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Contractile activity and calcium cycling in ventricular myocytes exposed to NaCI hyperosmotic solution

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Author(s):
Rafael de Almeida Ricardo
Total Authors: 1
Document type: Master's Dissertation
Press: Campinas, SP.
Institution: Universidade Estadual de Campinas (UNICAMP). Faculdade de Engenharia Elétrica e de Computação
Defense date:
Examining board members:
José Wilson Magalhães Bassani; Eduardo Tavares Costa; Antonio Augusto Fasolo Quevedo; Idagene Aparecida Cestari
Advisor: Rosana Almada Bassani; José Wilson Magalhães Bassani
Abstract

Intravenous injection of hyperosmolar NaCI solution has been used as the sole treatment for hemorrhagic shock, but its effects on heart muscle are not completely elucidated. In this work, we developed instrumentation for cell shortening measurement and investigated the direct effects of hyperosmolar NaCI solution on contractile activity and cytosolic Ca2+ concentration ([Ca2+]i) in isolated rat ventricular myocyte. Cell shortening (LlEC) and Ca2+ transient amplitude (?[Ca2+]j, measured with indo-1) were recorded in myocytes stimulated at 0.5 Hz before and after increasing extracellular osmolarity in 85 mOsm/l by sucrose (HiperSac) or NaCI (HiperNac) addition to the perfusate. Sarcoplasmatic reticulum (RS) Ca2+ load and fractional release were estimated. Computational simulation (LabHeart, v. 4.9.5) of Ca2+ transient and Na+-Ca2+ exchange voltage-current relationship was performed. HiperNac perfusion caused transient decrease of ?[Ca2+]i and LlEC, followed bya gradual recovery. HiperSac perfusion caused a monophasic decrease of LlEC, but did not change ?[Ca2+]i. Increased fractional RS Ca2+ release (pc:; 0.05) in the presence of HiperNac may have contributed to the delayed recovery of ?[Ca2+]i. Hyperosmolarity per se prolonged cell relaxation, but did not affect [Ca2+]i decline kinetics, possibly by increased intracellular viscosity. Slower [Ca2+]i decay during caffeine-induced transients indicates decreased NCX-mediated Ca2+ efflux transport following progressive intracellular [Na+] accumulation due to extracellular hyperosmolarity. Computational simulation results agree with this hypothesis (AU)