Morphological Characteristics of a Rat Model of Reexpansion Pulmonary EdemaShinichi Otani1, Takashi Yashiro2, Yasunori Sohara1 and Shunsuke Endo1*
- Corresponding Author:
- Shunsuke Endo
Department of Thoracic Surgery
School of Medicine, Jichi Medical University
3311-1, Yakushiji, Shimotsuke, Tochigi, Japan
E-mail: [email protected]
Received Date: January 25, 2017; Accepted Date: February 27, 2017; Published Date: February 28, 2017
Citation: Otani S, Yashiro T, Sohara Y, Endo S (2017) Morphological Characteristics of a Rat Model of Reexpansion Pulmonary Edema. J Pulm Respir Med 7:396. doi:10.4172/2161-105X.1000396
Copyright: © 2017 Otani S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Reexpansion pulmonary edema (RPE) is a severe disorder, and its pathophysiology is not well understood. One proposed mechanism for RPE is that chemical substances such as cytokines increase alveolar permeability. Another possible mechanism is that alveolar distention during reexpansion causes physical damage. To test the hypothesis that sudden alveolar distention damages alveolar cellular structure and identify the underlying cause of RPE, we developed and evaluated the morphological characteristics of a rat RPE model.
Methods: Lung from a rat model of RPE was observed by using live imaging from intravital fluorescence microscopy with fluorescein isothiocyanate labelled albumin as tracer, light microscopy, and electron microscopy (with and without horseradish peroxidase [HRP] as tracer).
Results: Intravital fluorescence microscopy and light microscopy showed that RPE developed almost immediately after lung reexpansion and that blood flow in pulmonary capillaries slowed substantially. In some capillaries, however, blood flow had stopped entirely; in others, anterograde and retrograde flow alternated. Electron microscopy revealed pores in type I pneumocytes and overt fissures in alveolar walls. Electron microscopic observation with HRP revealed that HRP moved from capillaries to the inner surfaces of alveolar epithelia in reexpanded lungs. In addition, diaminobenzidine reaction products from the HRP enzyme reaction were visible in areas with pores.
Conclusions: RPE occurred almost immediately after lung reexpansion. Pores developed in type I pneumocytes in alveolar epithelium. These pores, together with overt fissures in alveolar walls, allowed leakage of plasma components into alveoli. These findings appear to be important features of RPE development.