Application of an end-systolic pressure-segment length relationship for measuring regional contractility.
A method for estimating regional contractility is described using the end-systolic relationship between left ventricular pressure and myocardial segment-lengths in rapidly volume-loaded beats. The approach was based on the success of previously developed end-systolic relationships between left ventricular pressure and volume and between variable ejection force and fiber length used to describe global contractility in beating hearts. The regional end-systolic relationship was more complicated than its global counterpart, which was load independent, and appeared curvilinear to rapid volume loading. As an approximation of this relationship, a linear slope was constructed between maximum and minimum (pre-ejection) loaded beats of equal cycle length. Because of its load dependency and in order to compare slope relationships between interventions, slope functions were derived only from similarly loaded beats either within or between interventions. Slopes generated by this technique had a reasonable constancy at control conditions and coronary flows with an average SEM of 9.1% of the slope means. End-systolic slopes also appeared sensitive to changes in contractile state, increasing appropriately following treatments with dobutamine and decreasing after propranolol. Following shifts in the end-systolic slopes were unreliable, however, in describing the regional changes in contractility with ischemia. At milder levels of flow restriction, the slopes declined as expected. At moderate levels of flow restriction, the pressure-segment loops shifted markedly rightward and the slope increased. At advanced levels of ischemia, the loops were so distorted, that end-systole could not be identified accurately and the loops essentially described the diastolic compliance characteristics of the left ventricle. Thus the slope estimates of regional contractility as described in this report provided a reliable assessment of inotropic background during modifications with positive and negative inotropic drugs but became invalid as systolic shortening was replaced by aneurysmal bulging during high-grade ischemia.
D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology; D004280:Dobutamine / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D008722:Methods; D009200:Myocardial Contraction / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D013552:Swine; D013599:Systole / Q000187:drug effects
D004280:Dobutamine; D011433:Propranolol