Key result
NOS inhibition increases O2 consumption and decreases efficiency in hypoxic trout and goldfish myocardium.
Why the study?
The roles of nitric oxide synthase activity, nitrite, and myoglobin in regulating myocardial function during hypoxia in trout and goldfish were unclear.
Nitrite reduces oxygen consumption and increases myocardial efficiency during hypoxia in hypoxia-intolerant trout but not in hypoxia-tolerant goldfish, correlating with differences in myoglobin oxygen affinity.
Hypothesis-generating for NO-mediated myocardial efficiency in hypoxia; leaves open mammalian relevance and precludes clinical translation.
The roles of nitric oxide synthase activity (NOS), nitrite and myoglobin (Mb) in the regulation of myocardial function during hypoxia were examined in trout and goldfish, a hypoxia-intolerant and hypoxia-tolerant species, respectively. We measured the effect of NOS inhibition, adrenaline and nitrite on the O(2) consumption rate and isometric twitch force development in electrically paced ventricular preparations during hypoxia, and measured O(2) affinity and nitrite reductase activity of the purified heart Mbs of both species. Upon hypoxia (9% O(2)), O(2) consumption and developed force decreased in both trout and goldfish myocardium, with trout showing a significant increase in the O(2) utilization efficiency, i.e. the ratio of twitch force to O(2) consumption, suggesting an increased anaerobic metabolism. NOS inhibition enhanced myocardial O(2) consumption and decreased efficiency, indicating that mitochondrial respiration is under a tone of NOS-produced NO. When trout myocardial twitch force and O(2) consumption are enhanced by adrenaline, this NO tone disappears. Consistent with its conversion to NO, nitrite reduced O(2) consumption and increased myocardial efficiency in trout but not in goldfish. Such a difference correlates with the lower O(2) affinity measured for trout Mb that would increase the fraction of deoxygenated heme available to catalyze the reduction of nitrite to NO. Whereas low-affinity trout Mb would favor O(2) diffusion within cardiomyocytes at high in vivo O(2) tensions, goldfish Mb having higher O(2) affinity and higher nitrite reductase activity appears better suited to facilitate O(2) diffusion and nitrite reduction in the heart during severe hypoxia, a condition particularly well tolerated by this species.
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Pedersen et al. (2010) studied Hypoxia tolerance in trout and goldfish. NOS inhibition, adrenaline, and nitrite was evaluated on O(2) consumption rate and isometric twitch force development during hypoxia. In trout and goldfish myocardium, NOS inhibition enhanced myocardial O2 consumption and decreased efficiency during hypoxia, indicating mitochondrial respiration is under a tone of NOS-produced NO.
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