StatusThe thesis was presented on the 7 December, 2007
Approved by NCAA on the 28 February, 2008
Abstract– 0.34 Mb / in romanian
0.89 Mb /
During this study was included 87 patients with chronic obstructive pulmonary disease (COPD) associated with pulmonary hypertension (PAH) and cardiac dysfunction. In accordance with international recommendation COPD 75% from 58 patients with gr. II medium gravity and gr. III severe gravity of disease, but in cases with gr. IV 25,00% – very severe evolution. Peripherical bronchial obstruction of respiratory airways, lesions of parenchyma and vascular pulmonary dysfunction are factors that leads to decrease of gas exchange in lungs producing in 58,82 % cases patients –gr. I and in 41,18 % cases - gr. II severity of arterial hipoxemy. Development in advenced stages of hypercapny lead to accentuated changes with arterial pressure growing of paCO2 we found in 71,43% cases, but relative changings of paCO2 was only in 28,51%. PAH is basic cardiovascular complication in COPD that provoced ulterior development of cord pulmanary with increasing diastolical sizes RA 46,03 ± 0,67 mm, RV 30,41 ± 0,63 mm, LV in 26,92% cases with 59,3 ± 1,7 mm presion level in PA being between 46,16 ± 1,54 mmHg.
The in vitro study were included 29 patients whom were prelivated pulmonary vessel in accordance with surgery indications, 17 patients with PAH (study group) and 12 pacients (control group) without PAH were operated upon because of hidactic pulmonary cyst. PA was tested in action conditions of the following constrictor agents: ET-1, NE, Phe (same NE), AngII, 5-HT. Our experimental study showed that pacients with PAH constrictor answer of PA at action of ET-1 was increased. So, PA in vitro answer at action of ET-1 is significant increased,fact that was been dictated by ”higher reglation” of ETA receivers in association with ETB endotelinical recievers disfunction,coherent possible its reglation ”lower”. Significant was increased constrictor stage of PA at action ET-1, NE, Phe (same NE), AngII, 5-HT pointing out when these agents act in higher concentrations. So, the role of the neuroendocrine activation in the PAH evolution these vascular reactivity distinction can be viewed as an opportune contribution to PAH pathogenesis.
Evolution of vascular elasticity at pacients with PAH confirmed,elasticity of large arteries has an affected grad at the limit of norm, but certain was determined that elasticity of small had a bigger grad of affection,that determine a endothelial disfunction.
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