The impact of L-NAME and L-arginine chronic toxicity induced lesions on ascites--pulmonary hypertension syndrome development in broiler chickens.

The impact of L-arginine (LA), a precursor for synthesis of nitric oxide (NO), and N-omega-nitro-L-arginine methyl ester (L-NAME, LN), a non-selective inhibitor of the enzyme producing nitric oxide (nitric oxide synthase; NOS) chronic toxicity induced lesions on Ascites - Pulmonary hypertension syndrome (PHS) development was investigated in 140 one-day-old male broiler chickens (ROSS) during the first 5 weeks of life. Every second day the animals were treated intraperitoneally (ip) with L-NAME (10 mg/kg of body weight; BW), L-arginine (100 mg/kg BW), L-arginine and L-NAME in combination (100 mg/kg BW and 10 mg/kg BW respectively), and with physiological saline (0.90% w/v of NaCl; 0.5 mL/kg BW). Seven birds from each group were euthanized every week. The histopathological examination of the heart, the liver, the lungs, the blood vessels and the lymphoid organs, was performed. Also the organ index values were determined. At the end of the experiment the pre-ascitic condition or ascites - PHS was confirmed in five dead animals in the L-NAME-treated group. In the same group the edema was the most prominent histopathological change confirmed in the heart and in the lungs of the sacrificed chickens. In L-arginine-treated group the congestion and the haemorrhages were the striking changes in the same organs with the highest degree in the last two weeks of trial. While the focal disruption of myocardiofibriole and hepatocytes were predominant lesions in L-NAME-treated chickens (5th and 4th weeks, respectively), in L-NAME/L-arginine-treated group only the mild focal myocardial degeneration was seen. According to the most of the results of present investigation, it was concluded that the consecutive treatment with L-NAME provoked ascites - PHS, while L-arginine has protective effect in this animal model of disease.