In the study of the diaphragm thickness of patients of four subgroups, it was established that with an increase in the duration of the course of COPD and CID, the thickness increases , reaching maximum values ​​in the stage of compensated pulmonary heart. In the stage of decontamination of the CID, the thickness of the diaphragm decreased as compared with subgroups A, B and control. In patients with CLL with the presence of PH, but without a broncho-obstructive process in the lungs, the thickness of the diaphragm is slightly less than in the control group. Microscopic This study of the diaphragm revealed changes in myocytes and stroma. In all subgroups, mean myocytes prevailed. The greatest number of them was observed in subgroup A, in subgroups B and C there was a decrease in this indicator. A change in the number of large myocytes had a reverse tendency compared to the average muscle fibers, a greater number of them were diagnosed in patients with decompensated HPS. The same tendency was observed in the study of small muscle fibers. Chronic hypoxia, persistent energy hunger due to hyperfunction of the diaphragm as a result of COPD and HLS contributed to dystrophic and necrobiotic changes in the striped muscle fibers of the diaphragm. The cross-sectional hair contours with a long COPD course (subgroups B and C) looked less rounded,in places with retractions and bulges. In the stage of decompensated HPS, areas with necrosis of myocytes appeared. The number of stroma in subgroups A (12.2 ± 0.35%) and B (13.5 ± 0.4%) exceeded the control indicators (P <0.001), however, they did not differ significantly between them (P> 0.05 ). The largest number of stromal elements was observed in subgroup C – 28.4%, which significantly exceeded the control indicators of other study groups (P <0.001). In subgroup C in the stroma of the diaphragm there were areas of lipomatosis. Significant differences between morphometric data of the main and control subgroups (patients with COPD and PH without sopahowever, they did not differ significantly (P> 0.05). The largest number of stromal elements was observed in subgroup C – 28.4%, which significantly exceeded the control indicators of other study groups (P <0.001). In subgroup C in the stroma of the diaphragm there were areas of lipomatosis. Significant differences between morphometric data of the main and control subgroups (patients with COPD and PH without sopahowever, they did not differ significantly (P> 0.05). The largest number of stromal elements was observed in subgroup C – 28.4%, which significantly exceeded the control indicators of other study groups (P <0.001). In subgroup C in the stroma of the diaphragm there were areas of lipomatosis. Significant differences between morphometric data of the main and control subgroups (patients with COPD and PH without sopa lymphoproliferative disease) was not detected. Morphofunctional to artin reflects the compensatory-adaptive processes that occur in the diaphragm due to bronchopulmonary pathology and the hypoxia and hyperfunction caused by it. These factors lead to the development of hypertrophy, and then dystrophy of the striated myocytes of the diaphragm. With a long course of COPD and HPS, dystrophic changes reach a maximum, leading to fatty degeneration and necrosis of muscle fibers. In patients with CLL, in contrast to patients with CAS without lymphoproliferative disease, lymphoid infiltration of the diaphragm and lymphocytic stasis in the vessels of the diaphragm is noted . These changes, as well as compression of the diaphragm by the enlarged liver and splenic This contributes to impaired function of the diaphragm and the progression of the identified morphological changes . Morphological changes in the diaphragm in patients with subgroup D (CLL patients with PH, without COPD).

The morphological and morphometric studies of small circulation vessels (ISC) in CLL patients in combination with COPD at different stages of the formation of HLS were performed . The degree and frequency of identified changes increases with the progression of CPH. In patients with COPD and HLS, CLL in the arteries and arterioles of the ICC had changes of I – V degrees, in the veins – I – III degrees. Changes in the vessels of the ICC are characteristic of both the main patients (COPD on the background of CLL) and additional control subgroups (COPD without concomitant lymphoproliferative disease), at similar stages of the formation of the CPH. The morphological features of the vessels of the LA system in CLL patients were the following changes, which are not characteristic of patients with additional controls groups: filling gaps from vessels of different caliber with lymphocytes with the development of leukostasis, in some cases completely blocking the gaps of small vessels and causing a significant impairment of microcirculation ; in some patients, infiltration of the pulmonary vascular walls with tumor cells and multiple perivascular lymphoid cell lesions were noted.

In subgroup D, changes in the vascular ICC were less pronounced. In 13 cases, changes in arteries were noted and arterioles corresponding to the I degree (72.2%) – hypertrophy of the middle envelope, in 5 cases (27.8%) there were no changes. Changes in the veins were either absent or were not pronounced (I degree). We explain the less pronounced changes in the ICC vessels as compared with other subgroups by the shorter duration of PH in patients with CLL without COPD. Patients with I degree changes are mostly patients with significant liver enlargement and spleen. ki The duration of the disease is shorter than the duration of COPD in patients of the other subgroups. In patients without pathological changes in the vessels of the ICC, there was no significant increase in the liver and spleen. Consequently, an increase in pressure in the LA system in them is associated with a severe and prolonged course of inflammatory and specific leukoses in the lungs, an increase in lymph nodes in the chest cavity, and so on. That is, the duration of PH in this situation is even shorter and serious morphological changes detected in patients from other subgroups did not have time to occur in the vessels of the ICC.