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Protective effect of melatonin on liver ischemia-reperfusion induced pulmonary microvascular injury in rats
Objective:
Reactive oxygen species generated during liver reperfusion have been implicated in remote lung injury. In this study, we evaluate the protective effects of melatonin pretreatment against the increased pulmonary microvascular permeability.
Methods:
Male Sprague-Dawley rats were divided into three groups: shame-operated, liver ischemia-reperfusion (I/R), and melatonin pretreated (15 mg/kg, intraperitoneally) 15 minutes prior to the liver I/R). The duration of ischemia was 30 minutes, followed by 2 hours of reperfusion. Lungs were isolated in situ and parameters of the capillary filtration coefficient (K(fc)), lung wet-to-dry weight ratio (W/D), lung weight-to-body weight (LW/BW), and protein concentration in bronchial lavage fluid (PCBAL), the percentage of macrophages and neutrophils in bronchial lavage fluid (BALF), and lung tissue malonedealdehyde were used to assess the lung injury.
Results:
Liver I/R-induced lung injury was noted by the markedly increased K(fc), W/D, LW/BW, PCBAL, and the presence of neutrophils and macrophages in BALF. Lipid peroxidation was also increased (P < .05). All indicators were markedly decreased in melatonin-pretreated rats (P < .05), suggesting that lung injury was attenuated.
Conclusions:
Melatonin pretreatment prior to liver I/R can effectively reduce the pulmonary microvascular permeability and attenuate lipid peroxidation in the lungs.
Insights
Melatonin pretreatment protects against liver ischemia-reperfusion (I/R) induced lung injury by reducing pulmonary microvascular permeability and lipid peroxidation.
Area of Science:
- Physiology
- Pathology
- Pharmacology
Background:
- Reactive oxygen species from liver reperfusion contribute to remote lung injury.
- Pulmonary microvascular permeability is a key indicator of lung damage.
- Melatonin's antioxidant properties are being investigated for protective effects.
Purpose of the Study:
- To evaluate the protective effects of melatonin pretreatment against liver ischemia-reperfusion (I/R) induced lung injury.
- To assess melatonin's impact on pulmonary microvascular permeability and oxidative stress.
Main Methods:
- Male Sprague-Dawley rats underwent liver ischemia-reperfusion (I/R) or sham operation.
- Melatonin (15 mg/kg) was administered intraperitoneally 15 minutes before liver I/R.
- Lung injury was assessed using capillary filtration coefficient, wet-to-dry ratio, lung weight-to-body weight ratio, protein concentration in bronchial lavage fluid, inflammatory cell counts, and malondialdehyde levels.
Main Results:
- Liver I/R significantly increased lung injury markers, including capillary filtration coefficient, wet-to-dry ratio, lung weight-to-body weight ratio, and protein concentration in bronchial lavage fluid.
- Increased neutrophils and macrophages were observed in bronchoalveolar lavage fluid (BALF) post-I/R.
- Melatonin pretreatment significantly attenuated these I/R-induced lung injury indicators and reduced lipid peroxidation.
Conclusions:
- Melatonin pretreatment effectively mitigates liver I/R-induced lung injury.
- Melatonin reduces pulmonary microvascular permeability and oxidative stress in the lungs following liver I/R.
