dc.creatorDias-Junior, CA
dc.creatorVieira, TF
dc.creatorMoreno, H
dc.creatorEvora, PR
dc.creatorTanus-Santos, JE
dc.date2005
dc.date2014-11-15T14:59:44Z
dc.date2015-11-26T16:11:49Z
dc.date2014-11-15T14:59:44Z
dc.date2015-11-26T16:11:49Z
dc.date.accessioned2018-03-28T23:00:19Z
dc.date.available2018-03-28T23:00:19Z
dc.identifierPulmonary Pharmacology & Therapeutics. Academic Press Ltd Elsevier Science Ltd, v. 18, n. 3, n. 181, n. 186, 2005.
dc.identifier1094-5539
dc.identifierWOS:000227311400005
dc.identifier10.1016/j.pupt.2004.11.010
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/75578
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/75578
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/75578
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1267182
dc.descriptionSelective pulmonary vasodilators attenuate acute pulmonary embolism (APE)-induced pulmonary hypertension. We examined the effects of intravenous sildenafil on the hemodynamic and respiratory changes caused by APE in anesthetized dogs. Sham operated animals (n = 3) received only saline infusions. APE was induced by intravenous injections of microspheres in amounts adjusted to increase mean pulmonary artery pressures (MPAP) by 20 mmHg. Hemodynamic evaluation was performed and arterial blood samples were drawn for blood.-as analysis at baseline, 15 and 30 min after APE was induced, and then 15, 30, and 45 min after the sildenafil infusion (1 mg kg(-1) infused intravenously in 15 min followed by 0.3 mg kg(-1)h(-1) for 30 min) started in the Sildenafil group (n = 7), or saline infusion started in the control group (n = 8). APE induced sustained pulmonary hypertension and 325% increase in pulmonary vascular resistance index (PVRI) without significant changes in the other hemodynamic parameters. While the animals in the control group showed no further changes in MPAP and PVRI, a significant decrease in MPAP and PVRI (-25 and -45%, respectively; P < 0.05 both) was observed with sildenafil. No significant changes in the other hemodymamic parameters were observed in both groups. APE decreased PaO2, whereas sildenafil attenuated the decrease in PaO2 (P < 0.05). We conclude that intravenous sildenafil can selectively attenuate the increases in MPAP and PVRI after APE. (C) 2005 Elsevier Ltd. All rights reserved.
dc.description18
dc.description3
dc.description181
dc.description186
dc.languageen
dc.publisherAcademic Press Ltd Elsevier Science Ltd
dc.publisherLondon
dc.publisherInglaterra
dc.relationPulmonary Pharmacology & Therapeutics
dc.relationPulm. Pharmacol. Ther.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectsildenafil
dc.subjectpulmonary embolism
dc.subjectpulmonary hypertension
dc.subjectpharmacology
dc.subjectphosphodiesterase inhibitors
dc.subjectInhaled Nitric-oxide
dc.subjectEndothelin-receptor Antagonism
dc.subjectAttenuates Hemodynamic-changes
dc.subjectVenous Air Infusion
dc.subjectAcute Lung Injury
dc.subjectTherapeutic Implications
dc.subjectRecurrent Microembolism
dc.subjectArterial-hypertension
dc.subjectVascular-resistance
dc.subjectOral Sildenafil
dc.titleSildenafil selectively inhibits acute pulmonary embolism-induced pulmonary hypertension
dc.typeArtículos de revistas


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