Nitric oxide increases myocardial efficiency in the hypoxia-tolerant turtle Trachemys scripta

Abstract

Nitric oxide (NO) may influence cardiac mechanical performance relative to O2 consumption by depressing respiration rate and by affecting the excitation-contraction coupling. Such effects of NO should be particularly important during hypoxia in species such as the hypoxia-tolerant turtle Trachemys scripta. In heart ventricle preparations from this species, the ratio of twitch force to O2 consumption increased by approximately 15% during full oxygenation and by approximately 60% during hypoxia in the presence of added L-arginine [the substrate for nitric oxide synthase (NOS)]. This effect was primarily due to a decrease in O2 consumption and may represent an increase in the twitch force obtained per ATP and/or in the ATP obtained per O2. Lactate production during hypoxia did not differ between preparations treated with either L-arginine or asymmetric dimethylarginine (ADMA), an inhibitor of NOS, suggesting that NO does not elicit a compensatory increase in anaerobic metabolism. ADMA did not reverse the effects of L-arginine on O2 consumption significantly, although pre-treatment with ADMA abolished the effect of L-arginine, consistent with the competitive binding of L-arginine and ADMA to NOS. Histochemical studies using the fluorescent probe 4,5-diaminofluorescein diacetate (DAF-2 DA) revealed NO production in the presence of added L-arginine. In conclusion, NO may augment heart contractility obtained per O2 by deceasing O2 consumption without affecting either lactate production or developed force. This effect was particularly pronounced under O2 deficiency and may therefore contribute towards preserving cardiac function and to the overall excellent hypoxic tolerance of the turtle.