2001
DOI: 10.1097/00003246-200111000-00015
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Influence of aminosteroid and glucocorticoid treatment on inflammation and immune function during cardiopulmonary bypass

Abstract: These data confirm that, during cardiopulmonary bypass, pro- and anti-inflammatory systems are activated at the same time, whereas monocyte-based immune functions are depressed. Treatment with MP abrogates proinflammatory mediators and induces a shift toward anti-inflammation at the cost of further functional monocyte deficits, whereas treatment with TM apparently has neither anti-inflammatory nor immunosuppressive actions in this setting.

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Cited by 45 publications
(28 citation statements)
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“…Third, medication effects on circulating CRP and other inflammatory markers should also be considered. Systemic corticosteroids, for instance, may decrease CRP levels 32 while slightly increasing circulating levels of leukocytes and platelets. 33 Exclusion of individuals who were taking oral corticosteroids made no difference to the overall findings, which suggests that this medication was not an important confounder in the analysis.…”
Section: Discussionmentioning
confidence: 99%
“…Third, medication effects on circulating CRP and other inflammatory markers should also be considered. Systemic corticosteroids, for instance, may decrease CRP levels 32 while slightly increasing circulating levels of leukocytes and platelets. 33 Exclusion of individuals who were taking oral corticosteroids made no difference to the overall findings, which suggests that this medication was not an important confounder in the analysis.…”
Section: Discussionmentioning
confidence: 99%
“…They suggest that glucocorticoid action may represent another mechanism for the development of innate immune dysfunction. Similarly, Volk et al demonstrated that the administration of methylprednisolone in the setting of cardiopulmonary bypass resulted in an exacerbation of innate immunosuppression over that which was seen with byass alone [54].…”
Section: Mechanisms Of Immunoparalysismentioning
confidence: 99%
“…The clinical manifestation of SIRS following CPB is mediated via cell-derived cytokines that target end-organ receptors. After CPB, elevated serum levels of the pro-inflammatory cytokines, tumor necrosis factor (TNF)-a, interleukin (IL)-6 and IL-8, as well as the anti-inflammatory cytokine IL-10 have been found 2,3 . The potent vasodilator nitric oxide (NO) has also been implicated in SIRS pathophysiology.…”
Section: Introductionmentioning
confidence: 99%