phenylephrine-hydrochloride has been researched along with Hypertension--Pulmonary* in 4 studies
1 review(s) available for phenylephrine-hydrochloride and Hypertension--Pulmonary
Article | Year |
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Low flow oxygen therapy. Treatment of the ambulant outpatient.
Topics: Acute Disease; Ambulatory Care; Blood Pressure; Brain; Chronic Disease; Diphosphoglyceric Acids; Erythrocytes; Follow-Up Studies; Humans; Hypertension, Pulmonary; Hypoxia; Intubation; Lung Diseases, Obstructive; Nose; Oxygen; Oxygen Inhalation Therapy; Partial Pressure; Physical Exertion; Polycythemia; Prognosis; Psychology; Respiratory Insufficiency; Spirometry; Vascular Resistance | 1974 |
1 trial(s) available for phenylephrine-hydrochloride and Hypertension--Pulmonary
Article | Year |
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Acute hemodynamic effects of pulsed delivery of low flow nasal nitric oxide in children with pulmonary hypertension.
We studied 8 children, ages 8 months to 14 years, during cardiac catheterization in order to determine the acute hemodynamic effects of pulsed nasal cannula delivery of nitric oxide (NO) in children with pulmonary hypertension. NO was administered by continuous mask or pulsed nasal cannula in random order. All patients effectively triggered the NO pulsing device. Pulsed delivery of inhaled NO lowered mean pulmonary artery pressure and pulmonary vascular resistance as effectively as mask delivery of NO. Pulsed inhaled NO delivery may potentially be useful for the long-term domiciliary treatment of pulmonary hypertension in children. Topics: Administration, Inhalation; Adolescent; Atrial Function, Right; Blood Circulation; Blood Pressure; Cardiac Catheterization; Cardiac Output; Catheterization; Child; Child, Preschool; Drug Administration Schedule; Hemodynamics; Home Care Services; Humans; Hypertension, Pulmonary; Infant; Long-Term Care; Masks; Nitric Oxide; Nose; Prospective Studies; Pulmonary Artery; Pulmonary Wedge Pressure; Vascular Resistance | 1998 |
2 other study(ies) available for phenylephrine-hydrochloride and Hypertension--Pulmonary
Article | Year |
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Malar rash with pulmonary hypertension and chronic obstructive pulmonary disease.
Topics: Aged; Anti-Arrhythmia Agents; Anti-Bacterial Agents; Cheek; Diagnosis, Differential; Digoxin; Diuretics; Exanthema; Female; Humans; Hypertension, Pulmonary; Nose; Oxygen; Pulmonary Disease, Chronic Obstructive | 2017 |
[Nose-only cigarette smoke exposure plus airway lipopolysaccharide inhalation induced chronic obstructive pulmonary disease and associated pulmonary hypertension in mice].
To establish a mouse model of chronic obstructive pulmonary disease (COPD) and associated pulmonary hypertension (COPD-PH) induced by nose-only cigarette smoking exposure plus airway lipopolysaccharide (LPS) inhalation.. There were 24 male C57B6 mice divided into a control group and a model group at random. The model group was given LPS by intranasal inhalation on day 1 and day 14 and exposed to the cigarette smoke in a nose-only exposure system, while the control group was given physiological saline and exposed to normal air. The model establishment was evaluated according the following parameters: the lung function and the right heart pressure, the total and differential cell numbers in bronchial alveolar lavage fluid (BALF), and the pathological changes of lung tissues.. The functional residual capacity data of the model group and the control group were (0.402 ± 0.057) and (0.243 ± 0.064) ml respectively (P<0.05). The inspiratory resistance data of the model group and the control group were (1.056 ± 0.121) and (0.789 ± 0.063) cmH(2)O · ml(-1) · s(-1) (1 cmH(2)O=0.098 kPa) respectively (P<0.05). The static lung compliance data of the model group and the control group were (0.084 ± 0 .007) and (0.056 ± 0.004) cmH(2)O/ml respectively (P<0.05). The right ventricular mean pressure of the model group and the control group were (11.3 ± 1.3) and (7.9 ± 1.1) mmHg (1 mmHg=0.133 kPa) respectively (P<0.05), while the right ventricular hypertrophy index of the model group and the control group were (0.267 ± 0.019) and (0.195 ± 0.023) respectively (P<0.05). Moreover, the histological staining showed that goblet cell hyperplasia, lung inflammation and thickening of smooth muscle layers of bronchial and pulmonary small vessels occurred in the model group, which indicated ongoing airway and blood vessel remodeling.. A COPD-PH mouse model was established by nose-only cigarette smoking exposure plus airway LPS inhalation in a short period of time, and this method was more similar to the smoking behavior of human. Topics: Administration, Inhalation; Animals; Bronchoalveolar Lavage Fluid; Disease Models, Animal; Hypertension, Pulmonary; Lipopolysaccharides; Lung; Male; Mice; Mice, Inbred C57BL; Nicotiana; Nose; Pneumonia; Pulmonary Disease, Chronic Obstructive; Respiratory Function Tests; Smoking | 2015 |