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Cytokine activation (tumor necrosis factor - α) and clinical response induced by cardiopulmonary bypass

Systemic inflammatory response syndrome induced by cardiopulmonary bypass (CPB) is responsible for organ dysfunctions observed in some patients. The tumor necrosis factor-alpha (TNF-α) has been implicated in many clinical manifestations following cardiac operations with CPB, mainly in the vasoplegic syndrome. The purpose of this study was to verify the TNF-α release and its possible effects in patients with coronary atherosclerosis undergoing coronary artery surgery with and without CPB. Twenty patients were studied, 10 with CPB(Group I) and 10 without CPB(Group II). Serial blood samples were obtained during and until 48 hours after surgery in order to measure circulating TNF-α presence (using enzyme-linked immunosorbent assay-ELISA), leukocyte count and erythrocytes sedimentation rate. Hemodynamic parameters as blood pressure and cardiac rate, body temperature, orotracheal tubing time, postoperative bleeding and inotropic drugs requirements were also compared. Statistical significance was assumed when the p value was less than 0.05. Serum levels of TNF-α (limit detection of the assay = 10 pg/mL) were detected in 6 patients from Group I (60%). This cytokine was detected in Group II. The TNF-α peaked soon after the CPB starting and remained detectable 48 hours postoperatively. The patients of Group I had hypotension in relation to Group II (7.4 ± 1.0 vs 8.5 ± 0.67). They also required more inotropic drugs (8 vs 1), had a higher cardiac rate (114.2 ± 8.0 vs 98 ± 10 bpm), hyperthermia (37.17 ± 0.54 vs 36.67 ± 0.35ºC), more postoperative bleeding (820 ± 120 mL vs 360 ± 84 mL), a longer orotracheal tubing time (13.6 ± 2.2 vs 9.3 ± 1.4 horas) and a more pronounced leucocytosis. We concluded that CPB induces the TNF α release and leads hemodynamic and organic alterations that can be deleterious to patients. It may play a role on the pathophysiology of the alterations observed in this study and the inhibition of the TNFα could contribute to minimize these effects.

Tumor necrosis factor; Tumor necrosis factor; Myocardial revascularization; Extracorporeal circulation


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