TY - JOUR
T1 - Morphometric analysis on myocardial injury related to the use of high volume potassium cardioplegic solution during ischemic arrest
AU - Li, Qui yan
AU - MacAulay, M. A.
AU - Landymore, R. W.
AU - Marble, A.
AU - Dean, S.
AU - Fris, J.
AU - Kerstein, F.
PY - 1992
Y1 - 1992
N2 - We correlated the effects of high volumes of K+ cardioplegic solution on myocardial structure and function in 16 dogs following open-beart surgery. Eight animals received high volume potassium cardioplegic solution (25 cc/kg body weight, every 30 min) during 90 min of ischemic arrest (HVK-C group). The others received sufficient cardioplegic solution to maintain complete electrical arrest as defined by voltage monitoring criteria (VM group). Cardiac index (CI), left ventricular stroke work index (LVSWI), and myocardial contractility (dp/dt) were determined before arrest and after 90 min of ischemia and 45 min of reperfusion. Biopsies were taken for EM ultrastructure and ATP estimation. Morphometric analysis of EM micrographs found increased volume of damaged mitochondria (DMR) (p < 0.025), damaged myofibrils (DMF) (p < 0.001), intermyofibrilar edema (p < 0.005), T-tubule and sarcoplasmic reticulum (p < 0.05) in the HVK-C group. Left ventricular (LV) function was more depressed in animals receiving HVK-C. CI decreased by 1.8 ± 0.4 l/min/square meter (p < 0.01), LVSWS fell by 3.3 ± 0.8 gm-m/beat/Kg (p < 0.01), dp/dt decreased by 684 ± 135 (p < 0.0025). ATP decreased by 26% in HVK-C and by 12% in VM group (0.1 < p < 0.05). Structural damage (scores of injured volume of mitochondria and myofibrils) correlated with post-ischemic depression of LV function (Cardiac output and myocardial contractility), r -0.72 and -0.66 (p < 0.001 and 0.004).
AB - We correlated the effects of high volumes of K+ cardioplegic solution on myocardial structure and function in 16 dogs following open-beart surgery. Eight animals received high volume potassium cardioplegic solution (25 cc/kg body weight, every 30 min) during 90 min of ischemic arrest (HVK-C group). The others received sufficient cardioplegic solution to maintain complete electrical arrest as defined by voltage monitoring criteria (VM group). Cardiac index (CI), left ventricular stroke work index (LVSWI), and myocardial contractility (dp/dt) were determined before arrest and after 90 min of ischemia and 45 min of reperfusion. Biopsies were taken for EM ultrastructure and ATP estimation. Morphometric analysis of EM micrographs found increased volume of damaged mitochondria (DMR) (p < 0.025), damaged myofibrils (DMF) (p < 0.001), intermyofibrilar edema (p < 0.005), T-tubule and sarcoplasmic reticulum (p < 0.05) in the HVK-C group. Left ventricular (LV) function was more depressed in animals receiving HVK-C. CI decreased by 1.8 ± 0.4 l/min/square meter (p < 0.01), LVSWS fell by 3.3 ± 0.8 gm-m/beat/Kg (p < 0.01), dp/dt decreased by 684 ± 135 (p < 0.0025). ATP decreased by 26% in HVK-C and by 12% in VM group (0.1 < p < 0.05). Structural damage (scores of injured volume of mitochondria and myofibrils) correlated with post-ischemic depression of LV function (Cardiac output and myocardial contractility), r -0.72 and -0.66 (p < 0.001 and 0.004).
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U2 - 10.1016/S0344-0338(11)80077-4
DO - 10.1016/S0344-0338(11)80077-4
M3 - Article
C2 - 1409109
AN - SCOPUS:0026806952
SN - 0344-0338
VL - 188
SP - 668
EP - 671
JO - Pathology Research and Practice
JF - Pathology Research and Practice
IS - 4-5
ER -