PRESENCE AND QUANTIFICATION OF NEUROPEPTIDE Y IN PULMONARY EDEMA FLUIDS IN RATS
Ossama Hamdy
Abstract
Ossama Hamdy
Abstract
The present study was undertaken to determine the contribution of neuropeptide Y to edema occurrence in neurogenic and hydrostatic pulmonary edema. To induce neurogenic pulmonary edema, fibrinogen and thrombin were injected into the cisterna magna; and to evoke hydrostatic pulmonary edema, saline was infused intravenously. Concentrations of neuropeptide Y in serum and edema fluid were measured using enzyme-linked immunosorbent assay (ELISA), which showed a mean value of 158 nM (95% confidence limit 124-202 nM) in the neurogenic edema fluid, significantly higher than that in the hydrostatic one. Using immunohistochemistry, fluorescent signals reactive to neuropeptide Y were found in the alveolar macrophages and edema fluid in case of fibrin-induced pulmonary edema, but were almost absent in hydrostatic edema and absent in normal lungs. Mean ratio of protein concentrations in edema fluid to that in serum was 74.9 +/- 0.9% in fibrin-induced pulmonary edema, being higher than that in hydrostatic one. From these results, we conclude that neuropeptide Y has a relationship to the high protein concentration ratio, i.e., to increased pulmonary vascular permeability, and consequently may contribute to the development of neurogenic pulmonary edema in rats.
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The present study was undertaken to determine the contribution of neuropeptide Y to edema occurrence in neurogenic and hydrostatic pulmonary edema. To induce neurogenic pulmonary edema, fibrinogen and thrombin were injected into the cisterna magna; and to evoke hydrostatic pulmonary edema, saline was infused intravenously. Concentrations of neuropeptide Y in serum and edema fluid were measured using enzyme-linked immunosorbent assay (ELISA), which showed a mean value of 158 nM (95% confidence limit 124-202 nM) in the neurogenic edema fluid, significantly higher than that in the hydrostatic one. Using immunohistochemistry, fluorescent signals reactive to neuropeptide Y were found in the alveolar macrophages and edema fluid in case of fibrin-induced pulmonary edema, but were almost absent in hydrostatic edema and absent in normal lungs. Mean ratio of protein concentrations in edema fluid to that in serum was 74.9 +/- 0.9% in fibrin-induced pulmonary edema, being higher than that in hydrostatic one. From these results, we conclude that neuropeptide Y has a relationship to the high protein concentration ratio, i.e., to increased pulmonary vascular permeability, and consequently may contribute to the development of neurogenic pulmonary edema in rats.
Key concepts: Pulmonary edema, Neuropeptide, Edema, Neuropeptide Y receptor, Pathology, Internal medicine, Chemistry, Medicine