Actual studies suggest that a calcium activated chlorid channel (TMEM16A) may play a relevant role in the pathogenesis of pulmonary arterial hypertension (PAH). The inhibition of this channel led to pulmonary vasorelaxation in preclinical studies. Benzbromarone is a well known inhibitor of the TMEM16A channel and is used in patients with gout. In this pilot study the investigators plan to investigate if Benzbromarone has an acute effect on the pulmonary arteries in humans. This will be investigated within the frame of a right heart catheterization performed in patients with known PAH due to clinical reasons. The investigators hypothesize that the application of Benzbromarone leads to pulmonary vasodilation, which can be recognized by the decrease in pulmonary vascular resistance. In addition, the change in pulmonary and systemic arterial pressure, pulmonary arterial wedge pressure, heart rate and arterial oxygen saturation will be assessed. Due to clinical reasons patients will receive NO (15 ppm) during right heart catheterization. Hemodynamic changes upon NO and Benzbromarone may be compared.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
10
1x200mg Benzbromarone will be applied after baseline measurements during right heart catheterization. The effects of the drug on the pulmonary hemodynamics will be assessed after 2 hours.
Medical University of Graz
Graz, Austria
Pulmonary vascular resistance (Wood units) assessed by right heart catheterization
Time frame: 2 hours
Mean pulmonary arterial pressure (mmHg) assessed by right heart catheterization
Time frame: 2 hours
Mean systemic arterial pressure (mmHg) assessed by sphygmomanometer
Time frame: 2 hours
arterial oxygen saturation 8%) assessed by arterial blood gas analysis
Time frame: 2 hours
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