Efficacy of tadalafil in chronic hypobaric hypoxia–induced pulmonary hypertension: possible mechanisms
Abstract
The present study was carried out to investigate the effects of long-acting phosphodiesterase five inhibitor, tadalafil, on pulmonary hypertension induced by chronic hypobaric hypoxia in rats. Adult Albino Wistar rats were exposed to 2 weeks of hypobaric hypoxia for 8 h daily and treated with tadalafil or tempol, a standard antioxidant agent. Right ventricular systolic pressure (RVSP) was taken as an index for pulmonary arterial pressure; malondialdehyde, reduced glutathione and superoxide dismutase were chosen as the markers of oxidative stress; serum tumour necrosis factor alpha (TNF-α) levels and inflammatory changes in lungs were assessed for inflammation. Chronic hypobaric hypoxia was found to induce pulmonary hypertension, as it significantly (P < 0.001) increased RVSP. Chronic hypobaric hypoxia also leads to an increase in oxidative stress as was evidenced by an increase in malondialdehyde levels (P < 0.001) and a significant decrease in (P < 0.001) reduced glutathione levels and superoxide dismutase activity. Chronic hypobaric hypoxia-induced inflammation was revealed by lung histology and increase in serum TNF-α levels. Tadalafil significantly prevented (P < 0.001) rise in hypobaric hypoxia-induced rise in RVSP. Tadalafil partially while tempol completely reversed hypobaric hypoxia-induced oxidative stress. Lung inflammation and serum TNF-α levels were significantly attenuated by both tadalafil and tempol. However, effect of tadalafil on inflammation was more marked…
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