---start--- regional blood flow: realize that as each organ system changes its needs for blood flow the overall control of arterial BP has to take that into account. when you take a large meal, splanchnic circulation increases. during excercise, muscle circulation increases. pressure is maintained relatively constantly. the precapillary sphincters act to change resistance to flow at the entry to the various capillary beds. all organ systems are maintained in parallel, so are not interdependent. the total peripheral resistance is determined by the parallel arrangement of the individual resistances. so you can lower flow to muscle without losing flow to skin or GI tract. 1 total resistance = ------------------- 1/R1 + 1/R2 + 1/Rn so flow Q through any system n is calculated as Qn = (Pa-Pv)/Rn where Pa is arterial pressure and Pv is venous pressure. the components or renal circulation are set up in series, and the liver is in series with the splanchnic circulation, these are special circumstances. what determines flow through these systems? local factors, hormonal factors, etc. RELATIVE blood flow among organs p 2 handout renal flow is HUGE relative to other organs...because it filters plasma. it's pretty maxed out under normal conditions, and can't increase flow more than about twice. it can decrease about the same amount. the BRAIN and HEART you don't ever decrease flow to. youcan increase flow to the heart about 4 times and the brain about 3 times, but you do NOT want to decrease flow to those organs, so vasoconstriction doesn't occur. LIVER: can increase flow about 5 times, can decrease a little bit. INTESTINES can increase flow by factor of 10 and can also decrease flow muscle can increase flow about 20 times, and can also decrease. note that at rest, most capillaries are closed due to vasomotion anyway. skin can increase flow about 30 times. this is for thermoregulatory purposes.can also decrease flow. to measure blood flow, there are flow meters where you can put a probe over a vessel, there are thermal dilution and dye dilution techniques, but the classic method is the Fick method, from 1870 (see p 3 handout). the FICK BEAN MACHINE beans are fed into buckets, wheel goes around, beans are dropped into bucket. at a steady state there is a rate of rotation that is steady, a steady number of beans per bucket coming down, and a steady number going back, so there is a steady accumulation of beans in the bucket. if you know number of beans/bucket going down and back you can determine the rate of rotation. rate of accumulation Rate of rotation = --------------------------------------- beans/bucket down - beans/bucket up now, if this were blood, use oxygen and blood...as on page 4. oxygen uptake by lungs ml/min O2 rate of flow = ------------------------------- arterial mlO2/mL blood - venous mLO2/mL blood so, Q* = rate of flow, U*O2 = oxygen uptake, AO2= arterial ox. content, VO2 = venous ox content. Q* = U*O2/(AO2 - VO2) so you take blood from artery and from pulmonary artery, and you measure these things and you then figure out the rate of flow, in mL blood/minute. 240mL O2/min ------------- = 6000 mL blood/minute .18 - .14 note: arterial sample can be from any artery but venous sample has to be MIXED sample so must be from close to heart. CEREBRAL circulation anatomic considerations: supplied mainly by internal carotid and vertebral arteries. regulation: little autonomic regulation. Autoregulation important. Increased PCO2 is potent local vasodilator. this is couopled to secondary autonomically mediated reflex constriction in other systemic beds. so if PCO2 goes up in the brain, more flow is sent to the brain at the expense of other systems. "the boss is in trouble, everybody go help." flow is regulated over wide range of pressure with this mechanism: 60-140 mmHg arterial pressure.) Now, flow is relatively constant, due to bone can only increase by factor of 3. the blood brain barrier restricts capillary exchange - endothelium very tightly packed, can only pass H2O, CO2, O2 - but this barrier isn't present in hypothalamic region. SKELETAL MUSCLE: large capillary reserve. 70-8% of capillaries closed at rest. autonomic regulation by high resting alpha sympathetic vasoconstrictor tone. beta receptors dominate, so circulating epi causes vasodilation. parasymp.innervation is present. autoregulation: STRONG vasodilatory effects of metabolite buildup eg lactic acid, adenosine, increased pCO2. CORONARY circulation main l and r coronary arteries originate at ostia in sinuses of valsava just distal to aortic valve cusps. autonomic regulation predominantly HR. sympathetic beta 1 receptors respond to norepi by increasing HR, and circulating epi causes vasodilation. autoregulation: coronary vasodilation in response to increase in pCO2 and decrease in O2. most of flow goes to L heart, only 15% to right. flow can increase by factor of 4. flow is cyclic - occurs mostly during diastole esp in L heart. during systole L coronary flow drops to near zero, then increases during diastole, because the coronary vessels are occluded as pressure within ventricle builds up. this effect is less present in right heart. note: these notes of circulations are in the handout... SPLANCHNIC: liver, spleen, pancreas, stomach, intestines: many anastomoses. autonomic regulation mainly alpha sympathetic vasoconst. but there is also parasymp innervation present (vasodil.). autoregulation: can override prolonged sympathetic vasoconstriction as metabolites accumulate. flow is dynamic and state-dependent (excercise, feeding, etc). flow can fall to allow distribution to other higher priority organs. endothelial lining of liver sinuses VERY permeable allowing discrete components to pass into parenchyma. all splanchnic circ feeds into portal vein which goes into these sinuses. hepatic artery feeds liver CT. RENAL circ. glomerular and tubular circulations are arranged IN SERIES autonomic reg: rich alpha sympathetic vasoconstriction. greatest effect on efferent arteriole so flow can fall while still maintaining glomerular filtration - eg, you don't slow flow at the FRONT end of the bed, but at the output end. so you maintain a filtration pressure at glomerulus. no apparent parasympathetic control. autoregulation: renal capsue provides mechanical regulation during increased blood pressure- similar to bony covering of brain. high resting flow rate, can only increase 2x, can significantly fall though to allow distribution to brain, heart. renin/angiotensin mechanism important bp regulator look at anatomic diagram in handout to see why the efferent arteriole is used for decreasing flow instead of afferent. PULMONARY: bronchial arterial flow bypasses pulmonary capillaries (3%) autonomic regulation by alpha sympathetic vasoconst. autoregulation: decrease in O2, pH, and incresase in CO2 causes VASOCONSTRICTION to shunt blood to better ventilated area of lung. eg, if you have ventilation perfusion problem, blood is shunted to better area. flow can be decreased about 30% in response to symp. stim. high compliance vessels can accomodate large flow by vasodialtion associated w/small pressure increase with exercise. due to low hydrostatic pressure colloid osmotic pressure keeps alveoli dry ACH, histamine cause bronchiolar constriction symp stimulation causes bronchiolar dilation - asthma tx sympathomimetic amines. SKIN circ anatomy: capillary loops ascend in skin papillae and return to subcapillary plexus. forms radiator effect...warm blood goes into skin and loses heat efficiently to environment. good way to lose heat. there are arteriovenous anastomoses to shunt blood for thermoregulation. the rich venous plexus has a whole pool of blood. to conserve heat you use the anastomoses to shunt blood away from the heat exchange mechanism, going directly into vein instead of going through papillary capillary loops. SOURCE TRANSMIT RECEPTOR ACTION --------------- ---------- ----------- --------- parasymp. n ACH nicotinic vasodilation sympath. n. NOREPI alpha vasoconstriction adrenal EPI alpha vasconstriction adrenal EPI beta2 vasodilation how smooth muscles constrict or relax in the small vessels effects vasodilation or vasoconstriction, and that depends on receptors and neurotransmitters (NTs). If a smooth muscle cell has a nicotinic receptor and sees ACH released by parasympathetic nerve it will vasodilate. now, sympathetic stimulation releases norepi, and if the muscle has alpha receptors, you get vasoconstriction then. adrenal gland releases epi into blood. if you have alpha receptors, epi will cause vasoconstriction, if there are beta 2, will vasodilate. beta1 are in the heart, beta2 are in the periphery. now, peripherally, there is a high density of alpha receptors, so sympathetic outflow causes vasoconstriction, mostly. ---end---