Ischemia-reperfusion lung injury limits lung transplantation. Neutrophil activation and/or xanthine oxidase-mediated purine degradation may cause toxic oxygen metabolite production and lung injury. We investigated whether circulating blood elements are involved in the pathogenesis of ischemia-reperfusion lung injury. Isolated rat lungs were perfused with physiological salt solution (PSS) stabilized with Ficoll until circulating blood elements were not detected in the lung effluent. Lungs were then rendered ischemic by stopping ventilation and perfusion for 45 min at room temperature. Lung injury occurred and was quantitated by the accumulation of 125I-bovine serum albumin into lung parenchyma and alveolar lavage fluid during reperfusion. Lung injury occurred, in the absence of circulating blood elements, when ischemic lungs were reperfused with PSS-Ficoll solution alone. Reperfusion with whole blood or PSS-Ficoll supplemented with human or rat neutrophils did not increase lung injury. Furthermore, during lung ischemia, the presence of neutrophils did not enhance injury. Experiments using PSS-albumin perfusate and quantitating lung injury by permeability-surface area product yielded similar results. Microvascular pressures were not different and could not account for the results. Toxic O2 metabolites were involved in the injury because addition of erythrocytes or catalase to the perfusate attenuated the injury. Thus reperfusion after lung ischemia causes injury that is dependent on a nonneutrophil source of toxic O2 metabolites.

Preoperative psychological disturbances during the waiting weeks before cardiac surgery may influence the plasma levels of IL-6 immediately prior to the procedure. The clinical implications of these findings remain to be determined.

Patients with sustained ventricular tachycardia or ventricular fibrillation who receive an AICD that delivers only high-energy shock therapy are at moderate risk for experiencing loss of consciousness during AICD shocks. No clinical variables were found to be predictors of syncope. Therefore, driving and other activities that require patients to be extra vigilant should not be assumed to be safe after implantation of an AICD that delivers only high-energy shock.

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Seventy-four patients (16 women, 58 men, age 58 +/- 11 years, mean +/- standard deviation) who received an implantable cardioverter defibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 +/- 5 months in both groups) and the frequency of ICD shocks (0.3 +/- 0.2/month in group A vs 0.4 +/- 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P less than 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge.(ABSTRACT TRUNCATED AT 250 WORDS)