The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo

Kisch-Wedel, Hille; Kemming, Gregor; Meisner, Franz; Flondor, Michael; Kuebler, Wolfgang M.; Bruhn, Sebastian; Koehler, Carolina; Zwißler, Bernhard

doi:10.1007/s00134-003-1891-z

Cited by 37 publications

(43 citation statements)

References 29 publications

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“…This is in concordance with Rex et al, 22 who tested a low dose of iloprost in pigs subjected to acute pulmonary hypertension and did not show any improvement in RV function. This is also supported by Kisch-Wedel et al, 10 who reported a positive inotropic response in the LV of the pig during administration of iloprost at a supratherapeutic dose. Nitroprusside, which is a systemic arterial vasodilator, was titrated to produce the same drop in MAP as was and cardiac output (CO; B) in percent difference from placebo treatment after injection of Ilo10 and Ilo100.…”

Section: 19supporting

confidence: 75%

Iloprost Improves Ventricular Function in the Hypertrophic and Functionally Impaired Right Heart by Direct Stimulation

et al. 2013

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Right heart function is an important predictor of morbidity and mortality in patients suffering from pulmonary arterial hypertension and congenital heart diseases. We investigated whether the prostacyclin analog iloprost has a direct inotropic effect in the pressure-overloaded hypertrophic and dysfunctional right ventricle (RV). Rats were randomized to monocrotaline injection (60 mg/kg; n ¼ 8), pulmonary trunk banding (PTB; n ¼ 8), or a sham operation (n ¼ 8). RV function was evaluated with magnetic resonance imaging, echocardiography, and invasive pressure measurements at baseline, after intravenous administration of placebo, iloprost 10 ng/kg/min, or iloprost 100 ng/kg/min (Ilo100). Infusion of Ilo100 induced a 12% AE 4% (P ¼ 0:022) increase in stroke volume in the sham group and a 12% AE 3% (P ¼ 0:005) increase in the PTB group. RV dP=dt max was elevated by 11% AE 5% (P ¼ 0:039) in the sham group and by 12% AE 3% (P ¼ 0:016) in the PTB group. An elevation in cardiac output of 14% AE 3% (P ¼ 0:0008) and an 11% AE 2% (P ¼ 0:0021) increase in RV systolic pressure were found in the PTB group. Iloprost caused a decrease in mean arterial blood pressure (MAP) in all groups of animals. An equal reduction in MAP induced by the arterial vasodilator nitroprusside did not improve any of the measured parameters of RV function. We conclude that iloprost has inotropic properties directly improving ventricular function in the hypertrophic and dysfunctional right heart of the rat.

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Section: 19supporting

confidence: 75%

Iloprost Improves Ventricular Function in the Hypertrophic and Functionally Impaired Right Heart by Direct Stimulation

et al. 2013

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“…64,65 Afterload reduction, however, cannot be achieved in many cases, but the increased right ventricular wall thickness and reversal of a fetal gene expression program have not yet been investigated as potential targeted treatments. Chronic intravenous epoprostenol infusion therapy in patients with pulmonary arterial hypertension appears to improve right ventricular function 66,67 (although dilation and hypertrophy may not reverse over a 1-year period of observation 68 ), and the effects of the endothelin receptor antagonist bosentan on echocardiographic right ventricular parameters have also suggested a similar improvement in right ventricular function. 69 However, the specific myocardial effects of these or other therapies for pulmonary arterial hypertension remain incompletely understood.…”

Section: Treatment Of Right Ventricular Dysfunctionmentioning

confidence: 99%

Right Ventricular Function and Failure

et al. 2006

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“…45 And although it is quite possible that these observations are correct, it is of concern that the prostanoids have inotropic effects which results in a marked increase in stroke work of the right ventricle. 47,48 The experience with inotropic agents in patients with LV failure, 49 including intravenous epoprostenol, 50 showed an improvement in cardiac output that translated into an improvement in exercise tolerance in the short term, but an increase in mortality in the long term. This lesson requires us to remain diligent of this possibility in PAH as well.…”

Section: Prostacyclinsmentioning

confidence: 99%

The Effects of Vasodilators in Pulmonary Hypertension

Rich

2009

Circ: Heart Failure

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W hen primary pulmonary hypertension (PPH) was first described in the medical literature, it was characterized from a cardiac catheterization on a young woman who had an elevated pulmonary arterial pressure of unknown origin which, after the intravenous administration of acetylcholine, promptly fell. 1 The sentinel description of this phenomenon led to the acceptance of PPH as a medical entity in which inappropriate pulmonary vasoconstriction was a central feature. 2 Since then many series of patients with PPH (now referred to as idiopathic pulmonary arterial hypertension [IPAH]) have been published which document a variable ability to respond to acute vasodilator challenge. Although, the approach to therapy has emphasized the initial classification of responder or nonresponder, most patients demonstrate only a small decrease in pulmonary pressure (PAP) in response to vasodilators. 3 However, vasodilators are widely prescribed in patients who are nonresponders, based on clinical trials that established the response to a 6-minute walk (6 MW) test as the primary end point. 4 The consistent improvement in 6 MW reflects the complexity of exercise intolerance, which may be strongly influenced not only by cardiopulmonary factors, but by peripheral factors such as the muscle ergoreflex. 5 Who is a Responder?In the current era, patients with PAH 6 who undergo acute vasoreactivity testing at the time of diagnosis are classified as responders or nonresponders based on the change in PAP from select agents. 7 The definition of a responder has changed many times, the most recent being a fall in the mean PAP of at least 10 mm Hg to a level below 40 mm Hg without any fall in cardiac output. 4 However, the response is in reality a continuum, and not an all or none phenomenon. It is notable that in 2 large series of patients who were deemed acute responders, the characteristic of those who had near perfect survival on calcium blockers (CCB) for up to 18 years had an acute fall in mean PAP of 39% and an acute fall in pulmonary vascular resistance (PVR) of 50%. 3,8 It is remarkable how similar the experiences from the 2 series are, supporting the validity of the observations. Who is a Nonresponder?The majority of patients with IPAH are nonresponders. Although this implies lack of vasoreactivity, this is clearly not the case. In an observational study of patients with IPAH who were monitored with a pulmonary artery catheter over 6 hours without an intervention, considerable variability was noted in the PAP (Ϯ8%) and PVR (Ϯ13%), suggesting that changing vasomotor tone is common in these patients. 9 In the 2 series on long-term calcium blocker therapy, the nonresponders also had an acute fall in mean PAP and PVR, but of a lesser magnitude than the responder group. In one series, the fall in PAP was 8%, and fall in PVR was 17%. 8 In the other, nonresponders were noted to have a fall in PVR of less than 20%. 3 Thus, the characterization of a patient as a nonresponder actually means a minimal response, not lack of response. Although the...

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The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo

Cited by 37 publications

References 29 publications

Iloprost Improves Ventricular Function in the Hypertrophic and Functionally Impaired Right Heart by Direct Stimulation

Iloprost Improves Ventricular Function in the Hypertrophic and Functionally Impaired Right Heart by Direct Stimulation

Right Ventricular Function and Failure

The Effects of Vasodilators in Pulmonary Hypertension

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