Changes in ultrastructural calcium distribution in goat atria during atrial fibrillation

It has been suggested that Ca2+ content of atrial cardiomyocytes is increas ed at the onset of atrial fibrillation (AF). Whether this phenomenon is tra nsient is currently unknown, Therefore, in this study the time-related chan ges in Ca2+ location in atrial myocytes from goats with chronic AF have bee n investigated. The distribution of calcium was assessed with the electron microscope using the cytochemical phosphate-pyroantimonate and oxalate-pyro antimonate methods in atrial biopsies from goats in sinus rhythm and goats with 1-16 weeks of burst-pacing-induced AF. In atrial myocytes from control goats in sinus rhythm, a normal Ca2+ distribution was observed, with regul ar deposits along the sarcolemma (an average of 3.4 deposits per mu m at a regular distance), The number of sarcolemma-bound Ca2+ deposits substantial ly increased after 1 and 2 weeks of atrial fibrillation. After this period the amount of Ca2+ precipitate decreased at 4 and 8 weeks, and became below control level at 16 weeks, A similar time-related redistribution of Ca2+ o ccurred in mitochondria, Whereas mitochondria From control goats displayed very few Ca2+ deposits (average 4.0 deposits per mu m(2)), their number mar kedly increased after 1 and 2 weeks of atrial fibrillation, which indicates cellular Ca2+ overload, From 4 weeks, Ca2+ deposits reached control levels and were below control level after 16 weeks of atrial fibrillation (2.5 de posits per mu m(2)). Our findings are consistent with the previously observ ed Ca2+ overload early after the onset of atrial fibrillation. The present study shows that this overload persists for at least 2 weeks, after which t he cardiomyocytes apparently adapt to a new Ca(2+)homeostasis, thereby avoi ding Ca(2+)overload. This protection against Ca(2+)overload co-occurs with dedifferentiation like cellular remodeling. (C) 2000 Academic Press.