Efeitos da acidose lática nos processos da contratilidade cardíaca do teleósteo de água doce matrinxã, Brycon cephalus
Lopes, André Guelli
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In the majority of the fish species already studied, cardiac force contraction is sensitive to small changes in the extracellular pH. During intense swimming, the increased lactic acid (LA) levels significantly reduce the Fc, impairing the myocardial contractile performance. The freshwater teleost matrinxã, Brycon cephalus, is a reofilic species presenting a high capacity for swimming against rapids during migration and feeding, constituting an interesting model for studies of exercise and growth. Additionally, a considerable amount of contractile Ca2+ in cardiac myocytes of this species derives from intracellular stores (sarcoplasmic reticulum - SR). The goal of this study was to evaluate the effects of the extracellular lactic acidosis on Fc and mechanisms of excitation-contraction coupling. Ventricle strips were mounted for isometric force recordings during 40 minutes to evaluate: (a) the effects of 22 mM of lactic acid; (b) the combined effects of 22 mM of lactic acid and 10 μM of ryanodine (a specific SR calcium channels blocker); (b) the combined effects of 22 mM of lactic acid and 1mM of amiloride (a Na+/H+ exchanger - NHE blocker); (c) the effects of the replacement of NaCl by LiCl in the physiological solution (to test the role of the Na+/Ca2+ exchanger - NCX). Acidosis produced a biphasic inotropic curve: a significant Fc reduction (~80%) after 5 min of exposure and a complete Fc recovery after 20 min. b. This initial Fc reduction seems to be caused by a decreased myofibrilar Ca2+ sensitivity since the NCX blockade by lithium did not alter this response. Ryanodine blocked the Fc recovery during lactic acidosis (58.3%), evidencing the role of SR in increasing intracellular Ca2+ and, therefore, in the Fc recovery during acidosis. Additionally, the NHE is also crucial for Fc recovery during acidosis since it was abolished by amiloride. Taken together, the results indicate that matrinxã is an acidosis-tolerant species, presenting efficient mechanisms to counteract the negative inotropic effects of lactic acidosis.