The most premature motion change following coronary occlusion is early diastolic thinning of the ischemic left ventricular (LV) wall with concomitant thickening of the normoperfused wall. We aimed 1) to demonstrate that these early changes are due to the absence of fluid within the ischemic myocardium (hydraulic skeleton) rather than to cell anoxia, and 2) to quantitate the contribution of the lack of hydraulic skeleton to left ventricular asynergy of contraction in 7 anesthetized dogs submitted to acute, short-lasting circumflex artery (Cx) occlusion (ischemia) and to perfusion of the Cx with an oxygen-free solution (anoxia). We analyzed the time course of regional work index (WI, area of the LV pressure-wall thickness loop) and regional efficiency (RE, defined as the ratio of WI to the maximum possible work). Inter wall asynergy was defined as the difference between the regional efficiency of the anterior and posterior walls. After 9-10 seconds, posterior wall efficiency decreased 37±6% with anoxia and 72±3% with ischemia (P0.025), and inter wall asynergy was 0±6% with anoxia and 32±5% with ischemia (P<0.05). The contribution of absent hydraulic skeleton to inter wall asynergy (calculated as the difference between % asynergy in anoxia and % asynergy in ischemia, was 30±8% (P<0.05). In conclusion, the earliest wall motion change observed after acute coronary occlusion, namely ischemic wall thinning concomitant with normoperfused wall thickening during isovolumic relaxation, is due to the absence of intracoronary fluid. The lack of hydraulic skeleton within the myocardium contributes about 30% to inter wall asynergy.