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These results suggest that DiOHF may have therapeutic potential in the treatment of cardiovascular diseases. ""What is the central question of this study? This study tested the hypothesis that hyperthermia attenuates the increase in cerebral perfusion during cognitive activation. Mean middle Nutlin3 cerebral artery blood velocity (MCAVmean) served as an index of cerebral perfusion, while the nBack test (a test of working memory) was the cognitive task. Hyperthermia was characterized by elevations (P RO4929097 molecular weight This cascade commences with increases in neural and metabolic activity that are ultimately accommodated by increases in cerebral blood flow (Girouard & Iadecola, 2006; Rosengarten et al. 2012). This ��coupling�� between cognitive activation and cerebral perfusion enables the cognitive task to be suitably accomplished. Interestingly, however, the capacity to increase cerebral perfusion during cognitive activation is modulated by changes in baseline (i.e. before cognitive activation) blood flow. For instance, chronic suppression of resting cerebral perfusion (by 10�C20%) is accompanied by an impaired increase in cerebral perfusion during cognitive activation in healthy older individuals (Sorond et al. 2008) and in patients with essential hypotension (Duschek & Schandry, 2004). Acute reductions in brain INPP5D blood flow, induced via hypocapnia, likewise attenuate the increase in perfusion during a subsequent cognitive task (Szabo et al. 2011). On the contrary, however, acute elevations in resting perfusion, whether induced via hypercapnia (Rosengarten et al. 2003), acetazolamide (Yonai et al. 2010) or exercise (Willie et al. 2011b), have little impact on the increase in cerebral perfusion in response to such tasks. Thus, it is clear that acute or chronic reductions in cerebral perfusion deleteriously affect the capacity to increase perfusion during cognitive activation. Hyperthermia, i.e. elevations in both mean skin and internal temperatures, reduces resting cerebral perfusion by 10�C30% (Wilson et al. 2006; Brothers et al. 2009; Nelson et al. 2011). This decrease is, at least partly, a result of hypocapnia occurring concomitant to hyperthermia-induced hyperventilation (Fujii et al. 2008; Brothers et al. 2009; Ross et al. 2012).