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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:Modulation of pulmonary vasomotor tone in the fetus and neonate | Available online http respiratory-research.eom content 2 3 139 Review Modulation of pulmonary vasomotor tone in the fetus and neonate Nancy S Ghanayem and John B Gordon Department of Pediatrics Medical College of Wisconsin Milwaukee Wisconsin USA Correspondence John B Gordon MD Children s Hospital of Wisconsin MS 681 9000 W Wisconsin Ave Milwaukee WI 53226 USA. Tel 1 414 266 3360 fax 1 414 266 3563 e-mail j gordon@mcw.edu Received 2 February 2001 Revisions requested 9 February 2001 Revisions received 12 February 2001 Accepted 13 February 2001 Published 8 March 2001 Respir Res 2001 2 139-144 2001 BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract The high pulmonary vascular resistance PVR of atelectatic hypoxic fetal lungs limits intrauterine pulmonary blood flow PBF to less than 10 of combined right and left ventricular output. At birth PVR decreases precipitously to accommodate the entire cardiac output. The present review focuses on the role of endothelium-derived nitric oxide NO prostacyclin and vascular smooth muscle potassium channels in mediating the decrease in PVR that occurs at birth and in maintaining reduced pulmonary vasomotor tone during the neonatal period. The contribution of vasodilator and vasoconstrictor modulator activity to the pathophysiology of neonatal pulmonary hypertension is also addressed. Keywords nitric oxide perinatal potassium channels prostacyclin pulmonary hypertension Introduction During late fetal development PVR is high and PBF is limited to less than 10 of combined ventricular output. This provides adequate nutrition and stimulus for growth to the lung while optimizing flow to other fetal tissues and the placenta. At birth mechanical distention of the lungs increased oxygen tension and increased shear stress result in a precipitous decrease in PVR and increase in PBF to 100 of cardiac output. Failure of this normal transition leads to persistent right-to-left shunting across fetal cardiovascular channels .
