Figure 2 Plasma adrenaline levels during hypoxic, normoxic, and hyperoxic endotoxeimia.
Fig. 2 Suggested salivary markers for SNS activity and their relationship with plasma adrenaline after exhaustive exercise.
Maximum plasma concentration.
Fig. 1 Plasma adrenaline, salivary α-amylase activity, chromogranin A and α-amylase secretion rate response to exhaustive exercise.
Hypoxia resulted in a profound increase of plasma adrenaline levels, which were not influenced by hyperoxia (Figure 2).Furthermore, inverse correlations between adrenaline and the pro-inflammatory cytokines IL-6 and IL-8 (r=-0.48, p=0.007 and r=-0.47, p=0.004, respectively) and a positive correlation between adrenaline and IL-10 (r=0.52, p=0.004) were found.
Correlations between plasma adrenaline concentration and salivary parameter post exercise were significant for sAA (r = 0.60, P = 0.01), but not for sCgA (r = 0.06, P = 0.79, Fig. 2).
Plasma adrenaline is originated from adrenal medulla, while plasma noradrenaline reflects the release from sympathetic nerves in addition to the secretion from adrenal medulla.
Saliva and blood samples were taken pre, post and 30 min post exercise and analysed for sAA, sCgA and plasma adrenaline concentration, respectively.
Time to maximum plasma concentration.
Intracerebroventricularly administered furegrelate [1.8 μmol (500 μg)/animal] (an inhibitor of thromboxane A2 synthase) abolished the elevations of both noradrenaline and adrenaline induced by vasopressin, while the reagent only attenuated the elevation of plasma adrenaline evoked by CRH.
