THE ROLE OF NITRIC OXIDE IN ACUTE LUNG INJURY: A HISTOLOGICAL AND BIOCHEMICAL STUDY | ||||
| The Egyptian Journal of Anatomy | ||||
| Article 8, Volume 26, Issue 1, January 2003, Page 195-218 PDF (3.42 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejana.2003.5876 | ||||
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| Authors | ||||
| Mohamed EI Wasseef1; Dina Radwan2 | ||||
| 1Department of Anaesthesia and Intensive care. National Cancer Institute. Cairo University. | ||||
| 2Histology Department, Faculty of Medicine, Cairo University | ||||
| Abstract | ||||
| Acute lung injury (ALI) is a disease characterized by an early phase of diffuse and severe inflammatory reaction of the lung parenchyma with loss of compartmentalization followed by a late fibroproliferative phase with fever (without a source of infection) and inability to improve the lung function (Meduri et al., 1995), It remains an important contributor to the morbidity and mortality of patients in intensive care units throughout the world (Bernard et al., 1994), The most common causes are infection, sepsis. aspiration and trauma, Since trials of anti-inflammatory therapies in ALI have shown little benefit the exact mechanism by which the lungs are injured remains controversial (Numata et al., 1998). Recent investigations suggested that nitric oxide (NO) may playa role in acute lung injury, both beneficial and detrimental roles have been proposed (Koristof et al., 1998 and Matsuo, 1999). Nitric oxide (NO) is a highly reactive radical synthesized from the amino acid L-arginine by the action of nitric oxide synthases (NOS) (Palmer et al., 1987). Several isoforms of NOS have been identified and divided into two categories with different regulation and activities (Moncada et al., 1991). The constitutive NOS (c-NOS) which exits in endothelial and neuronal cells and comprises the low output path on demand in homeostatic processes such as neurotransmission or blood pressure regulation (Lowestein et al., 1994). In addition, there are inducible isoforms (i-NOS) that may be expressed after exposore to endotoxin and certain cytokines (lL-l. TNF) in macrophages, mast cells, neutrophils and endothelial cells (Gelleret et al., 1993). | ||||
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