EUROMEDICA  Hanover 3-4  Juni 2010	Advanced methods of diagnosis, treatment and prophylactics
	European Academy of Natural Sciences, Hanover European Scientific Society, Hanover Berliner Medizinischen Gesellschaft, Berlin

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Despite the fact that morphological lung substrate in condition of pulmonary hypertension is well studied and classified, there is still no integrated information about aerohaematinic barrier submicroscopic structure and microcirculation in lungs in condition of the so called hypoxia of “stress” caused by physical activity of different modes. Taking into consideration the above-stated we set ourselves a task to study rats’ respiratory lung field in condition of chronic stress.

The experiment was performed on 30 white outbred male rats of 150-180 grams who were subjected to chronic exercise stress, i.e. running in rotating treadmill 2 times a week in 2-hour sessions in the course of 2 months, speed of rotation - 19 revolutions per minute.

During the experiment histological and electron microscopic methods were applied.

Peculiar features of the rats’ lung samples are as follows: dystonia of interalveolar capillaries and wider vessels located next to dilated air vesicles as well as distelectatic parts, dilatation and plethora of capillaries and pulmonary artery branches of terminal bronchiole level.

In central and subpleural parts of lungs along with air vesicle atelectasis there were found overdilated air vesicles, dilatation and plethora of vessels of all gauges, plasmatic impregnation of small vessels walls, hemorrhage, especially subpleurally; nonuniform opening of acinus airspace took place.

It is worth noting that after exercise stress in aerohaematinic barrier occurred changes which indicate that hemodynamic adaptive mechanisms of lesser pulmonary circulation turned on in the form of uneven thickening of artery and lung vein walls; focal indurations in and around basement membranes of interalveolar capillaries. Besides changed capillaries vessels with normal wall structure were often found, mostly in central lung parts.

So, on the basis of acquired data we can conclude that deep derangements in lung aerohaematinic barrier occur as a result of chronic exercise stress as well as noncompensated respiratory acidosis, which altogether testify inadequacy of exercise stress of this mode. From the practical viewpoint it is undoubtedly very important to research lung aerohaematinic barrier morphological substrate lesions in conditions of alterations caused by exercise stress of different intensity including conditions of hypoxia. Thus, our work opens new prospects of integrated study of cardiopulmonary reactions which provide oxygen supply of organism in experimental conditions.