Evaluation of Plasma Nitric Oxide and Serum Endothelial Nitric Oxide Synthase in Pulmonary Hypertensive Dogs: A Clinical and Echocardiography Investigation
Siwayu Rattanakanokchai | Numfa Fungbun | Ketmanee Senaphan | Supranee Jitpean | Trasida Ployngam
Nitric oxide (NO), an endogenous vasodilator, has been proposed as a biomarker for pulmonary hypertension (PH) in humans. NO is synthesized by endothelial nitric oxide synthase (eNOS). Alterations in NO/eNOS have not been studied in dogs with PH. We assessed alterations in NO and eNOS in the blood of dogs with PH (<i>n</i> = 17) and healthy dogs (<i>n</i> = 10) and analyzed their correlations with echocardiographic parameters. The results showed significantly higher plasma NO and serum eNOS levels in dogs with PH compared with healthy dogs. Dogs with PH and ascites (<i>n</i> = 11) had significantly lower plasma NO levels than those without ascites (<i>n</i> = 6) and presented a decreasing eNOS trend. In dogs with PH, plasma NO was positively correlated with left ventricular hemodynamics, right ventricular compliance, and pulmonary distensibility, but was negatively correlated with pulmonary vascular resistance and right cardiac remodeling. Serum eNOS was positively correlated with the main pulmonary artery diameter. Increments in NO/eNOS reflected compensatory responses to cardiovascular changes in PH. These compensations were downward in the advanced stages. Other factors may also impact NO/eNOS compensation. Although the role of NO/eNOS as biomarkers for PH in dogs remains equivocal, they may indicate compensatory consequences of cardiovascular alterations.
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