| Summary: | Grizzly bears, Ursus arctos horribilis , tolerate extended periods of low heart rate during hibernation without developing congestive heart failure or chamber dilation. We evaluated myocardial response to hibernation‐induced bradycardia by measuring myosin heavy‐chain (MyHC) isoform expression in the left atria and left ventricles of active and hibernating bears, as well as relative mRNA expression of a set of genes important to muscle plasticity. We supplemented these data with echocardiographic measurements of systolic and diastolic function in unanesthetized bears. Relative MyHC‐α protein expression increased by 10% in the atria during hibernation, uncharacteristic of bradycardia in non‐hibernators. The left ventricle expressed 100% MyHC‐β protein in both groups. Insulin‐like growth factor (IGF‐I) mRNA expression was reduced by ~50% in both chambers during hibernation, consistent with observed ventricular atrophy. A 50% decrease in atrial creatine kinase mRNA expression occurred in hibernators. Taken in context with hemodynamic assessment of increased atrial afterload and ventricular stiffness, these data suggest a potential downregulation of atrial chamber function during hibernation to prevent fatigue and dilation due to excessive work against an optimally filled ventricle. Supported by NIH MBRS SCORE 2 S06 GM063119 , the Autzen Foundation and the WSU Bear Center.
|
|---|