nitrites has been researched along with Familial Primary Pulmonary Hypertension in 3 studies
Nitrites: Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)
Familial Primary Pulmonary Hypertension: Familial or idiopathic hypertension in the PULMONARY CIRCULATION which is not secondary to other disease.
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 3 (100.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Klinger, JR | 1 |
| Zuckerbraun, BS | 1 |
| George, P | 1 |
| Gladwin, MT | 1 |
| Malinovschi, A | 1 |
| Henrohn, D | 1 |
| Eriksson, A | 1 |
| Lundberg, JO | 1 |
| Alving, K | 1 |
| Wikström, G | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Dose Escalation Study to Evaluate the Effect of Inhaled Nitrite on Cardiopulmonary Hemodynamics in Subjects With Pulmonary Hypertension[NCT01431313] | Phase 2 | 48 participants (Actual) | Interventional | 2012-06-30 | Completed | ||
| A Phase 2, Multi-Center, Open-label, Randomized, Parallel-Dose Study to Determine the Safety and Efficacy of AIR001 in Subjects With WHO Group 1 Pulmonary Arterial Hypertension (PAH)[NCT01725256] | Phase 2 | 29 participants (Actual) | Interventional | 2012-11-30 | Terminated (stopped due to Terminated early dt to acquisition of Sponsor and change in corporate priorities) | ||
| A Phase 2, Multicenter, Open-Label Study to Evaluate the Intermediate/Long Term Safety and Efficacy of AIR001 in Subjects With WHO Group 1 Pulmonary Arterial Hypertension[NCT01725269] | Phase 2 | 17 participants (Actual) | Interventional | 2013-03-31 | Terminated (stopped due to Terminated early dt acquisition of Sponsor and change in corporate priorities) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Basal platelet oxygen consumption measured in isolated platelets by extracellular flux analysis (XF24, Seahorse Biosciences, Billerica, MA). (NCT01431313)
Timeframe: Maximal effect at 15 minutes post 45mg or 90mg inhalation vs Pre dose
| Intervention | picomoles O2/min (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -17.58 |
| WHO Group II Pulmonary Hypertension (PH) | 8.62 |
| WHO Group III Pulmonary Hypertension (PH) | -11.64 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of plasma nitrite concentrations in mixed venous blood over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Pre-dose, 15 minutes post 45mg and 90mg inhalation
| Intervention | micromolar (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 9.9 |
| WHO Group II Pulmonary Hypertension (PH) | 7.0 |
| WHO Group III Pulmonary Hypertension (PH) | 7.4 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of pulmonary artery occlusion (capillary) pullback nitrite concentration over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Pre-dose, 15 minutes post 45mg and 90mg inhalation
| Intervention | micromolar (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 9.2 |
| WHO Group III Pulmonary Hypertension (PH) | 2.4 |
Characteristic impedance (Zc) which may be related to compliance effects in the large, conduit arteries. (NCT01431313)
Timeframe: Pre dose and 60 minutes post last dosage inhaled
| Intervention | dyne*sec/cm5 (Median) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -0.004 |
| WHO Group II Pulmonary Hypertension (PH) | -0.34 |
| WHO Group III Pulmonary Hypertension (PH) | -0.20 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. Since pulmonary vascular resistance (PVR) was not normally distributed, it was transformed to natural log prior to analysis. The reported mean is the change from baseline of PVR over all subsequent times and doses (beta from the mixed effects model, converted back from natural log to Woods units), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | Woods units (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 0.77 |
| WHO Group II Pulmonary Hypertension (PH) | 0.40 |
| WHO Group III Pulmonary Hypertension (PH) | -0.39 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of MAP over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | mmHg (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -5.1 |
| WHO Group II Pulmonary Hypertension (PH) | -3.4 |
| WHO Group III Pulmonary Hypertension (PH) | -9.5 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. Since systemic vascular resistance was not normally distributed, it was transformed to natural log prior to analysis. The reported mean is the change from baseline of SVR over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | mmHg⋅min/L (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -0.43 |
| WHO Group II Pulmonary Hypertension (PH) | 1.19 |
| WHO Group III Pulmonary Hypertension (PH) | -2.04 |
Time in minutes to maximum PVR decrease. During study procedure, hemodynamics were measured at 0, 15, 30, 45, and 60 minutes after 45 mg followed by same times after 90 mg dose. The time point at which each patient's maximal decrease in PVR occurred was recorded and reported as the mean and standard deviation in each cohort. (NCT01431313)
Timeframe: 0, 15, 30, 45, and 60 minutes after 45 mg followed by same times after 90 mg dose
| Intervention | minutes (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 42.0 |
| WHO Group II Pulmonary Hypertension (PH) | 33.0 |
| WHO Group III Pulmonary Hypertension (PH) | 42.5 |
1 review available for nitrites and Familial Primary Pulmonary Hypertension
| Article | Year |
|---|---|
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
Nitrite in pulmonary arterial hypertension: therapeutic avenues in the setting of dysregulated arginine/nitric oxide synthase signalling.
Topics: Arginine; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitric Oxide; Ni | 2011 |
2 other studies available for nitrites and Familial Primary Pulmonary Hypertension
| Article | Year |
|---|---|
Plasma nitrite/nitrate levels: a new biomarker for pulmonary arterial hypertension?
Topics: Biomarkers; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Nitrates; Nitr | 2016 |
Increased plasma and salivary nitrite and decreased bronchial contribution to exhaled NO in pulmonary arterial hypertension.
Topics: Adult; Aged; Breath Tests; Bronchi; Case-Control Studies; Exhalation; Familial Primary Pulmonary Hyp | 2011 |