Sildenafil Is a Pulmonary Vasodilator in Awake Lambs with Acute Pulmonary Hypertension

Weimann, Jörg; Ullrich, Roman; Hromi, Jonathan; Fujino, Yuji; Clark, Martin; Bloch, Kenneth D.; Zapol, Warren M.

doi:10.1097/00000542-200006000-00030

Cited by 204 publications

(140 citation statements)

References 37 publications

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“…[6][7][8][9] Sildenafil was studied in animal models of pulmonary hypertension, revealing to be a selective pulmonary vasodilator with no effects on systemic arterial pressure, enhancing the effects of inhaled nitric oxide (iNO) when given orally or intravenously. 5,10 It is a potent inhibitor of phosphodiesterase-5, which is responsible for the conversion of cGMP into GMP. The inhibition of this enzyme results in an increase of cGMP concentration in the lungs, with consequent relaxation of the smooth muscle of the vascular wall (Figure 1).…”

Section: Discussionmentioning

confidence: 99%

Sildenafil no tratamento da hipertensão pulmonar após cirurgia cardíaca

Bentlin¹,

Saito²,

Luca³

et al. 2005

J. Pediatr. (Rio J.)

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Objective: To report on the use of sildenafil for pulmonary hypertension treatment of a newborn patient after cardiac surgery.Description: A female, full term newborn infant with diagnosis of double outlet right ventricle, pulmonary hypoplasia and subaortic ventricular septal defect, was submitted to Blalock surgery in the first week of life. In postoperative the newborn had pulmonary hypertension and persistent hypoxia, without response to nitric oxide, but with improved oxygenation after continuous intravenous infusion of prostaglandin E1. After several failed attempts to discontinue prostaglandin E1, oral sildenafil was used. There was a decrease in pulmonary vascular resistance with consequent oxygenation improvement and 48 hours later it was possible to discontinue prostaglandin E1 infusion.Comments: Sildenafil can be an alternative therapy for pulmonary hypertension, especially when there is no response to conventional therapy.J Pediatr (Rio J). 2005;81(2):175-8: Sildenafil, pulmonary hypertension, prostaglandin.

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Section: Discussionmentioning

confidence: 99%

Sildenafil no tratamento da hipertensão pulmonar após cirurgia cardíaca

Bentlin¹,

Saito²,

Luca³

et al. 2005

J. Pediatr. (Rio J.)

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“…66 Sildenafil proved to be a potent pulmonary selective vasodilator when used for treating PAH in animal experiments with very little fall in systemic pressure. 67 An acute vasodilatory effect on the pulmonary circulation was seen in patients with iPAH when combined with inhaled iloprost in the study by Wilkens and colleagues. 68 The fall in PVR was dose dependent in this study using intravenous sildenafil during right heart catheterisation.…”

Section: Sildenafilmentioning

confidence: 98%

“…There is genetic anticipation in familial PAH, i.e. the onset of disease occurs at an Indian Heart Journal 6401 (2012) [60][61][62][63][64][65][66][67][68][69][70][71][72][73] earlier age in successive generations. 8,9 Group 1 of Dana Point classification also includes drugs and toxins associated with development of PAH; the most notorious of these include the appetite suppressants fenfluramine and dexfenfluramine.…”

Section: Epidemiologymentioning

confidence: 99%

Pulmonary hypertension—“state of the art” management in 2012

Saxena

2012

Indian Heart Journal

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A B S T R A C TPulmonary artery hypertension (PAH) is a pathological condition of small pulmonary arteries, characterised by vascular proliferation and remodelling. The pulmonary artery pressure and pulmonary vascular resistance progressively rise, leading to right heart failure and death. Pulmonary artery hypertension may be secondary to various conditions, or it may be idiopathic where no underlying cause is identifiable. Earlier, only symptomatic treatment was available for such patients which did not change the natural history of the disease. However, over the years, improvement in understanding the pathogenesis has resulted in the development of targeted approaches to the treatment of PAH. Survival advantage has also been shown with some of the pharmacologic agents. This review article discusses the current management strategy for PAH with special emphasis on an idiopathic variety, in an Indian context.

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“…Sildenafil is a specific inhibitor of PDE5 that increases the pulmonary vasodilating effect of inhaled nitric oxide [5][6][7][8] , prevents pulmonary hypertensive crises after weaning of nitric oxide in patients with severe pulmonary hypertension 5,9 , and has its own pulmonary vasodilating effect 10,11 by increasing the GMPc levels 12 .…”

Section: Case Reportmentioning

confidence: 99%

“…In an experimental study, Weimann et al 10 showed that the pulmonary vasodilating effect of sildenafil is dose-dependent, beginning 5 minutes after its administration and reaching its maximum effect in 10 minutes.…”

Section: Case Reportmentioning

confidence: 99%

Sildenafil melhora a função ventricular direita no receptor de transplante cardíaco

Paez¹,

Araujo²,

Hossne³

et al. 2005

Arq. Bras. Cardiol.

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The use of a female donor for a male recipient is known to have a greater early mortality (OR=1.11, P=0.3), similarly to that of a recipient using vasoactive drugs and waiting in the intensive care unit (OR=2.51, P<0.0001) [13][14][15] .We report the case of a patient undergoing orthotopic cardiac transplantation, who experienced cardiogenic shock due to right ventricular dysfunction secondary to pulmonary hypertension associated with vasoplegia. Because the recipient's clinical condition was critical, a marginal donor was used.In the national literature, we did not find reports of the use of sildenafil for pulmonary hypertension in the postoperative period. The objective of this report is to propose a new and safe manner to treat right ventricular failure secondary to pulmonary hypertension in the postoperative period of cardiac transplantation. Case ReportThe patient was a 33-year-old man with idiopathic dilated cardiomyopathy, who had been in NYHA functional class IV for the preceding 2 years and was hospitalized with low cardiac output and was using catecholamines (dobutamine, 6.6 mcg/kg/min, and dopamine, 8 mcg/kg/min). The patient was hypotensive (blood pressure of 70x40 mmHg), slightly dyspneic at rest, and had hepatomegaly and pulmonary congestion (basal rales in both bases).The patient underwent orthotopic cardiac transplantation on 08/02/2003. Due to his rapid clinical worsening, a marginal organ was used. The marginal donor was a 60-kg female, who had experienced cardiac arrest for 15 minutes 3 days before, was using 12 mcg/kg/min of dopamine, and, on the echocardiogram, had diffuse, mild hypokinesia and preserved overall function.The transplantation was performed according to the bicaval technique with 165 minutes of extracorporeal circulation and 117 minutes of anoxia, under mild hypothermia (32 o C) and use of intermittent anterograde blood cardioplegia. The patient was removed from the extracorporeal circulation after the third attempt and sent to the ICU receiving 0.11 mcg/kg/min of isoproterenol, 0.75 mcg/ kg/min milrinone, and 20mcg/kg/min of dobutamine. His mean blood pressure was 40 mmHg and mean pulmonary arterial pressure was 45 mmHg. His right ventricular contractility was very poor, and he received adrenaline in bolus during transportation and in the first hours at the ICU. Twelve hours after transplantation, the patient was receiving 10mcg/kg/min of dobutamine, 0.96 mcg/kg/min of adrenaline, 0.13 mcg/kg/min of isoproterenol, and 0.41 mcg/kg/ The use of inhaled nitric oxide reduces pulmonary artery pressure, increasing the production of guanosine 3',5'-cyclic monophosphate (GMPc) in the smooth muscle cells of the lung 1 . Specific inhibitors of GMPc phosphodiesterase (PDE5), which hydrolyzes GMPc in vascular smooth muscle, cause pulmonary vasodilation 2-4 .Sildenafil is a specific inhibitor of PDE5 that increases the pulmonary vasodilating effect of inhaled nitric oxide 5-8 , prevents pulmonary hypertensive crises after weaning of nitric oxide in patients with severe pulmonary hypertensio...

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Sildenafil Is a Pulmonary Vasodilator in Awake Lambs with Acute Pulmonary Hypertension

Abstract: Sildenafil is a selective pulmonary vasodilator in an ovine model of acute pulmonary hypertension. Sildenafil induces pulmonary vasodilation via a NO-dependent mechanism. In contrast to zaprinast, sildenafil did not prolong the pulmonary vasodilator action of inhaled NO.

Cited by 204 publications

References 37 publications

Sildenafil no tratamento da hipertensão pulmonar após cirurgia cardíaca

Sildenafil no tratamento da hipertensão pulmonar após cirurgia cardíaca

Pulmonary hypertension—“state of the art” management in 2012

Sildenafil melhora a função ventricular direita no receptor de transplante cardíaco

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