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Upper Respiratory Tract Illnesses and Fatigue
Published in Gerald Matthews, Paula A. Desmond, Catherine Neubauer, P.A. Hancock, The Handbook of Operator Fatigue, 2017
While it has been difficult to identify the viral or immunological pathways that lead to malaise, it has been easier to show which CNS changes may be involved. The starting point for this research was a study which showed that caffeine removed many of the impairments induced by URTIs (Smith, Thomas, Perry & Whitney, 1997). At the same time studies were in progress to examine whether changes in central noradrenaline could explain lapses of attention (Smith & Nutt, 1996) and the effects of caffeine in fatigued individuals (Smith, Brice, Nash et al., 2003). This led to a study examining whether increases in the turnover of central noradrenaline (produced by the drug idazoxan) could remove the impairments seen in those with a cold (Smith, Sturgess et al., 1999). The results confirmed that changes in central noradrenaline occur when a person has an URTI and that compounds that increase noradrenaline may reverse such effects. It is, of course, quite likely that changes in other neurotransmitter systems are also involved in the malaise induced by URTIs.
Endogenous neuroprotection after perinatal hypoxia-ischaemia: the resilient developing brain
Published in Journal of the Royal Society of New Zealand, 2019
Joanne O. Davidson, Simerdeep K. Dhillon, Guido Wassink, Kelly Q. Zhou, Laura Bennet, Alistair J. Gunn
The latent phase after HI is associated with reduced brain blood flow and metabolism (Wassink et al. 2018). This active suppression is partly mediated through endogenous neuroinhibitors such as noradrenaline acting on the α2-adrenoreceptor (Lagercrantz et al. 2001). For example, α2-adrenergic receptor blockade with idazoxan in post-hypoxic preterm fetal sheep attenuated EEG suppression and worsened neuronal death (Dean et al. 2006). Moreover, low-dose but not high-dose infusion (10 or 100 µg/kg/h) with an α2-adrenoreceptor agonist, clonidine-hydrochloride, during the latent phase was associated with significant striatal and thalamic neuroprotection in preterm fetal sheep (Dean et al. 2008). In neonatal mice treated with ibotenate, a potent excitotoxin, pretreatment with clonidine or the highly selective α2-adrenoreceptor agonist, dexmedetomidine, reduced cortical and white lesions in a concentration-dependent manner, which was abolished with the α2-antagonist yohimbine (Laudenbach et al. 2002). However, it is worth noting that clonidine is less selective for α2-adrenoreceptors than dexmedetomidine and thus high-dose-associated loss of neuroprotection might have been mediated through non-specific α1-receptor stimulation.