Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
57 Cards in this Set
- Front
- Back
ACUTE control of local and humoral control of tissue blood flow occurs within what time frame
|
seconds to minutes
|
|
ACUTE control of local and humoral control of tissue blood flow occurs via what mechanisms
|
local and neurohormonal
|
|
LONG-TERM control of local and humoral control of tissue blood flow occurs within what time frame
|
over days to months
|
|
LONG-TERM control of local and humoral control of tissue and blood flow is due to what
|
change in size or number of blood vessels
|
|
baseline tone is acheived how
|
by partial constriction of the resistance vessels which allows both vasodilation and further vasoconstriction
|
|
the walls of resistance vessels are composed of what
|
primarily of smooth muscle
|
|
variation of smooth muscle contraction allows for what to occur
|
*preferential distribution of blood flow throughout the body
*control of arterial & venous tone *total peripheral resistance |
|
muscle can increase how much from resting to active state
|
20 fold
|
|
smooth muscle contraction develops slowly or rapidly
|
very slowly
|
|
smooth muscle contraction develops low or high forces
|
high
|
|
smooth muscle maintains contraction for how long
|
long periods
|
|
what are the mechanisms for contraction of smooth muscle
|
*electromechanical coupling
*pharmacmechanical coupling |
|
what is occuring with electromechanical coupling
|
increased myoplasmic Ca+ via voltage gated Ca channels when an AP arrives
|
|
what is pharmacomehanical coupling
|
*occurs via receptor mediated Ca channels
*occurs in the ABSENCE of electrical excitation |
|
what is the primary mechanism for smooth muscle contraction
|
pharmacomechanical coupling
|
|
what are the theories of local blood flow regulation
|
1-vasodilator theory
2-oxygen lack theory |
|
what is the vasodilator theory
|
vasodilator substances produced and released d/t and increase in metabolism or a decrease in supply of o2 or other nutrients
|
|
what are the proposed vasodilator substances r/t to the vasodilator theory
|
*adenosine
*CO2 *histamine *K+ or H+ ions *nitric oxide *prostaglandins **combo of these** |
|
what does the oxygen lack theory state
|
*in the absence of adequate o2 (or some other nutrient) the smooth muscle is not able to maintain contraction
*when it relaxes the blood vessel dilates allow more blood & o2 to be provided |
|
what would occur with too much blood flow or hyperoxygenation
|
it would allow for increased contraction of smooth muscle thereby decreasing blood vessel diameter & returning blood flow to acceptable level
|
|
what is reactive hyperemia
|
*following occulusion of blood supply to tissue upon release of the occlusion the blood flow may increase to several times the baseline
|
|
with reactive hyperemia what is the duration
|
it is related to duration of occlusion
|
|
what is active hyperemia
|
increased blood flow in highly active tissue
(e.g. exercising skeletal muscle) |
|
what is autoregulation
|
maintenance of or rapid return to approximately normal blood flow following abrupt changes in arterial pressure
|
|
what are the proposed mechanisms for autoregulation
|
1-metabolic theory
2-myogenic theory |
|
what is metabolic theory
|
*similar to o2 lack theory of local blood flow regulation
*excess o2 or other nutrient causes increased smooth muscle contraction w/ subsequent decrease in blood flow |
|
what is myogenic theory
|
increase or decrease in pressure initially increases or decreases flow, but the change in transmural pressure initiates contraction or relaxation of vascular smooth muscle
|
|
with myogenic theory what allows rapid Ca+ entry resulting in contraction
|
stretch induced vascular depolarization
|
|
myogenic theory of autoregulation is independent of what factors
|
*neurohumoral influences
*intact endothelium |
|
what is the myogenic theory of autoregulation overriden by
|
metabolic needs of the tissue
|
|
locally mediated vasodilation affects only what vessels
|
the small arteries and arterioles
|
|
locally mediated vasodilation does NOT affect what vessels
|
larger upstream arteries
|
|
what occurs when vasodilation occurs downstream
|
*it increases flow through the larger arteries upstream
*this increased flow places a shear stress on the vascular endothelium upstream which releases EDRF (primarily NO) w/ subsequent vasodilation of these vessels |
|
what is baseline tone of blood vessels INDEPENDENT of
|
nervous system input
|
|
baseline vascular tone is possibly d/t what factors
|
*myogenic activity in response to stretch imposed by the blood pressure
*high o2 content of arterial blood *presence of Ca+ *some unknown plasma factor |
|
regarding neurohormonal control how are substances produced and released
|
both centrally and locally
|
|
vasoconstrictors include what substances
|
*norepi
*epi *angiotension II *vasopressin (ADH) *endothelin |
|
where is norepi released from
|
sympathetic nerve endings and the adrenal medulla
|
|
where is epi released from
|
the adrenal medulla
|
|
what does angiotension II cause to occur
|
widespread constriction of small arterioles resulting in increased peripheral resistance
|
|
vasopressin (ADH) is released from where
|
the posterior pituitary
|
|
vasopressin (ADH) has what function
|
functions to increase tubular reabsorption of water
|
|
endothelin is released from where
|
damaged endothelial cells
|
|
what does endothelin cause to occur
|
local vasoconstriction and reduced bleeding
|
|
vasodilators include what substances
|
*bradykinin
*histamine |
|
what is enzyme kallikrein
|
it is activated by many factors and acts on alpha-2 globulin to release kallidin which is converted to bradykinin
|
|
what does bradykinin do
|
produces arteriolar dilation and increased capillary permeability
|
|
which substance is an importat factor in capillary leakage in inflammation and in regulation of skin blood flow
|
bradykinin
|
|
what does histamine do
|
causes arteriolar dilation and increases capillary permeability following release from inflammed or damaged tissues
|
|
what are other factors that cause vasodilation
|
*increased K
*increased Mg *increased H *acetate *citrate *increased CO2 (cerebral) |
|
what are other factors that cause vasoconstriction
|
*increased Ca
*decreased H *increased CO2 (systemically via SNS) |
|
long term regulation of blood flow regulates blood flow fairly well b/t what blood pressures
|
50-250 mmHg
|
|
long term blood pressure control occurs in what time frame
|
over days to months
|
|
long term regulation of blood flow is primarily acheived how
|
through change in vascularity of tissues
|
|
angiogenesis is stimulated by what factors
|
*inadeqate o2
*lack of other necessary nutrients |
|
what are the mediators of angiogenesis
|
(multiple substances id'd which stimulate vascular growth)
*vascular endothelial growth factor (VGEF) *fibroblast growth factor *angiogenin |
|
what is stimulation of angiogensis dependent on
|
MAXIMUM need rather than average need
|