Key result
Acute hypobaric hypoxia in 22-month-old rats caused mild uncoupling and increased NO production in brain mitochondria, while heart mitochondria showed decreased NO production (53%) and increased cytochrome oxidase activity (39%).
Why the study?
Rat brain and heart display different endogenous protective responses against hypobaric hypoxia in an age-dependent way, motivating an evaluation of acute hypobaric hypoxia on mitochondrial function and nitric oxide in old rats.
In senile rats, acute hypobaric hypoxia induces a self-protective mechanism in heart mitochondria characterized by decreased NO and ROS production alongside increased cytochrome oxidase activity, contrasting with brain mitochondrial responses.
Hypothesis-generating in aged rat models; leaves open whether organ-specific mitochondrial adaptations to hypoxia apply in humans.
Rat brain and heart display different endogenous protective responses against hypobaric hypoxia in an age-dependent way. The aim of the present work was to evaluate the effects of acute hypobaric hypoxia (HH, 48 h) on brain and heart mitochondrial function as well as the participation of nitric oxide (NO) in old rats (22-month old). Cortical mitochondria from rats exposed to HH decreased respiratory rates (37 %, state 3) and membrane potential (20 %), but NO and H2O2 production increased by 48 %, and 23 %, respectively. Hippocampal mitochondria preserved O2 consumption and H2O2 production, decreased membrane potential (18 %) and increased NO production (46 %). By contrast, HH decreased NO production (53 %) in mitochondria from left heart ventricles associated with increased cytochrome oxidase activity (39 %) and decreased NADPH oxidase activity (31 %). Also, a tendency to increase complex I-III (24 %) and complex II-III (65 %) activity was observed. In conclusion, after HH hippocampal and cortical mitochondria showed mild uncoupling and increased NO production. However, only the hippocampus preserved O2 consumption and H2O2 levels. Interestingly, heart mitochondria showed a decreased ROS production through increased cytochrome oxidase activity associated with a decrease in NO production. This may be interpreted as a self-protective mechanism against hypoxia.
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Padula et al. (2023) studied Acute hypobaric hypoxia. Acute hypobaric hypoxia was evaluated on Mitochondrial function (respiratory rates, membrane potential, NO and H2O2 production) in brain and heart. Acute hypobaric hypoxia in 22-month-old rats caused mild uncoupling and increased NO production in brain mitochondria, while heart mitochondria showed decreased NO production (53%) and increased cytochrome oxidase activity (39%).
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