The air-blood barrier represents the maturity of developing lung. The development of air-blood barrier in human fetal lung was studied by transmission electron microscopy. The results obtained were as follows. 1. The formation of air-blood barrier started at 16 week of postcoitum, which was the end of pseudoglandular period. The basement membranes began to be fused with each other as the capillaries penetrated between epithelial cells of primitive alveoli. 2. The flattening of the type II alveolar cells was observed only around the site of fused basement membranes, which seemed to be developed not by mechanical force but by induction of the fused basement membrane. 3. The basement membranes of capillaries and alveoli were relatively flat until the fusion occurred, but they showed severe folds with the occurrence of fusion. But with the proceeding of the terminal sac period, the folds greatly decreased. In summary, the air-blood barrier began to develop at the end of pseudoglandular period and was formed as capillaries penetrated the cytoplasms of epithelial cells devoided of the nuclei. The fused basement membranes seems to play an important role in the development of air-blood barrier.
Basement Membrane ; Blood-Air Barrier* ; Capillaries ; Cytoplasm ; Epithelial Cells ; Humans* ; Lung* ; Microscopy, Electron, Transmission ; Pulmonary Alveoli

Lung tissues of rats from two different age groups (2-12 and 16-26 months of age) were studied by both light and electron microscopy. Proliferation of granular pneumocytes in pulmonary alveolar lining was a frequent occurrence in older rats. Lungs of older rats showed not only an increase in number of granular pneumocytes, but also a remarkable increase of lamellar bodies and other forms of lipid vacuoles in individual granular pneumocytes. Spontaneously-occurring nodular lesions characterized by the accumulation of macrophages in the alveolar spaces were accompanied by desquamation and proliferation of granular pneumocytes. These lesions developed only in the lungs of rats older than l7 months of age. Such lessions in lungs of old rats were similar in many respects to desquamative interstitial pneumonitis of human lungs. Atrophy of alveolar walls and emphysematous areas seen in senile rats was characterized by irregular cytoplasmic breakdown of Type I alveolar lining epithelial cells. Obliteration of capillaries by spontaneously-occurring thrombus formation or a herniated cytoplasm of the septal cell and collagen fibers was considered to be a cause of atrophy of alveolar walk. Degeneration and actual breakdown of endothe1ial cytoplasm of puImonary capillaries enhanced herniation of the septal tissue. Vacuolar degeneration of epithelial cytoplasm was occasionally observed, but only in rats older than 20 months of age. The basement membrane of pulmonary alveolar walls was often thicker in old rats than in younger rats. Hyperplasia of granular pneumocytes invariably accompanied large septal cells, some of which contained many of the organelles found in granular pneumocytes.
Aging* ; Animal ; Female ; Macrophages/cytology* ; Male ; Pulmonary Alveoli/anatomy & histology* ; Pulmonary Alveoli/cytology ; Rats

Calculi ; Humans ; Lung Diseases ; Male ; Middle Aged ; Pulmonary Alveoli ; pathology

We describe a case of pulmonary alveolar proteinosis in a male adult with lung cancer. To achieve the successful operation of lung cancer, we used percutaneous veno-venous extracorporeal membrane oxygenation (ECMO) during whole lung lavage (WLL) of the contralateral lung. We performed successful WLL under ECMO support.
Adult ; Bronchoalveolar Lavage* ; Extracorporeal Membrane Oxygenation* ; Humans ; Lung Neoplasms* ; Lung* ; Male ; Pulmonary Alveolar Proteinosis* ; Pulmonary Alveoli

OBJECTIVETo report a newborn infant who died of alveolar capillary dysplasia (ACD). The literature on about 20 cases of ACD was reviewed.

METHODSA retrospective review of records of infants from Medline with a diagnosis of ACD was carried out.

RESULTSThe case was a newborn female infant who developed respiratory distress 5 hours after an uncomplicated delivery. She died at the fourth day after birth despite full ventilatory support. The lung autopsy provided a diagnosis of ACD. In the 21 infants, 7 were male and 14 were female; 19 infants were born full-term and 2 were born pre-term. The birth weight of 19 infants and Apgar score of 15 infants were normal; 16 infants developed progressing tachypnea and cyanosis within 24 hours of age, 5 developed cyanosis at 1 day to 19 days. Echocardiography demonstrated a right to left shunt in the hearts of all the 21 infants, and pulmonary hypertension in 20 infants. Twenty infants were treated with conventional mechanical ventilation, 7 infants with high-frequency oscillatory ventilation and 12 infants with extracorporeal membrane oxygenation (ECMO). Fourteen infants were also treated with inhaled nitric oxide therapy and 4 with exogenous surfactant. Diagnostic open lung biopsy was performed in 6 infants. The chest radiography showed normal findings in 3 infants, pneumothoraces in 9 infants, reticular markings, granular, patchy or diffuse opacity in lungs of 7 infants, and decreased pulmonary vascular markings in two infants. All the 21 infants died; 8 of them died within 10 days of age, 7 within 30 days of age, and one died at the age of 4 months who was the longest survivor. Fourteen infants were associated with congenital malformations, such as cardiovascular, gastrointestinal, and genitourinary systems, including one infant associated with chromosomal abnormalities, two infants of familial genetic predisposition.

CONCLUSIONSAt present, ACD is still a disease with poor prognosis, significant medical expenses and no specific treatment. When respiratory failure or persistent pulmonary hypertension (PPHN) is persistent after routine treatment in an infant, ACD should be highly suspected and conventional open-lung biopsy should be preformed to confirm the diagnosis.

Female ; Humans ; Infant, Newborn ; Male ; Persistent Fetal Circulation Syndrome ; diagnosis ; pathology ; Pulmonary Alveoli ; abnormalities ; pathology

The inhalation and deposition of particles in human pulmonary acinus region can cause lung diseases. Numerical simulation of the deposition of inhaled particles in the pulmonary acinus region has offered an effective gateway to the prevention and clinical treatment of these diseases. Based on some important affecting factors such as pulmonary acinar models, model motion, breathing patterns, particulate characteristics, lung diseases and ages, the present research results of numerical simulation in human pulmonary acinus region were summarized and analyzed, and the future development directions were put forward in this paper, providing new insights into the further research and application of the numerical simulation in the pulmonary acinus region.
Aerosols ; Computer Simulation ; Humans ; Lung ; physiology ; Models, Biological ; Particle Size ; Pulmonary Alveoli ; physiology

Diffuse alveolar hemorrhage (DAH) is a clinical syndrome with major clinical manifestations of hemoptysis, anemia, and diffuse infiltration in the lung. DAH has a high mortality rate in the acute stage and is a life-threatening emergency in clinical practice. Compared with adult DHA, childhood DHA tends to have a specific spectrum of underlying diseases. It has long been believed that idiopathic pulmonary hemosiderosis (IPH) is the main cause of childhood DAH; however, with the increase in reports of childhood DAH cases, the etiology spectrum of childhood DAH is expanding. The treatment and prognosis of DAH with different etiologies are different. This review article gives a general outline of childhood DAH, with focuses on DAH caused by IPH, systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody-related vasculitis, COPA syndrome, or IgA vasculitis.
Antibodies, Antineutrophil Cytoplasmic ; Child ; Hemorrhage ; Humans ; Lung Diseases ; Pulmonary Alveoli ; Vasculitis

All physiologic textbooks deal with pleural cavity pressure, alveolar wall pressure and pressure inside the lung, but they have not stated these ideas clearly. The present study reveals production and Law of variation of the intrinsic pressure of pleural cavity, the pressure of alveolar wall and the intrinsic pressure in the alveoli. Pleural cavity intrinsic pressure is produced by the pressure from pleura expanding or compressing force of the lungs. When the lungs calmly inhale, the thorax expands, pleural cavity negative pressure increase. When the lungs calmly exhale, thorax reduces, but thorax and lungs are still in the extended state, pleural cavity is still in negative pressure. With thorax reducing, negative pressure decreases. When the lungs are at the forced expiration, the lung pleura and wall pleura extrude pleural cavity, only to produce positive pressure. The pressure of alveolar wall is the algebraic sum of the intrinsic pressure of pleural cavity, the intrinsic pressure of pulmonary tissue and the additional pressure of alveolar wall. We did the calculation of additional pressure on the alveolar wall by using Laplace formula of spherical elastic membrane. The intrinsic pressure of alveoli depends on the moving speed or slowness of expansion or compression of alveolar wall and the size of trachea resistance.
Humans ; Pleural Cavity ; physiology ; Pressure ; Pulmonary Alveoli ; physiology ; Respiration ; Respiratory Mechanics ; physiology

OBJECTIVETo explore the possible mechanisms of lung necrosis by examining the effects of Streptoccus pneumoniae (S.p) on the ultrastructure of alveolar epithelial cells type Ⅱ(AEC-Ⅱ) in the lung tissues of mice and children.

METHODSThe suspended solutions of S.p strains cultured from the blood of a child with pneumococcal necrotizing pneumonia (PNP) (0.3 mL, CFU: 1×108/L) were instilled into the trachea of pathogen-free mice to prepare PNP model. The same amount of normal saline was given for the control group (10 mice). The samples (1 mm3) from the lower lobe of right lung of the mice were obtained 92 hrs later and fixed in 2.5% glutaraldehyde. Normal and abnormal lung tissues (1 mm3) were obtained while operation for the left lower lobe pulmonary cavity excision in the child with PNP. The specimens were fixed in 2.5% glutaraldehyde and stored at 4℃. A transmission electron microscope was employed for the examination of the ultrastructure of AEC-Ⅱ in the lung tissues.

RESULTSQuantitative reduction and exfoliation of microvilli in S.p-infected AEC-Ⅱ were observed in both mice and this child compared with the control. Enlarged size, enhanced evacuation and reduced density of the lamellar bodies were also presented. The number of mitochondria was obviously reduced. The nucleolus chromatin concentrated and showed an inhomogeneous distribution.

CONCLUSIONSS.p infection results in comparable damage to the ultrastructure of AEC-Ⅱ in mice and children that may represent one of the primary causes responsible for S.p-induced lung tissue necrosis.

Animals ; Child ; Epithelial Cells ; ultrastructure ; Female ; Humans ; Mice ; Pneumonia, Pneumococcal ; pathology ; Pulmonary Alveoli ; ultrastructure

Adult ; Haploidy ; Hematopoietic Stem Cell Transplantation ; Hemorrhage ; Humans ; Lung Diseases ; Male ; Pulmonary Alveoli