reproduction of new endothelial cells from the vessel towards the growth factor
4. Form tubes and capillary loops, and connect with other vessels
5. If growth is large enough smooth mm. proliferate

Front 25

Long term vascular control is regulated by:

Back 25

Maximum bloos flow needed rather then average flow. Maximum flow only a couple of minutes a day in hard exercise release enough VEGF from muscles to increase their vascularity to a sufficient amount.

Front 26

Development of collateral circulation:

Back 26

Dilation of vascular loops around the blockage (acute phase).
Then growth of many new and small collateral vessels over weeks- months. (Long- term).
This is very common after thrombosis of coronary arteries.

Front 27

Humoral control of the circulation means:

Back 27

Control by substances secreted or absorbed into the body fluids such as hormones and locally produced factors.

Front 28

Vasoconstrictor agents:

Back 28

1. Norepinephrine and Epinephrine
2. Angiotensin II
3. Vasopressin

Front 29

Vasodilator agents:

Back 29

1. Bradykinin
2. Histamine

Front 30

(Nor) Epinephrine:

Back 30

Vasodilatation of coronary arteries.
Constricts arterioles and veins.

Front 31

Angiotensin II:

Back 31

Constricts small arteriolses in the whole body --> increases total peripheral resistance==> rising arterial pressure

Front 32

Vasopressin:

Back 32

(Antidiuretic hormone) is a powerful vasoconstrictor. Produced in hypothalamus and secreted to blood by the posterior pituitary gland. Can rise arterial pressure by 60 mmHg and increase water reabsorption in kidneys.

Front 33

Bradykinin:

Back 33

Causes arteriolar dilation and increased capillary permeability. Enzymes cleave alpha2- globulins into kinins such as kallidin which is the cleaved by tissue enzymes to bradykinin. Activated by maceration of blood and inflammation of tissue.

Front 34

Histamine:

Back 34

Histamine is released from mast cells and basophils in response to tissue damage or inflammation. Arteriolar vasodilator and increase capillary porosity increasing leakage of both fluid and proteins.