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Protective effect of lung inflation in reperfusion-induced lung microvascular injury
H B Srinivasan1, S M Vogel, D Vidyasagar
1Department of Pediatrics, University of Illinois, College of Medicine, Chicago, Illinois 60612, USA.
Abstract:
We used the isolated-perfused rat lung model to study the influence of pulmonary ventilation and surfactant instillation on the development of postreperfusion lung microvascular injury. We hypothesized that the state of lung inflation during ischemia contributes to the development of the injury during reperfusion. Pulmonary microvascular injury was assessed by continuously monitoring the wet lung weight and measuring the vessel wall (125)I-labeled albumin ((125)I-albumin) permeability-surface area product (PS). Sprague-Dawley rats (n = 24) were divided into one control group and five experimental groups (n = 4 rats per group). Control lungs were continuously ventilated with 20% O(2) and perfused for 120 min. All lung preparations were ventilated with 20% O(2) before the ischemia period and during the reperfusion period. The various groups differed only in the ventilatory gas mixtures used during the flow cessation: group I, ventilated with 20% O(2); group II, ventilated with 100% N(2); group III, lungs remained collapsed and unventilated; group IV, same as group III but pretreated with surfactant (4 ml/kg) instilled into the airway; and group V, same as group III but saline (4 ml/kg) was instilled into the airway. Control lungs remained isogravimetric with baseline (125)I-albumin PS value of 4.9 +/- 0.3 x 10(-3) ml x min(-1) x g wet lung wt(-1). Lung wet weight in group III increased by 1.45 +/- 0.35 g and albumin PS increased to 17.7 +/- 2.3 x 10(-3), indicating development of vascular injury during the reperfusion period. Lung wet weight and albumin PS did not increase in groups I and II, indicating that ventilation by either 20% O(2) or 100% N(2) prevented vascular injury. Pretreatment of collapsed lungs with surfactant before cessation of flow also prevented the vascular injury, whereas pretreatment with saline vehicle had no effect. These results indicate that the state of lung inflation during ischemia (irrespective of gas mixture used) and supplementation of surfactant prevent reperfusion-induced lung microvascular injury.
Insights
Lung inflation during ischemia, not oxygen levels, prevents reperfusion injury. Surfactant also protects against lung microvascular damage, highlighting key factors in preventing post-ischemic lung injury.
Area of Science:
- Pulmonary Medicine
- Cardiovascular Research
- Physiology
Background:
- Postreperfusion lung microvascular injury is a significant clinical concern.
- The role of lung inflation and ventilation during ischemia in mitigating this injury remains incompletely understood.
Purpose of the Study:
- To investigate the influence of pulmonary ventilation and surfactant instillation on postreperfusion lung microvascular injury.
- To determine if lung inflation state during ischemia impacts reperfusion injury development.
Main Methods:
- Utilized an isolated-perfused rat lung model.
- Assessed microvascular injury by monitoring lung wet weight and measuring albumin permeability-surface area product ((125)I-albumin PS).
- Compared groups with varying ventilation (20% O(2), 100% N(2), collapsed) and surfactant/saline pretreatment during ischemia.
Main Results:
- Collapsed, unventilated lungs (Group III) showed significant increases in lung weight and albumin PS, indicating severe injury.
- Ventilation with either 20% O(2) (Group I) or 100% N(2) (Group II) during ischemia prevented injury.
- Surfactant pretreatment of collapsed lungs (Group IV) also prevented injury, while saline did not (Group V).
Conclusions:
- Lung inflation during ischemia, regardless of the gas mixture, is critical in preventing reperfusion-induced lung microvascular injury.
- Surfactant administration can protect against this injury in non-inflated lungs.
- Findings suggest that maintaining lung inflation and considering surfactant therapy are important strategies for mitigating lung injury after ischemia.