Abstract

Pathophysiological hypoxia induces changes in the structure, function, and gene expression of the developing heart. Recent work in reptiles exposed to hypoxia during development revealed cardiac hypertrophy and a reduction in both resting heart rate and blood pressure. The purpose of the current study was to further investigate these responses at the level of the cardiac myocyte. America alligators (Alligator mississippiensis) were reared in normoxic and hypoxic conditions until 90% development. The heart was quickly excised and single ventricular myocytes were liberated via a modified langendorf perfusion using digestive enzymes. Ventricular myocytes were long and thin with clear sarcomeric striations. Sarcomeric shortening and calcium transients were simultaneously measured as contraction frequency was increased from 0.5 to 2.0 Hz. Data are presented as means ± SEM from n=7–15 cells under each condition from N=20 animals. There were no differences between normoxic and hypoxic resting sarcomere length (SL) (1.78±0.04 and 1.77±0.05 um, respectively) and resting SL decreased (~3%) in both treatments with increased frequency. SL shortening was significantly greater in the hypoxic (9.9±1.4%) than the normoxic (4.6±1.4%) myocytes at 0.5 Hz but the differences were reduced as frequency increased. Calcium transient amplitude data mirrored that of sarcomeric shortening.

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