TY - JOUR
T1 - Reversal of dysfunction in postischemic stunned myocardium by epinephrine and postextrasystolic potentiation
AU - Becker, Lewis C.
AU - Levine, Joseph H.
AU - DiPaula, Anthony F.
AU - Guarnieri, Thomas
AU - Aversano, Thomas
N1 - Funding Information:
From the Cardiology DivI~ion, Department of Medicine, Johns HopkIns University School of MedicIne, Baltimore, Maryland, This study was supported by the Specialized Center for Research in Ischemic Heart Disease Grant HL 17b55 from the National Institutes of Health, Bethesda, Mary• land. Drs. Levine and Aversano were recipients of National Research Service Award-Training Grant 5 T32 HL 07227 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, Manuscnpt received August 20, 1985; revised manuscnpt received October 9, 1985, accepted October 23, 1985, Address for reprints: LeWIS C Becker, MD, Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe Street, Halsted 500, Bal• timore, Maryland 21205.
PY - 1986
Y1 - 1986
N2 - After brief coronary occlusions, myocardium may become "stunned," exhibiting prolonged depression of function despite the absence of necrosis. Because of the accompanying decline in adenosine triphosphate and adenine nucleotide precursors, a deficiency of energy supply has been proposed as the basis for postischemic dysfunction. This study examined whether sufficient functional and metabolic reserve exists in stunned myocardium to sustain a prolonged, maximal inotropic response to epinephrine and postextrasystolic potentiation. In 11 open chest dogs, the left anterior descending coronary artery was occluded for 5 minutes, followed by 10 minutes of reflow, repeated 12 times, with a final 1 hour recovery period. Regional myocardial function was measured using pairs of ultrasonic dimension crystals implanted in ischemic and nonischemic zones. During repetitive reflows a progressive decrease in mean systolic segment shortening occurred: baseline 21.8%, 1st reflow 15.2%, 12th reflow 4.3%, 1 hour recovery 7.9%. Intravenous epinephrine, titrated to produce a maximal inotropic response, caused segment shortening to increase to 21.6% after 10 minutes and to 24.8 % after 1 hour of infusion, despite a 20 mm Hg increase in systolic pressure. The same dose of epinephrine given before ischemia increased segment shortening to 30.5%. In six of the dogs, postextrasystolic potentiation before ischemia increased segment shortening from 21.8 to 31.1%, and after 1 hour of recovery from ischemia, from 7.9 to 24.8%. Lesser increases in segment shortening were also seen in nonischemic segments. The results indicate that stunned myocardium possesses considerable functional reserve. Deficient energy stores are therefore not likely to be the basis for depressed function seen at rest in stunned myocardium.
AB - After brief coronary occlusions, myocardium may become "stunned," exhibiting prolonged depression of function despite the absence of necrosis. Because of the accompanying decline in adenosine triphosphate and adenine nucleotide precursors, a deficiency of energy supply has been proposed as the basis for postischemic dysfunction. This study examined whether sufficient functional and metabolic reserve exists in stunned myocardium to sustain a prolonged, maximal inotropic response to epinephrine and postextrasystolic potentiation. In 11 open chest dogs, the left anterior descending coronary artery was occluded for 5 minutes, followed by 10 minutes of reflow, repeated 12 times, with a final 1 hour recovery period. Regional myocardial function was measured using pairs of ultrasonic dimension crystals implanted in ischemic and nonischemic zones. During repetitive reflows a progressive decrease in mean systolic segment shortening occurred: baseline 21.8%, 1st reflow 15.2%, 12th reflow 4.3%, 1 hour recovery 7.9%. Intravenous epinephrine, titrated to produce a maximal inotropic response, caused segment shortening to increase to 21.6% after 10 minutes and to 24.8 % after 1 hour of infusion, despite a 20 mm Hg increase in systolic pressure. The same dose of epinephrine given before ischemia increased segment shortening to 30.5%. In six of the dogs, postextrasystolic potentiation before ischemia increased segment shortening from 21.8 to 31.1%, and after 1 hour of recovery from ischemia, from 7.9 to 24.8%. Lesser increases in segment shortening were also seen in nonischemic segments. The results indicate that stunned myocardium possesses considerable functional reserve. Deficient energy stores are therefore not likely to be the basis for depressed function seen at rest in stunned myocardium.
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U2 - 10.1016/S0735-1097(86)80468-5
DO - 10.1016/S0735-1097(86)80468-5
M3 - Article
C2 - 3950238
AN - SCOPUS:0022624277
SN - 0735-1097
VL - 7
SP - 580
EP - 589
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 3
ER -