engleski

Respiratory plasticity following acute intermittent hypoxic or hypercapnic stimulus – maintenance of the breathing stability

Plasticity is a key property of neural systems, manifested as a persistent change in the neural control system based on a prior experience. It includes the respiratory control system, and promotes effective homeostatic regulation. Acute intermittent hypoxia can evoke long-lasting increase of phrenic nerve activity known as phrenic long-term facilitation (pLTF). On the other hand, it has been shown that acute intermittent hypercapnia can evoke long-lasting decrease of phrenic nerve activity, known as phrenic long-term depression (pLTD) in anesthetized rats. This study was performed to investigate the effects of acute intermittent hypoxia and acute intermittent hypercapnia, as well as combined acute intermittent hypoxic and hypercapnic stimulus on phrenic nerve activity. Adult male urethane-anesthetized, vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats were exposed to: acute intermittent hypoxia (AIH), acute intermittent hypercapnia (AIHc), or combined intermittent hypercapnia and hypoxia (AIHcH). Peak phrenic nerve activity (pPNA) and burst frequency were analyzed during baseline (T0), hypercapnia or hypoxia exposures at 15, 30, and 60 minutes (T60) after the end of the stimulus. Exposure to AIH elicited increase of pPNA at T60 to 241.0±28.2% compared to baseline (P=0.015), i.e., phrenic long-term facilitation was induced. Exposure to AIHc elicited decrease of phrenic nerve frequency from 44.25±4.06 at T0 to 35.29±5.21 at T60 (P=0.038), i.e., frequency phrenic long-term depression was induced. Exposure to AIHcH protocol failed to induce long-term plasticity of the phrenic nerve. Phrenic nerve frequency was 40.5±2.2 breaths/min at T0 and 38.14±1.82 breaths/min at T60 (P>0.05) and pPNA was 172.6±38.4%, (P>0.05) 60 min after the last combined stimulus compared to baseline values. Thus, we conclude that combined intermittent hypercapnic and hypoxic stimulus might be responsible for maintenance of breathing stability.

respiratory plasticity; hypoxia; hypercapnia; breathing stability

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