title: Effects of acutely impaired regional function on remote myocardial wall motion and blood flow in the canine left ventricle studied by coronary occlusion and hypoxic perfusion.
abstract: OBJECTIVE
  The aim was to examine whether regional myocardial dysfunction has a significant effect on the wall motion and blood flow in remote non-ischaemic regions.
  
  
  METHODS
  Two different severities of regional dysfunction were produced by occluding the left anterior descending coronary artery and perfusing it with a hypoxic solution. Haemodynamic variables were otherwise identical in the two conditions. The relationship of regional dysfunction in the left anterior descending artery region to regional wall motion and regional myocardial blood flow in the left circumflex artery region were examined.
  
  
  METHODS
  22 anaesthetised mongrel dogs, 9-16 kg, were used for the studies: 14 for the regional wall motion studies, and eight for the regional myocardial blood flow studies.
  
  
  RESULTS
  Segment shortening in the left anterior descending artery region was impaired differently in the two conditions: arterial occlusion caused a bulge, while hypoxic perfusion caused only mild hypokinesis. Segment shortening and the myocardial blood flow in the left circumflex artery region were augmented similarly in the two conditions. Left ventricular end diastolic pressure and end diastolic segment length in the left circumflex region were increased and aortic pressure was slightly decreased by left anterior descending artery occlusion and hypoxic perfusion, but there was no significant difference between the two conditions. Heart rate was not affected.
  
  
  CONCLUSIONS
  The augmentation of wall motion and blood flow of the remote myocardium does not depend on the magnitude of acutely induced regional dysfunction per se. The augmented wall motion in the remote region is unlikely to be due to mechanical unloading of the remote myocardium due to an intraventricular regional interaction, but rather to the Frank-Starling mechanism and left ventricular afterload reduction following acute ischaemia.
authors.affiliation: Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ohtsuka
authors.forename: M
authors.initials: M
authors.lastname: Kakihana
authors.forename: T
authors.initials: T
authors.lastname: Doi
authors.forename: Y
authors.initials: Y
authors.lastname: Sugishita
authors.forename: I
authors.initials: I
authors.lastname: Ito
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood
chemical_list: D010100:Oxygen