Early biochemical indicators of the obliterative bronchiolitis syndrome in lung transplantation

The diagnosis of the obliterative bronchiolitis syndrome in lung transplantation is presently best established by evaluation of postoperative lung function tests. Unfortunately the decline in lung function occurs only when obliteration has progressed significantly and is therefore not an early predictive indicator. To distinguish patients at increased risk for the development of obliterative bronchiolitis, we regularly assessed the chemiluminescence response of polymorphonuclear leukocytes, opsonic capacity, and plasma elastase/beta-N-acetylglucosaminidase in 52 outpatients (25 women and 27 men; mean age 45 +/- 12 years) who underwent transplantation between January 1991 and January 1992. Recent onset bronchiolitis within the described observation period occurred in 16 patients (group obliterative bronchiolitis). A matched cohort of 16 patients was formed according to type of procedure, age and follow-up (control) from the remaining 36 patients. Data obtained from a period 6 months before clinical onset of the syndrome showed a significant drop of the opsonic capacity (group obliterative bronchiolitis = 87% +/- 7%; control = 100% +/- 9%; p < 0.023) and rise of the N-acetyl-D-glucosaminidase (group obliterative bronchiolitis = 7.5 +/- 2 U/L; control = 5.8 +/- 1.8 U/L; p < 0.04). No correlation was found between the number of infectious events or rejection episodes and the incidence of obliterative bronchiolitis. According to these results, it can be concluded that a decrease in the plasma opsonic capacity and a rise in beta-N-acetylglucosaminidase may be early markers before clinical onset of obliterative bronchiolitis. The nonspecific immune system may therefore play an important role in the development of obliterative bronchiolitis

Warm or cold ischemia in animal models of lung ischemia-reperfusion injury: Is there a difference?

Objective: Experiments were designed to compare large animal models for lung ischemia-reperfusion injury using either 90 minutes' warm or 24 hours' cold ischemia. Methods: In 6 pigs, the left lung was perfused in situ with cold LPD solution. Reperfusion was started after 90 min of warm ischemia. The left lung of 6 donor pigs was perfused with LPD solution and the lung transplanted after 24 hours of cold storage into 6 recipient pigs. In both groups the right pulmonary artery and main bronchus were clamped after reperfusion of the left lung. Bronchoalveolar lavage (BAL) was obtained before ischemia and after 2 h of reperfusion. Hemodynamic and respiratory parameters were monitored. Surfactant activity was determined from the BAL in a pulsating bubble surfactometer. Results: Moderate lung injury was evident after reperfusion, but without any significant differences between groups. Surfactant composition and function were mildly impaired after reperfusion in both groups. Conclusions: Our results suggest that short periods of warm ischemia might be accepted as an accelerated model for ischemia-reperfusion injury of the lung after cold storage