Subjects and methods I. Subjects: 63 patients in this group, 38 males and 25 females, aged 20-68 years old, average 46 years old. The clinical manifestations were complex, but all had symptoms of chest tightness, cough, dyspnea, and all had ventilation or ventilation dysfunction on pulmonary function tests. 45 of the 63 cases were clinically comprehensive diagnoses, 10 cases were confirmed by bronchoscopy, and 8 cases were confirmed by puncture or open chest biopsy. Examination methods: All 63 cases had CT scan, including 15 cases with HRCT; 55 cases had chest X-ray; 28 cases had CTPA examination. Analysis method: Two experienced radiologists analyzed the imaging data of 63 cases and made the preliminary diagnosis. Then a radiologist and a respiratory physician jointly compared and analyzed the imaging data with the clinical data, and discussed the etiology of the formation of uneven lung density. The main manifestations of uneven lung density in 63 cases were “mosaic-like” changes in the density of both lungs or one lung or one lobe of the lung in 56 cases; glandular vesicle-like, lobular-like and small lamellar solid shadows were seen in 3 cases within the ground glass shadow; and map-like or pavement-like changes in lung density were seen in 4 cases. In addition, among 39 cases of vascular disease, pulmonary aneurysmal dilatation, stenosis, thrombosis and irregularity of the vessel wall accounted for 35 cases. Second, the types of diseases that cause uneven lung density: in this group, pulmonary vascular diseases are: PE 16 cases, BS 7 cases, WG 5 cases, PAN 6 cases, metaplasia granulomatosis and vasculitis 2 cases, lung cancer invasion of the pulmonary artery 3 cases, a total of 39 cases accounting for 61.9%; small airway lesions are COPD 15 cases and BO 2 cases, accounting for 27%; while 7 cases of PAP pathological manifestations of the lung is not uniform filling. Discussion I. Mechanism of lung density alteration: Lung density is composed of four factors: density of air spaces in the lung, density of lung tissue, amount of extravascular body fluid in the lung, and pulmonary blood volume. Thus, any disease leading to changes in the above factors will certainly cause changes in lung density, but the most common is lung disease leading to changes in air cavity density and blood volume, which is the basic pathological basis for changes in lung density. Second, the formation mechanism and main etiology of pulmonary density inhomogeneity: 16 cases of PE in this group mainly involved lobar, segmental and sub-segmental pulmonary arteries, which is consistent with literature reports. In order to maintain normal cardiac output, the reduced blood volume will be redistributed to other unobstructed pulmonary arteries, resulting in an increase in local blood volume in the area and an increase in lung density, forming a mosaic perfusion. In 6 cases of PAN, the main manifestations were stenosis, obstruction and post-stenosis dilatation of the pulmonary artery lumen, which resulted in mosaic-like changes in pulmonary density due to the intersection of pulmonary artery stenosis and obstruction with normal pulmonary arteries, resulting in the uneven distribution of pulmonary blood volume. The pulmonary artery lesions, such as stenosis, obstruction and aneurysmal dilatation, can cause uneven perfusion of pulmonary blood, resulting in uneven lung density. COPD and BO are both small airway obstructive diseases, and gas trapping in the airspace where the obstructed bronchus belongs to can cause a decrease in lung density in this area, thus forming a mosaic with the normal lung airspace, resulting in uneven lung density; at the same time, the contraction of smooth muscle in the small pulmonary artery bed and/or structural changes in the vessel wall caused by hypoxia in the lesion area, resulting in a narrowing of the blood vessels and a decrease in blood flow in the lesion area, while the blood volume increases in the area without stenosis or with less stenosis. This results in mosaic perfusion. Therefore, it is suggested that the uneven lung density in the 17 small airway lesions was the result of uneven perfusion of pulmonary blood and air. In 7 cases of PAP, the main manifestations were multiple ground glass shadows and patchy solid shadows interspersed with each other, forming a map-like distribution and pavement-like changes in the normal lung areas/compensated emphysema areas. This is the main reason for the uneven filling of the lung cavities with these active substances. Third, the differential diagnosis of pulmonary density: uneven lung density mosaic-like changes without lobar emphysema, often suggest simple uneven pulmonary blood perfusion. In this group, 39 cases of vascular disease were not seen in the signs of emphysema, indicating that the pathological basis of such lung density changes is pulmonary vascular lesions, so it is not difficult to make a diagnosis by choosing CTPA and combining clinical data. When the hypodense area of uneven lung density is emphysema, which often indicates small airway obstructive lesions, then it may be COPD, BO, BOOP, RBILD and other diseases. When ground glass shadows are interspersed with solid shadows, and when high-density lesions are interspersed with low-density normal lung areas or emphysematous areas, this often indicates heterogeneous filling of the lung. In summary, there are many causes of pulmonary density heterogeneity, but they are mainly due to inhomogeneous perfusion of pulmonary blood and gas and inhomogeneous filling of the lung, and most commonly to inhomogeneous perfusion of pulmonary blood due to pulmonary vascular disease.