Objective-To amplify the description of myocardial stunning. Design-Co
ntrol versus 30 min after a 20 min no flow ischaemia. Experimental ani
mals-15 isolated rabbit hearts perfused with erythrocyte suspension. M
ain outcome measures-Left ventricular systolic function in terms of ao
rtic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end syst
olic pressure-volume relation (ESPVR); early relaxation from dP/dtmin
and rate of left ventricular pressure decay (tau). Passive properties:
ventricular and myocardial stiffness. Coronary resistance from corona
ry blood flow and perfusion pressure. Total myocardial oxygen consumpt
ion (MVO(2)tot). Total mechanical energy via pressure-volume area (PVA
). Contractile efficiency (Econ) and MVO(2) of the unloaded contractin
g heart (MVO(2)unl). External mechanical efficiency (Eext) from stroke
work and MVO(2)tot. Results-Systolic variables in stunned myocardium
were significantly decreased (mean (SD)): aortic flow: 38 (13) v 9 (11
) ml/min; LVPmax: 112 (19) v 74 (18) mm Hg; dP/dtmax: 1475 (400) v 107
5 (275) mm Hg/s. ESPVR was not significantly decreased, at 138 (73) v
125 (58) mm Hg/ml, but the volume axis intercept was shifted rightward
: 0.30 (0.37) v 0.65 (0.25) mi. Likewise, early relaxation was impaire
d: dP/dtmin (-1275 (250) v -975 (250) mm Hg/s) and tau (37 (7) v 46 (1
0) ms). LVPed was significantly decreased at 19 (12) v 12 (7) mm Hg, a
nd both the ventricular (end diastolic pressure-volume relation) and t
he myocardial stiffness (constant k) were increased by 75% and 31%, re
spectively. Coronary resistance increased non-significantly from 0.83
(0.31) to 1.04 (0.41) mm Hg/(ml/min/100 g). Decreases in PVA (570 (280
) v 270 (200) mm Hg . ml/100 g), MVO(2)tot (40 (9) v 34 (8) mu l/beat/
100 g), and MVO(2)unl (26 (9) v 22 (6) mu l/beat/100 g) did not reach
significance, in contrast to significant decreases in Econ (31 (18) v
14 (7)%) and Eext (0.75 (0.29) v 0.18 (0.25) arbitrary units). Conclus
ions-Ventricular systolic function is decreased after brief episodes o
f ischaemia. The decrease in diastolic function probably amplifies the
systolic deterioration during myocardial stunning. Passive diastolic
properties are also changed, shown by increases in both ventricular an
d myocardial stiffness. The increase in coronary resistance indicates
stunning at the vascular level which could limit oxygen supply. With m
aintained MVO(2)tot during stunning, external efficiency is decreased.
Possible candidates for this metabolic stunning are inadequate excita
tion-contraction coupling and disturbed O-2 utilisation by the contrac
tile apparatus.