Impairment of splanchnic and peripheral tissue perfusion during cardiopulmonary bypass (CPB) may be responsible for endotoxin-mediated systemic inflammation and acute phase responses. We examined the effects of dopexamine on hemodynamic parameters, creatinine clearance, systemic and splanchnic oxygenation, gastric mucosal pH (pHi), and mixed and hepatic venous plasma levels of endotoxin, interleukin-6 (IL-6), serum amyloid A (SAA), and C-reactive protein (CRP) in 44 patients scheduled for coronary artery bypass grafting. Patients were randomized to receive continuous infusions of 0.5, 1.0, or 2 micrograms.kg-1.min-1 dopexamine (n = 10 per group) or placebo (n = 14) prior to surgery, intraoperatively, and postoperatively. Dopexamine infusion increased systemic oxygen delivery (P < or = 0.01). Hepatic venous oxygen saturation did not change, and pHi decreased during and after CPB in all patients (P < or = 0.01). Postoperative increases in IL-6 were smallest in patients who received 2.0 micrograms.kg-1.min-1 dopexamine (P < or = 0.02). SAA and CRP increases during the postoperative period were less pronounced with dopexamine throughout the study. Creatinine clearance was elevated in all dopexamine groups (P < or = 0.025). This elevation was higher with lower dopexamine doses (P < or = 0.025). We conclude that dopexamine improves creatinine clearance and reduces systemic inflammation without affecting splanchnic oxygenation.
Eicosanoids partly develop from the metabolism of arachidonic acid through the cyclooxygenase or the lipoxygenase pathway. Lipoxygenase products are the leukotrienes (LTA4, LTB4, LTC4, LTD4, LTE4) and the 5-hydroxyeicosatetraenoic acid (5-HETE). Cyclooxygenase products are the prostanoids (prostaglandins [PG] D2, E2, F2, I2 and thromboxane A2). The other part of the eicosanoids develops from the metabolism of two other fatty acids over the same pathways; 8,11,14-eicosatrienoic acid leads to the prostaglandins D1, E1, F1, I1 and the leukotrienes A3, B3, C3, D3, E3. From 5,8,11,14,17-eicosapentaenoic acid result the prostaglandins D3, E3, F3, I3 and the leukotrienes A5, B5, C5, D5, E5. The pathophysiological changes in ARDS are mainly due to an imbalance of opposing effects of mediators. In this regard eicosanoids play an important role which has not yet been clearly determined. Bronchoconstriction and pulmonary hypertension are increased by thromboxane A2 and leukotrienes, whereas they are reduced by PGI2. Pulmonary edema is enlarged by leukotriene, especially, LTB4, whereas PGI2 has a protective effect. The aggregation of platelets is mediated through thromboxane A2, PGF2 and LTB4; PGE1 and PGI2 counteract these reactions. LTB4, in addition to 5-HETE, leads to the activation of inflammatory cells. Drug induced eicosanoid imbalances can be used for therapeutic interventions.
51 patients, who underwent direct laryngoscopy under general anesthesia, received either 250 mg Methyprednisolone or 10 ml NaCl 0.9% intraveneously in a prospective, double blind study. 4-5 hours after microlaryngoscopy they were examined in regard to edema and size of redness of certain anatomical structures of the larynx and hypopharynx. Findings were compared to the results which had been found on the eve of the operation. There was no statistically significant difference between the two groups. However, in the NaCl-Group there was a direct correlation between the edema formation and inflammatory reaction on one hand and the duration of surgery on the other hand. Routine prescription of Cortisone before mikrolaryngoscopy is not necessary, but is recommended, when the operation is expected to take a long time, around more than 30 min.
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