title: Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity.
abstract: BACKGROUND
  During maximal hyperemia, capillaries provide the greatest resistance to flow. A major determinant of capillary resistance is viscosity. We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion.
  
  
  RESULTS
  Maximal hyperemia was induced in 9 dogs using adenosine. Serum triglyceride levels were increased by incremental doses of Intralipid. A good correlation was noted between serum triglyceride levels and blood viscosity (r=0.82). Neither total coronary blood volume nor myocardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion. Myocardial vascular resistance (MVR) increased with increasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64). The decrease in hyperemic MBF was associated with a decrease in blood velocity (r=-0.56). These findings were confirmed with direct intravital microscopic observations in the mice cremaster muscle.
  
  
  CONCLUSIONS
  Increasing lipid levels in a fully dilated normal coronary bed causes no change in large or small vessel dimensions. Instead, the increase in blood viscosity causes capillary resistance to rise, which attenuates hyperemic CBF. Therefore, the abnormal CBF reserve associated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function.
authors.affiliation: Cardiovascular Imaging Center, Cardiovascular Division, University of Virginia, Charlottesville, VA, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: Rim
authors.forename: H
authors.initials: H
authors.lastname: Leong-Poi
authors.forename: J R
authors.initials: JR
authors.lastname: Lindner
authors.forename: K
authors.initials: K
authors.lastname: Wei
authors.forename: N G
authors.initials: NG
authors.lastname: Fisher
authors.forename: S
authors.initials: S
authors.lastname: Kaul
mesh_terms: D000241:Adenosine; D000818:Animals; D001160:Arterioles / Q000503:physiopathology; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D001809:Blood Viscosity; D001810:Blood Volume; D002122:Calcium Chloride / Q000494:pharmacology; D002200:Capillary Resistance; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004452:Echocardiography; D005217:Fat Emulsions, Intravenous; D006940:Hyperemia / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology; D006949:Hyperlipidemias / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008863:Microspheres; D018482:Muscle, Skeletal / Q000098:blood supply; D014280:Triglycerides / Q000097:blood; D014699:Venules / Q000503:physiopathology
chemical_list: D005217:Fat Emulsions, Intravenous; D014280:Triglycerides; D000241:Adenosine; D002122:Calcium Chloride