Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Egemnazarov, B.
Overview of the animal models of right ventricular dysfunction
Studium für die Gleichwertigkeit; Humanmedizin; [ Diplomarbeit ] Medical University of Graz; 2019. pp. 43
[OPEN ACCESS]
FullText
- Autor*innen der Med Uni Graz:
- Betreuer*innen:
- Kwapiszewska-Marsh Grazyna
- Altmetrics:
- Abstract:
- The function of the right ventricle (RV) determines the severity of the disease and survival of patients suffering from pulmonary hypertension. Chronic RV pressure overload leads to development of RV dysfunction, which culminates in heart failure. Mechanisms responsible for development of RV dysfunction are poorly investigated. One of the reasons could be the fact that the currently used animal models do not resemble the complexity of RV dysfunction in full and therefore are not satisfactory. The aim of the work is by performing a literature search elucidate some features of RV dysfunction, which are not reflected by existing animal models. Moreover, some aspects of RV pathophysiology, which are less investigated, should be identified. The obtained knowledge should deliver ideas for improvement of our models. The literature search was performed for this work. Results of our group were compared with findings of other groups. Currently, investigations on RV dysfunction are at the level of characterizeing it. Hypoxia induced RV dysfunction model appears as a model with fully compensated pressure overload. Pulmonary artery banding model (PAB) induces pronounced adaptive RV remodeling, which causes moderate dysfunction. Monocrotalin (MCT) and Sugen5416 (SU/HOX) induced models cause severer dysfunction. Although, none of the models demonstrates the phenotype of cardiac decompensation. Investigations using molecular biology approach show contribution of different signaling pathways partly known from the research on the left ventricular dysfunction. Characterization using invasive and non-invasive techniques demonstrates reduced cardiac function in PAB, MCT and SU/HOX models. At the same time, the aspect of RV/PA coupling remains mainly untouched. Summary. None of the investigated animal models resembles the clinical picture of cardiac failure. The machanisms of RV dysfunction seem to be partly specific for RV. Some questions of RV physiology, e.g. RV/PA coupling, remain poorly investigated.