ArticleAnimal models and experimental medicine2025
Effects of different nitric oxide synthases on pulmonary and systemic hemodynamics in hypoxic stress rat model.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Characterization of di-gital, tri-gital, and tetra-gital temporal movement of systolic blood pressure on the arterial pulse waveform of rats at different vascular stiffness.Animal models and experimental medicine · 2025Article
- Role of AT1angiotensin receptor antagonist in pulmonary complications induced by renal ischemia-reperfusion injury in male and female rats.BMC nephrology · 2025Article
- Effects of different nitric oxide synthases on pulmonary and systemic hemodynamics in hypoxic stress rat model.Animal models and experimental medicine · 2025Article
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5 authors.
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Abstract
backgroundUnder hypoxia, exaggerated compensatory responses may lead to acute mountain sickness. The excessive vasodilatory effect of nitric oxide (NO) can lower the hypoxic pulmonary vasoconstriction (HPV) and peripheral blood pressure. While NO is catalyzed by various nitric oxide synthase (NOS) isoforms, the regulatory roles of these types in the hemodynamics of pulmonary and systemic circulation in living hypoxic animals remain unclear. Therefore, this study aims to investigate the regulatory effects of different NOS isoforms on pulmonary and systemic circulation in hypoxic rats by employing selective NOS inhibitors and continuously monitoring hemodynamic parameters of both pulmonary and systemic circulation.
methodsForty healthy male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group (N
resultsUnder normoxia, mean arterial pressure and total peripheral vascular resistance were increased, and ascending aortic blood flow and serum NO concentration were decreased in the L-NAME and AG groups. During hypoxia, pulmonary arterial pressure and pulmonary vascular resistance were significantly increased in the L-NAME and AG groups.
conclusionsThis compensatory mechanism activated by inducible NOS and endothelial NOS effectively counteracts the pulmonary hemodynamic changes induced by hypoxic stress. It plays a crucial role in alleviating hypoxia-induced pulmonary arterial hypertension.
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