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Systemic consequences of oxidative stress following aortic surgery correlate with the degree of antioxidant defenses. | LitMetric

AI Article Synopsis

  • The study aimed to explore the relationship between preoperative antioxidant levels, measured by total antioxidant capacity (TAC), and the severity of postoperative inflammation, indicated by pulmonary injury after aortic surgery.
  • Twenty-four patients had their TAC measured before and after surgery, and they also underwent chest imaging and blood gas tests to assess pulmonary function and injury.
  • Results showed that lower TAC levels were linked to greater pulmonary dysfunction and edema after surgery, suggesting that antioxidant supplementation before surgery might help reduce inflammatory responses related to ischemia and reperfusion injury.

Article Abstract

The purpose of this study was to correlate the preoperative level of antioxidant defenses, measured by the plasma total antioxidant capacity (TAC), to the degree of postoperative systemic inflammatory response, measured by the severity of pulmonary injury following elective aortic surgery. Twenty-four patients had TAC measured preoperatively and 24 hr postoperatively. Chest radiography and arterial blood gases were obtained preoperatively and serially during the first 24 hr after surgery. Using objective radiologic criteria and blood gas analysis, the degree of pulmonary edema and pulmonary dysfunction were quantified. All patients showed evidence of pulmonary dysfunction in the first 24 hr following surgery. Fifteen of the 24 patients showed radiographic evidence of noncardiogenic pulmonary edema in the immediate postoperative period. In this group, the TAC was lower than in those without pulmonary edema immediately following surgery (p = 0.03). Preoperative TAC was associated with the degree of pulmonary edema in the postoperative period (r = -0.372, p = 0.067). These results suggest that preoperative antioxidant supplementation may favorably impact the severity of systemic inflammatory response following ischemia and reperfusion injury.

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Source
http://dx.doi.org/10.1007/s100169910006DOI Listing

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