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Reversal of Ischemia/Reperfusion Lung Injury by Inhibition of Polymorphonuclear Leukocytes*

Joseph W. Barnard, PhD; K. Shappell, BA; M. Yoshitake, MS
Author and Funding Information

*From Otsuka America Pharmaceuticals Inc (Dr. Barnard and Messrs. Shappell and Yoshitake), Rockville, MD; and Rush Medical College (Dr. Barnard), Chicago, IL.

Correspondence to: Joseph W. Barnard, PhD, Maryland Research Laboratories, 9900 Medical Center Dr, Rockville, MD 20850



Chest. 1999;116(suppl_1):33S-34S. doi:10.1378/chest.116.suppl_1.33S-a
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Because polymorphonuclear leukocytes (PMNs) have been shown to mediate ischemia/reperfusion lung injury, we hypothesized that their inhibition by the agent OPC-6535, which blocks PMN adherence and superoxide production, would reverse ischemia/reperfusion injury in the isolated rat lung.

Lungs were isolated from rats using our established techniques, perfused with Earl’s balanced salt solution at 0.03 mL/g of body weight, and ventilated with air/5% CO2 except during ischemia (45 min) when flow was also stopped. Permeability was assessed by the filtration coefficient (Kf,c) and increased after 30 min of reperfusion (from 0.47 ± 0.08 to 1.27 ± 0.29 mL/min/cm H2O/100 g [p < 0.05]) and 90 min of reperfusion (1.77 ± 0.44 [p < 0.05] [n = 8]) resulting in severe edema (final wet weight, 4.24 ± 1.07 g [p < 0.05]). Treatment with 10 μM isoproterenol after 30 min of reperfusion reversed the increase (30 min of reperfusion increased Kf,c from 0.22 ± 0.02 to 0.41 ± 0.14), which was reversed by isoproterenol (back to 0.21 ± 0.06 at 90 min of reperfusion; final wet weight, 2.55 ± 1.27 g) as we have previously shown.


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