The selective pulmonary vasodilatory effect of inhaled DETA/NO, a novel nitric oxide donor, in ARDS—a pilot human trial

Lam, Chen-Fuh; Heerden, Peter Vernon van; Blott, John A.; Roberts, Brigit; Ilett, Kenneth F.

doi:10.1016/j.jcrc.2004.02.009

Cited by 19 publications

(20 citation statements)

References 16 publications

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“…Diethylenetriamine has a very slow half-life ($24 h), potentially allowing once a day therapy, and reverses experimental pulmonary vasoconstriction without causing systemic vasodilatation [54]. A pilot study confirmed our earlier animal studies, showing that nebulized diethylenetriamine (150 mmol) causes selective pulmonary vasodilatation in adult respiratory distress syndrome patients [55].…”

Section: Nono-atessupporting

confidence: 66%

An evidence-based approach to the management of pulmonary arterial hypertension

Archer

Michelakis²

2006

Current Opinion in Cardiology

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Section: Nono-atessupporting

confidence: 66%

An evidence-based approach to the management of pulmonary arterial hypertension

Archer

Michelakis²

2006

Current Opinion in Cardiology

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“…Effectiveness of acute or chronic administration of NONOates in attenuating PH has been shown in several animal studies and in a human clinical trial [12,15,16,18,27,31,32] . Previously, we have demonstrated that nebulization of a single dose of DPTA/NO attenuated GBS-induced PH in newborn piglets [18] .…”

Section: Discussionmentioning

confidence: 98%

Effects of Intermittent Nebulization of NONOate, DPTA/NO, on Group B <i>Streptococcus</i>-Induced Pulmonary Hypertension in Newborn Piglets

Dąbrowska¹,

Hehre²,

Ladino³

et al. 2010

Neonatology

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Background: A single dose of NONOate attenuates pulmonary hypertension (PH) induced by group B Streptococcus (GBS) infusion and this is accompanied by a decrease in systemic vascular resistance (SVR). Objective: The objective of the study was to determine whether two doses of the NONOate sustain the attenuation in GBS-induced PH without further systemic compromise. Methods: 15 anesthetized newborn piglets were randomized to receive placebo (n = 8) or two doses of nebulized DPTA/NO (n = 7) at 15 and 75 min after GBS-induced PH. Pulmonary artery (Ppa) and systemic (Psa) pressures, cardiac output (CO) and arterial blood gases were obtained at baseline and every 15 min until 180 min during GBS infusion. Results: Ppa and pulmonary vascular resistance (PVR) decreased significantly after the first dose of nebulized DPTA/NO and this effect was maintained after the second dose. Psa and SVR decreased after the first dose of DPTA/NO to values close to baseline and no further changes in systemic circulation were observed with repeated treatment. PVR/SVR increased with GBS infusion, but decreased after the first dose of DPTA/NO and remained significantly lower for 180 min. CO was significantly higher in the DPTA/NO group. Changes in Ppa, PVR, Psa, SVR, and CO with GBS infusion were not modified by placebo infusion. PaCO₂, base deficit, and pH did not differ between groups. PaO₂ was significantly lower in the DPTA/NO group after the second dose. Conclusion: These data demonstrated that GBS-induced PH is attenuated with two doses of DPTA/NO without significant systemic effect. The vasodilatory effect is more pronounced in the pulmonary than in the systemic vasculature, as suggested by lower PVR/SVR in the DPTA/NO group. We speculate that NONOates may have a clinical application in the management of PH in neonates.

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“…A small pilot Special Report study in five intubated acute respiratory distress syndrome patients also demonstrated a decreased pulmonary vascular resistance with a nebulized NONOate [57].…”

Section: Ino Adductsmentioning

confidence: 89%

“…Nebulised NONOate UOL 5 ARDS Acute Gas exchange, RHC [57] l-arginine COL 10 PAH a/w SCA 1 month ECG [61] l-arginine RCT 19 IPAH, CTEPH 5 days RHC, CPET [62] Sildenafil RCT 278 IPAH, PAH a/w CTD 3 months 6MWT, RHC, WHO FC [70] Sildenafil + iloprost UOL 14 IPAH, PAH a/w CTD 12 months 6MWT, RHC [74] Sildenafil + trepostinil UOL 9 IPAH 3 months CPET [75] Sildenafil + epoprostenol RCT 267 IPAH, PAH a/w CTD 4 months 6MWT, RHC, TTCW [76] Sildenafil RCT 19 CTEPH 3 months 6MWT, WHO FC, RHC [77] Sildenafil UOL 13…”

Section: Financial and Competing Interests Disclosurementioning

confidence: 99%

Pulmonary hypertension, nitric oxide and nitric oxide-releasing compounds

Hagan

Pepke‐Zaba

2011

Expert Review of Respiratory Medicine

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Nitric oxide (NO) is an important molecule in the mammalian cardiovascular system and the elucidation of its biological role has led to the awarding of a Nobel prize in medicine. There have been many significant discoveries in NO biology over the past two decades and translation of these developments from bench to bedside has allowed an explosion of therapies for pulmonary hypertension. This article provides an overview of the NO pathway in the pulmonary circulation in maintenance of normal vascular tone as well as its dysregulation in pulmonary hypertension, and a discussion of therapies based on inhaled NO or manipulation of its downstream signaling pathways. Several therapies such as phosphodiesterase inhibitors are already in use, and various experimental therapies are also discussed.

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The selective pulmonary vasodilatory effect of inhaled DETA/NO, a novel nitric oxide donor, in ARDS—a pilot human trial

Cited by 19 publications

References 16 publications

An evidence-based approach to the management of pulmonary arterial hypertension

An evidence-based approach to the management of pulmonary arterial hypertension

Effects of Intermittent Nebulization of NONOate, DPTA/NO, on Group B <i>Streptococcus</i>-Induced Pulmonary Hypertension in Newborn Piglets

Pulmonary hypertension, nitric oxide and nitric oxide-releasing compounds

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