TY - JOUR
T1 - Contribution of asynchrony and nonuniformity to mechanical interaction in normal and stunned myocardium
AU - Fan, Dongsheng
AU - Soei, Loe Kie
AU - Stubenitsky, Rene
AU - Boersma, Eric
AU - Duncker, Dirk J.
AU - Verdouw, Pieter D.
AU - Krams, Rob
N1 - Copyright © 1997 the American Physiological Society
PY - 1997/11
Y1 - 1997/11
N2 - In anesthetized pigs, we investigated whether asynchrony (ΔT) and nonuniformity (regional differences) in contractility (ΔE) could describe the interaction between normal and stunned myocardium. Mechanical interaction was evaluated by regional postsystolic work (PSW) before and after production of stunning by a 5-min occlusion of the left circumflex coronary artery [LCX (LCX stunning)] and a subsequent 10-min occlusion of the left anterior descending coronary artery [LAD (LAD stunning)]. ΔT and ΔE were intensified by intracoronary (LAD) infusions of dobutamine. From regional end-systolic pressure-segment length relationships, systolic segment shortening (SS), end- systolic elastance (E), external work (EW), and PSW were determined. LCX stunning decreased SS(LCX) from 14 ± 2 (mean ± SE, n = 9) to 10 ± 2% and E(LCX) from 103 ± 25 to 52 ± 7 mmHg/mm, whereas the LAD region was unaffected. EW(LCX) decreased from 165 ± 16 to 138 ± 20 mmHg · mm, whereas PSW(LCX) increased from -4 ± 6 to 8 ± 3 mmHg · mm. Additional LAD stunning reduced SS(LAD) from 16 ± 2 to 9 ± 3% and E(LAD) from 79 ± 10 to 31 ± 6 mmHg/mm, without affecting SS(LCX) and E(LCX). In the normal myocardium, PSW(LAD) increased and PSW(LCX) decreased, but, during local LAD dobutamine infusions after stunning, both PSW(LCX) and PSW(LAD) increased. In normal myocardium, the changes in PSW(LCX) could be described by ΔT (65 ± 11%) and ΔE (37 ± 15%). After stunning of the LAD area, the contribution of ΔE increased to 55 ± 14% at the expense of ΔT (37 ± 15%). Similar contributions of ΔE (54 ± 13%) and ΔT (57 ± 13%) were found when both the LCX and LAD distribution areas were stunned. In normal myocardium, both ΔT and ΔE modulate mechanical interaction, with the contribution of AT exceeding that of ΔE. In stunned myocardium, both factors contribute, but the contribution shifts in favor of ΔE.
AB - In anesthetized pigs, we investigated whether asynchrony (ΔT) and nonuniformity (regional differences) in contractility (ΔE) could describe the interaction between normal and stunned myocardium. Mechanical interaction was evaluated by regional postsystolic work (PSW) before and after production of stunning by a 5-min occlusion of the left circumflex coronary artery [LCX (LCX stunning)] and a subsequent 10-min occlusion of the left anterior descending coronary artery [LAD (LAD stunning)]. ΔT and ΔE were intensified by intracoronary (LAD) infusions of dobutamine. From regional end-systolic pressure-segment length relationships, systolic segment shortening (SS), end- systolic elastance (E), external work (EW), and PSW were determined. LCX stunning decreased SS(LCX) from 14 ± 2 (mean ± SE, n = 9) to 10 ± 2% and E(LCX) from 103 ± 25 to 52 ± 7 mmHg/mm, whereas the LAD region was unaffected. EW(LCX) decreased from 165 ± 16 to 138 ± 20 mmHg · mm, whereas PSW(LCX) increased from -4 ± 6 to 8 ± 3 mmHg · mm. Additional LAD stunning reduced SS(LAD) from 16 ± 2 to 9 ± 3% and E(LAD) from 79 ± 10 to 31 ± 6 mmHg/mm, without affecting SS(LCX) and E(LCX). In the normal myocardium, PSW(LAD) increased and PSW(LCX) decreased, but, during local LAD dobutamine infusions after stunning, both PSW(LCX) and PSW(LAD) increased. In normal myocardium, the changes in PSW(LCX) could be described by ΔT (65 ± 11%) and ΔE (37 ± 15%). After stunning of the LAD area, the contribution of ΔE increased to 55 ± 14% at the expense of ΔT (37 ± 15%). Similar contributions of ΔE (54 ± 13%) and ΔT (57 ± 13%) were found when both the LCX and LAD distribution areas were stunned. In normal myocardium, both ΔT and ΔE modulate mechanical interaction, with the contribution of AT exceeding that of ΔE. In stunned myocardium, both factors contribute, but the contribution shifts in favor of ΔE.
UR - https://www.scopus.com/pages/publications/20644471605
U2 - 10.1152/ajpheart.1997.273.5.h2146
DO - 10.1152/ajpheart.1997.273.5.h2146
M3 - Article
C2 - 9374747
SN - 0363-6135
VL - 273
SP - H2146-H2154
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 5
ER -