Table 1.
Stimulus | Interventions | In vitro | In vivo |
---|---|---|---|
Continuous elevation in flow |
Exercise Water immersion Heat therapy |
↑ eNOS ↓ Inflammatory cytokines ↑ Antioxidants ↑ Anti-inflammatory molecules |
↑ Basal blood flow ↑ Maximal flow-mediated dilation ↑ Cerebrovascular responsiveness |
Intermittent elevation in flow |
Exercise Heat therapy |
??? | ??? |
Oscillatory flow | Pneumatic compression |
Prolonged exposure: ↑ Inflammatory cytokines ↑ Adhesion molecules ↑ Vasoconstriction factors |
↑ Basal blood flow Improved functional outcomes |
Loss of flow | Ischemic preconditioning |
Prolonged exposure: ↑ Inflammatory cytokines ↑ Cellular dysfunction ↑ Cell death |
↑ Endothelium-dependent blood flow ↑ Maximal flow-mediated dilation |
Hypoxia |
Ischemic preconditioning Hypoxia |
↑ Inflammatory cytokines ↑ Oxidative stress ↑ Angiogenic factors ↑ eNOS |
??? |
Increased temperature (Febrile/ ~ 39 °C) | Heat therapy |
↓ IL-6 response to TNFa ↓ Future hyperthermic damage HSP protection against inflammation |
↑ Basal blood flow ↑ Maximal flow-mediated dilation ↑ Cerebrovascular conductance |
References for the stated responses can be found in Sects. “Ischemic preconditioning”, “Flow-independent adaptation in vivo” and 3.3
eNOS endothelial nitric oxide synthase, IL interleukin, VEGF vascular endothelial growth factor, heat shock protein 72 HSP72, tumor necrosis factor alpha TNFα, ↑ increase, ↓ decrease,??? response currently unknown