Untersuchung der pathophysiologischen Mechanismen bei Ausbildung einer pulmonalen Hypertonie ausgelöst durch pulmonal-venösen Rückstau

Beschreibung

Pulmonary hypertension has a poor prognosis and no cure. The most common of all forms of pulmonary hypertension (PH) is due to left heart disease and currently there are no firm guidelines for treating this disease complex. As the average age of the population increases, the number of patients with heart failure with preserves ejection fraction (HFpEF-PH) is growing. However, due to a lack of models, the search for promising drugs and new treatment modalities is difficult. As PH is a major determinant of quality of life and mortality in this context, it is becoming increasingly important to find appropriatea treatment strategies. Unfortunately, pulmonary arterial hypertension PAH-specific drugs are not effective in HFpEF-PH patients. With this thesis, we have established a promising model that addresses this challenge. The pulmonary vein banding (PVB) mimics venous congestion as it occurs in HFpEF-PH and leads to a remodeling process in pulmonary vessels. As a result, the echocardiographic and hemodynamic findings were consistent with mild PH. Right ventricular pressures were slightly elevated and ultrasound revealed an increase in right ventricular wall thickness. However, compared to already estab-lished PAH models, right ventricular failure was absent. Nevertheless, the diseased lungs showed a strong vascular remodeling process with inflammatory involvement of lymphocytes and siderophages. With the help of an additional stenosis of the right pulmonary veins, this effect could certainly be intensified, but animal welfare and questionable advantages for answering scientific questions should be taken into account. Overall, We were able to show that PVB induces cardiac and pulmonary changes that can be equated with pulmonary hypertension in humans. With the establishment of this animal model, the therapeutic effect of drugs on pure, vascular-associated pulmonary hypertension can be explored. Interfering factors such as cardiac dysfunction or metabolic diseases, as they occur in HFpEF-PH patients, can therefore be excluded in this model. New modes of drug action and the significance of PH in terms of mortality and quality of life in HFpEF-PH can thus be better explored.

Autor*in

Jonas Münks

Themen in »Untersuchung der pathophysiologischen Mechanismen bei Ausbildung einer pulmonalen Hypertonie ausgelöst durch pulmonal-venösen Rückstau«

Pulmonale Hypertonie (PH) HFpEF-PH (Herzinsuffizienz mit erhaltener Ejektionsfraktion und PH) Tiermodell – Pulmonalvenöses Banding (PVB) Gefäßremodelling der Lunge Rechtsventrikuläre Hypertrophie Medikamentenentwicklung PH / Translationales Modell

Stimmen zu »Untersuchung der pathophysiologischen Mechanismen bei Ausbildung einer pulmonalen Hypertonie ausgelöst durch pulmonal-venösen Rückstau«

Details

Link teilen