Background and Purpose Iron catalyzes the formation of damaging reactive species during cerebral reperfusion. Brain iron concentration is highest at birth, so the brain of the asphyxiated newborn may be at increased risk of iron-dependent injury. We investigated whether the ferric iron chelator deferoxamine could reduce hypoxic-ischemic brain injury in neonatal rats. Because deferoxamine has concentrationdependent activities other than iron chelation, we measured brain deferoxamine levels and calculated deferoxamine pharmacokinetic parameters.Methods We produced hypoxic-ischemic injury to the right cerebral hemisphere of 7-day-old rats by right common carotid artery ligation followed by 2.25 hours of hypoxia in 8% oxygen. At 5 minutes of recovery from hypoxia the rats received 100 mg/kg deferoxamine mesylate or saline subcutaneously. Rats (saline, n=33; deferoxamine, n=38) were killed at 42 hours of recovery to assess early acute edema by measurement of hemispheric water content. Other rats (saline, n=31; deferox-

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This case describes a 75-year-old man who developed pulmonary fibrosis. The onset of symptoms occurred three months after starting mexiletine. A computerized tomogram obtained eight months after initiating mexiletine documented findings consistent with chronic pulmonary fibrosis. The patient died from intractable respiratory difficulties 13 months after beginning mexiletine therapy. To date, there have been three cases of pulmonary fibrosis in patients receiving mexiletine spontaneously reported to the manufacturer.