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Although the precise causes of PRIS are unknown, there is both clinical and experimental evidence to suggest that propofol can trigger dysfunction of the mitochondrial respiratory chain, leading to depletion of ATP production and cellular hypoxia in tissues such as the heart and muscle [ 6].
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According to some of these theories, abnormalities in one of the two neurotransmission systems could trigger dysfunctions in the other.
Probably, the excessive intake of nicotine could be associated with an up-regulation of pineal nicotinic receptor α3β4[4], and this could trigger a dysfunction of melatonin release linked to the CH's chrono-biological profile.
In addition, these multiple risk factors trigger endothelial dysfunction in a summative fashion [ 35].
She also emphasized that epithelial-fibroblast interactions trigger fibroblast dysfunction during kidney injury.
A key mechanism by which particles could trigger vascular dysfunction is by down-regulating NO synthase.
These reactions are able to trigger endothelial dysfunction and a procoagulatory state with thrombus formation and promotion of atherosclerotic lesions.
In fact, Ang II robustly stimulates the production of molecular oxygen species that trigger mitochondrial dysfunction and cellular injury (de Cavanagh et al, 2007; Wilson, 1990).
Sleep loss and fragmentation could trigger endothelial dysfunction and immune response but its remains to be demonstrated if this occurs in patients with OSA.
Hypoxia characterised by an inadequate supply of molecular oxygen, can trigger mitochondria dysfunction through ineffective functioning of respiratory complexes of ETC [ 2, 3].
Indeed, oxidation of one or two reactive myosin cysteines (Cys707 and Cys696) could be crucial and may well trigger motor dysfunction (Crowder & Cooke, 1984).
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