Studies on prolonged acute regional ischemia. II. Implications of progression from dyskinesia to akinesia in the ischemic segment.
This study analyzed the pattern of regional wall motion in 58 dogs undergoing 4 to 6 hours of left anterior descending coronary artery occlusion. Regional wall motion was measured by ultrasonic crystals and ischemic muscle either remained dyskinetic (-40% of control systolic shortening, n = 26) or progressed toward akinesia (less than 20% of control systolic shortening or greater than 50% reduction in passive lengthening, n = 32). Ten dogs underwent unmodified blood reperfusion. Regional blood flow (radioactive microspheres), histochemical damage (triphenyltetrazolium chloride staining), and mitochondrial function were determined. Hearts showing persistent dyskinesia had more collateral flow (12 versus 2 ml/100 gm/min, p less than 0.05), less histochemical damage (26% versus 63% area at risk/area of nonstaining, p less than 0.05), and better retention of mitochondrial oxidative phosphorylation capacity (adenosine triphosphate, 622 versus 444 nmol/mg protein/min, p less than 0.05), and tended toward mitochondrial calcium accumulation (48 versus 64 nmol/mg protein). Unmodified blood reperfusion after 4 hours of ischemia produced prompt akinesia (-2% +/- 3% systolic shortening) and was associated with increased edema (82% water content), caused the low-reflow phenomenon (19% control subendocardial flow, 13 ml/100 gm/min), and increased histochemical damage (69% triphenyltetrazolium chloride nonstaining, p less than 0.05). These findings suggest that persistent dyskinesia during early ischemia (first 6 hours) may reflect a relatively optimistic sign, as regression to akinesia occurs in muscle with less collateral flow, more impaired mitochondrial function, worsened calcium homeostasis, and more severe histochemical and ultrastructural damage. These observations imply that careful evaluation of ischemic wall motion may provide a valuable insight into potential muscle salvage.
Division of Cardiothoracic Surgery, University of California, Los Angeles Medical Center 90024-1741.
F
F
Beyersdorf
F
F
Okamoto
G D
GD
Buckberg
F
F
Sjöstrand
B S
BS
Allen
C
C
Acar
H H
HH
Young
H I
HI
Bugyi
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001834:Body Water / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D004285:Dogs; D006439:Hemodynamics; D006651:Histocytochemistry; D008929:Mitochondria, Heart / Q000378:metabolism / Q000648:ultrastructure; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010710:Phosphates / Q000378:metabolism
D010710:Phosphates; D000255:Adenosine Triphosphate; D003402:Creatine Kinase; D002118:Calcium