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SUMMARY:Theoretical models for regulation of blood flow in the microcircul
 ation - Secomb\, T (Arizona)
DTSTART:20090721T093000Z
DTEND:20090721T094500Z
UID:TALK19137@talks.cam.ac.uk
CONTACT:Mustapha Amrani
DESCRIPTION:Local control of blood flow is achieved by contraction and dil
 ation of smooth muscle cells in microvessel walls\, particularly in arteri
 oles\, allowing rapid local responses to changing conditions. Several type
 s of vessel response are involved. In the myogenic response\, increased wa
 ll tension causes contraction. In the shear-dependent response\, increased
  wall shear stress causes dilation. In the metabolic response\, arteriolar
  diameters change according to the metabolic status sensed at downstream l
 ocations (capillaries and venules) after oxygen has been extracted from th
 e blood. Information is transferred upstream along vessel walls by conduct
 ed responses\, which involve electrical coupling of the cells. We have dev
 eloped theoretical models for flow regulation based on a mechanism for the
  metabolic response in which decreased oxygen levels in venules cause incr
 eased release of ATP\, which acts on vessel walls to initiate upstream con
 ducted responses leading to vasodilation. This model is used to explore th
 e roles of the various vessel responses in autoregulation\, in which flow 
 is almost constant independent of changes in blood pressure\, and in metab
 olic regulation\, in which flow is modulated in response to changing metab
 olic demands. It is shown that autoregulation is achieved by the combined 
 action of myogenic and metabolic responses\, which overcome the opposing e
 ffect of shear-dependent responses. Metabolic responses are primarily resp
 onsible for metabolic flow regulation\, but are opposed by the effects of 
 shear-dependent and myogenic responses. The model is based on an explicit 
 description of vascular network structure\, and has potential application 
 to the simulation of coronary flow regulation.
LOCATION:Seminar Room 1\, Newton Institute
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