Role of adrenergic mechanisms in regulation of phagocytic cell functions in acute stress response

Effect of adrenaline on the functions of rat peripheral blood phagocytes under stress and upon hydrocortisone administration

“…Summarizing our data and the results obtained earlier [1][2][3][6][7][8], it is possible to conclude that the stimulatory effect of catecholamines on the oxygen-dependent bactericide activity of phagocytes is mediated by α-adrenoreceptors. The administration of hydrocortisone completely eliminated the activating effect of adrenaline (p > 0.05, data not shown), which may be due to the hormone-induced enhancement of the expression of β-adrenoreceptors, because the blockage of β-adrenoreceptors under these conditions led again to the stimulatory effect of adrenaline in vitro (the extinctions in the experiment and control were, respectively, 0.44 ± 0.05 and 0.35 ± 0.03; p < 0.05).…”

“…Earlier, we showed that acute immobilization stress and treatment with hydrocortisone enhanced the phagocytic activity of peripheral blood leukocytes [1][2][3]. It is well known that glucocorticoid hormones have a permissive effect on catecholamines accounted for by the enhancement of the expression of adrenoreceptors in target cells of different organs [4,5].…”

“…Doses and schemes of drug introduction were based on the results of previous studies [9,10]. Samples of peripheral blood were taken from tail vessels of intact animals (the combined background) 6 and 24 h after the beginning of the experiment, i.e., when the changes were especially pronounced, according to earlier data [1][2][3].…”

“…The total phagocytic activity of leukocytes was studied in comparison with formalin-treated sheep erythrocytes of sheep as described earlier [1,2]. The oxygen-dependent bactericide activity of peripheral blood leukocytes was estimated by a modified spectrophotometric test with tetrazolium nitroblue (TNB test) [3,11]. The statistical significance of differences was estimated using paired Student's t test and Wilcoxon's sign T test.…”

Chlorisondamine, a sympathetic ganglionic blocker, moderates the effects of whole-body irradiation (WBI) on early host defense to a live bacterial challenge

“…Detrimental effects of the SNS appear to result from the sympathetic inhibition of innate immunity against Gram-negative bacteria reducing the host's ability to eliminate the pathogen, including peritoneal cytokine secretion [27], adhesion and influx of neutrophils and monocytes [22,24,[28][29][30], and phagocytosis of bacteria [24,31,32]. Additionally, the sympathetic hyperactivity in the splanchnic circulation directly influences bacterial growth, and promotes translocation from the gut and spreading of Escherichia coli [22,24,25,33].…”