We investigated if cyclooxygenase metabolites of arachidonic acid were involved in ischemia-reperfusion lung injury by determining if inhibition of their production attenuated the injury. Isolated rat lungs were perfused with physiologic salt solution osmotically stabilized with Ficoll until circulating blood elements were not detected in lung effluent. Ischemia was induced by stopping ventilation and perfusion for 90 min. Lung ventilation and perfusion were then resumed. Ischemia-reperfusion resulted in the production of prostacyclin and thromboxane assessed by lung effluent and tissue measurements of their respective stable metabolites, 6-keto-PGF1 alpha thromboxane B2 (TxB2). In contrast, prostaglandin F2 alpha did not increase. Ischemia-reperfusion also caused lung injury as assessed by increased lung 125I-BSA accumulation compared with nonischemic control lungs. Addition of the cyclooxygenase inhibitors, indomethacin, or flubiprofen to the lung perfusate before and after ischemia inhibited lung injury as well as the production of 6-keto-PGF1 alpha and TxB2. Addition of a thromboxane synthetase inhibitor (U 63557A) reduced lung injury as well as TxB2 formation without affecting the production of 6-keto-PGF1 alpha. The attenuation of lung injury was not explained by direct H2O2 removal by indomethacin, flubiprofen, or U 63557A because the concentrations of the inhibitors used in the isolated lung experiments did not remove exogenously added H2O2 from buffer in vitro. We conclude that cyclooxygenase metabolites of arachidonic acid are involved in ischemia-reperfusion injury to isolated rat lungs.
Patient outcome following coronary artery bypass grafting (CABG) has come under increasing governmental, social, and economic scrutiny. To insure quality patient outcome after CABG, many new policies and programs have been instituted. One of these, case management, was developed as a tool for identification and quantification of patient clinical sequences and resource utilization. This present study examines the influence of case management on length of stay and patient outcome following CABG. One hundred forty randomized, retrospectively analyzed CABG patients from 1990, prior to case management, were compared against 140 age‐and case‐matched randomly controlled CABG patients from 1994 after case management was in place. Patients' demographics were similar. The outcome data showed that intensive care unit (ICU) use and total length of stay were significantly decreased. Furthermore, resource utilization as monitored by chest X‐ray, electrocardiography, and laboratory testing were decreased as well. Finally, mortality was decreased despite an increase in risk‐adjusted acuity of the patients. There appeared to be no effect of gender or age on the benefit derived from case management. These data demonstrate that the influence of case management is beneficial for resource utilization and patient outcome following CABG and that these types of patient care policy advancements should be encouraged.
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