Meeting Abstract
P3-4 Sunday, Jan. 6 15:30 - 17:30 Force-velocity relationships in cardiac muscles of the American lobster, Homarus americanus KUKAJ, A.*; ESCALANTE, G.; ELLERS, O.; DICKINSON, P.; JOHNSON, A. S.; Bowdoin College; Bowdoin College; Bowdoin College; Bowdoin College; Bowdoin College akukaj@bowdoin.edu
Crustacean hearts provide a comparatively simple model for understanding the mechanics of heart function. As with all hearts, the work done by the lobster heart creates pressure that circulates blood, or hemolymph, throughout the body. The ability of the heart to do work depends on heartbeat frequency and amplitude. When tissues need more energy, the heart can increase the volume being pumped into and out of the heart by increasing these variables. Such functional changes can alter the stretch imposed on the heart by elastic pulls and pressure changes during contraction and relaxation, which, in effect, alter the length of the intrinsic muscles of the heart. Similarly, increases in frequency will alter the velocity at which the heart changes length. We assessed the characteristic length-tension and force-velocity relationships of the lobster heart and quantified how these relationships change with increased inotropy as induced by SGRNFLRFamide (SGRN), an endogenous neuropeptide in H. americanus. We found that (1) the lobster heart length-tension curves fit the general pattern observed for cardiac length-tension curves from other species in that the active force generated by the muscle increases up to a point with increasing muscle length, (2) the lobster heart force-velocity curve resembles the iconic curve in that contractility of the heart increases as lengthening velocity increases and decreases as shortening velocity increases, (3) SGRN shifts the length-tension curve up, thereby increasing heart contractility, and (4) SGRN decreases the effect of velocity on force during both lengthening and shortening of the heart. These relationships among tension, length and velocity and neuromodulators such as SGRN enable flexibility in the heart’s response to cardiac demand.