Meeting Abstract
Recent work on capture stress in sharks suggests that elevated levels of potassium in the blood (i.e., hyperkalemia) may be correlated with higher rates of post-release mortality. In teleosts, the negative effects of hyperkalemia appear to be exacerbated when combined with other common by-products of the stress response (i.e., hypoxia, acidosis) or with unfavorable environmental conditions (i.e., elevated temperature). This study investigates how hyperkalemia (7.4mM K+), hypoxia, acidosis (0.26 pH decline) and changes in temperature may affect myocardial function in three phylogenetically disparate (but sympatric) species of elasmobranchs (sandbar shark, smooth dogfish, and clearnose skate). We measured myocardial strip contractility and force production in vitro and evaluated the ability of a β-adrenergic agonist to ameliorate negative effects of simulated capture stress. All species demonstrated declines in the net force of contraction in response to hyperkalemia but only sandbar sharks showed a significant decline in force when compared to baseline levels of potassium (5 mM K+, p = 0.001). Clearnose skates were the only species to show a decrease in net force in response to hypoxia and acidosis (p=0.026) as well as in response to high temperature (p=0.0002). This study provides the first indication that hyperkalemia may negatively affect heart function in some elasmobranchs, however, there are likely important interspecific differences that allow varying tolerances to hyperkalemia resulting from capture-related stress.
