TY - JOUR
T1 - Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog
T2 - Comparison with myocardial stunning produced by repeated coronary occlusions
AU - Stahl, Lloyd D.
AU - Aversano, Thomas
AU - Ambrosio, Giuseppe
AU - Becker, Lewis C.
N1 - Funding Information:
From the Cardiology Division, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland. This study was supported by United States Public Health Service Grant (Specialized Center of Research in Ischemic Heart Disease) 17655-12 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Betheseda, Maryland. Dr. Stahl was supported by a Research Fellowship from the American Heart Association, recipient of a Fogarty International Fellowship Award I F05 TWO 3435 from the National Institutes of Health. Manuscript received July 28, 1986; revised manuscript received October 8, 1986, accepted November 3, 1986. Address for reprints: Lewis Halsted 500, 600 North Wolfe Street, Baltimore, Maryland 21205.
PY - 1987
Y1 - 1987
N2 - Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last druginduced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
AB - Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last druginduced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
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U2 - 10.1016/S0735-1097(87)80475-8
DO - 10.1016/S0735-1097(87)80475-8
M3 - Article
C2 - 3584722
AN - SCOPUS:0023257747
SN - 0735-1097
VL - 9
SP - 1339
EP - 1347
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 6
ER -