title: Contribution of myocardium hydraulic skeleton to left ventricular wall interaction and synergy in dogs.
abstract: The most premature motion change after 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 the result of 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 seven 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 (defined as the ratio of WI to the maximum possible work). Interwall asynergy was defined as the difference between the regional efficiency of the anterior and posterior walls. After 9-10 s, posterior wall efficiency decreased 37 +/- 6% with anoxia and 72 +/- 3% with ischemia (P < 0.025), and interwall asynergy was 0 +/- 6% with anoxia and 32 +/- 5% with ischemia (P < 0.05). The contribution of absent hydraulic skeleton to interwall 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 the result of the absence of intracoronary fluid. The lack of hydraulic skeleton within the myocardium contributes approximately 30% to interwall asynergy.
authors.affiliation: Department of Physiological, Favaloro University, C1078AAI Buenos Aires, Argentina. jgbarra@favaloro.edu.ar
authors.forename: Juan Gabriel
authors.initials: JG
authors.lastname: Barra
authors.forename: Alberto José
authors.initials: AJ
authors.lastname: Crottogini
authors.forename: Peter
authors.initials: P
authors.lastname: Willshaw
authors.forename: Elena Catalina
authors.initials: EC
authors.lastname: Lascano
authors.forename: Ricardo Horacio
authors.initials: RH
authors.lastname: Pichel
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology*; D004285:Dogs; D000860:Hypoxia / Q000503:physiopathology*; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000209:etiology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*