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Strong evidences support their participation in CDH and in the etiology of PH <jats:italic>via<\/jats:italic> the activation of ET<jats:sub>A<\/jats:sub> receptors (ET<jats:sub>A<\/jats:sub>\u2010Rs).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Evaluation of the effect of ABT\u2010627, a selective non\u2010peptidic ET<jats:sub>A<\/jats:sub>\u2010R antagonist, given from \u221215 to 210\u2003min post\u2010delivery (1\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup> bolus +0.01\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup>\u2003h<jats:sup>\u22121<\/jats:sup> infusion, i.v.), was conducted in the lamb model of CDH.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Severity of CDH was assessed in comparison to untreated controls (<jats:italic>n<\/jats:italic>=5). Untreated CDH lambs (<jats:italic>n<\/jats:italic>=7) had a higher mean pulmonary arterial pressure (MPAP; <jats:italic>P<\/jats:italic>&lt;0.0001), lower mean blood pressure (MBP; <jats:italic>P<\/jats:italic>=0.0004), higher MPAP \/ MBP ratio (<jats:italic>P<\/jats:italic>&lt;0.0001), lower arterial pH (<jats:italic>P<\/jats:italic>&lt;0.0001), higher paCO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>&lt;0.0001), lower paO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>&lt;0.0001) and lower post\u2010ductal pulsatile SaO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>&lt;0.0001) than untreated controls.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Treated controls (<jats:italic>n<\/jats:italic>=7) showed a higher MPAP, lower MBP, higher MPAP\/MBP ratio, lower arterial pH, higher paCO<jats:sub>2<\/jats:sub>, lower paO<jats:sub>2<\/jats:sub>, lower post\u2010ductal pulsatile SaO<jats:sub>2<\/jats:sub> and lower plasmatic ir\u2010ET ratios compared to untreated controls (<jats:italic>P<\/jats:italic>&lt;0.0001).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Treated CDH lambs (<jats:italic>n<\/jats:italic>=8) showed a higher MBP (<jats:italic>P<\/jats:italic>&lt;0.0001), lower MPAP \/ MBP ratio (<jats:italic>P<\/jats:italic>&lt;0.0001), higher arterial pH (<jats:italic>P<\/jats:italic>&lt;0.0001), lower paCO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>&lt;0.0001), higher paO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>=0.0228), higher post\u2010ductal pulsatile SaO<jats:sub>2<\/jats:sub> (<jats:italic>P<\/jats:italic>=0.0016) and lower plasmatic ir\u2010ET ratios (<jats:italic>P<\/jats:italic>=0.0247) when compared to untreated CDH lambs.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These observations revealed that, although acute perinatal treatment with a selective non\u2010peptidic ET<jats:sub>A<\/jats:sub>\u2010R antagonist had some adverse effects in controls, it attenuated the progressive cardiopulmonary deterioration that occurred after birth in CDH lambs.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2001) <jats:bold>134<\/jats:bold>, 1679\u20131688; 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