title: Vasodilator response assessment in porcine myocardium with magnetic resonance relaxometry.
abstract: BACKGROUND
  This research describes an early preclinical study of the biophysical mechanisms governing changes in myocardial T2 during vasodilation in normal myocardium.
  
  
  RESULTS
  Theoretical modeling and experimental studies in an instrumented pig model (n=7) provided measures of changes in myocardial T2, relative blood volume (BV), and microcirculation oxygen levels (%O2) during intracoronary adenosine infusion. Intracoronary adenosine increases perfusion without increasing blood volume or cardiac metabolic rate; thus, T2 elevations should reflect elevated microcirculation oxygen levels. Robust strategies were used for magnetic resonance imaging (MRI) data collection. Measures of myocardial and vascular T1 before and after Clariscan (Amersham Health) injection provided blood volume assessment. Changes in microcirculation oxygen levels were estimated via direct blood sampling from the left anterior descending (LAD) coronary vein. Perfusion changes were monitored using a Doppler flow wire within the left main coronary artery. Myocardial T2 elevations (DeltaT2=17+/-8%) within the LAD arterial perfusion bed were related to elevations in perfusion (coronary velocity reserve=3.2+/-0.4) and coronary venous %O2 [Delta(LAD CV%O2) =56+/-11%], whereas blood volume (DeltaBV=0 +/-2%) and cardiac metabolic rate [Delta(heart rate x blood pressure) = -4+/-11%] remained constant.
  
  
  CONCLUSIONS
  Myocardial T2 elevation during intracoronary adenosine infusion was significant and repeatable, caused by increases in microcirculation oxygen levels. Changes in microcirculation oxygen levels of approximately 40%O2 should be detectable by this technique. This sensitivity should suffice for differentiating normal from abnormal myocardium via measurement of myocardial perfusion reserve.
authors.affiliation: Department of Medical Biophysics, University of Toronto, and Sunnybrook and Women's College Health Sciences Centre, Toronto, Ontario, Canada. wfoltz@sten.sunnybrook.utoronto.ca
authors.forename: Warren D
authors.initials: WD
authors.lastname: Foltz
authors.forename: Hong
authors.initials: H
authors.lastname: Huang
authors.forename: Stephen
authors.initials: S
authors.lastname: Fort
authors.forename: Graham A
authors.initials: GA
authors.lastname: Wright
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001810:Blood Volume / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D013552:Swine; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine; D010100:Oxygen