Abstract
Diastolic heart failure (DHF) is characterized as heart failure with preserved systolic function; the mechanisms underlying this syndrome are incompletely understood. Accordingly, we studied myofilament function in an experimental model of DHF. DHF was induced by chronic Angiotensin II infusion via surgically implanted infusion pumps (400ng/kg/min)/saline pumps (0.9%) in female Dunkin Hartley Guinea pigs (400g). Following eight weeks of treatment, LV samples were snap frozen in liquid N2. Skinned myocyte fragments were prepared by mechanical dissociation and subsequently glued to a force transducer and motor attached to micropipettes that were positioned on the stage of an inverted microscope. Preliminary data indicate that myocyte myofilament function is depressed in the DHF group in terms of maximum Ca2+ saturated force development (15.8±0.9 vs. 28.1±0.9 mN/mm2) and cooperativity (Hill coefficient; 2.8±0.1 vs. 3.4±0.6), but not Ca2+ sensitivity (EC50; 2.21±0.06 vs. 2.23±0.13 μM). In addition, 2-D DIGE gel analysis revealed shifts in the phosphorylation profiles of the contractile proteins MyBP-C and Troponin I. We conclude that myofilament dysfunction underlies, in part, the decreased pump function that is seen in this guinea-pig experimental model of DHF and that this phenomenon may be caused by maladaptive contractile protein phosphorylation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
