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

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

Based on the principles of the sheet-flow model, oxygen transport in pulmonary capillaries was considered as a process in which oxygen first enters plasma through the respiratory membranes, and then combines with the Hbc. A novel mathematical model about oxygen transport in pulmonary capillaries was established according to the relationship of the oxygen concentration inside the red blood cells with the concentration of haemoglobin and the blood saturation, and according to the basic formula for the correlation between blood saturation and oxygen partial pressure. Furthermore, we adopted the Lax-Wendroff Finite Difference Method and obtained certain valuable results under different physiological states. It was well concluded that the established model could be used to provide useful data for medical researchers as well as doctors.
Biological Transport ; physiology ; Capillaries ; physiology ; Humans ; Models, Biological ; Oxygen ; blood ; Partial Pressure ; Pulmonary Alveoli ; blood supply ; Pulmonary Circulation ; physiology ; Pulmonary Gas Exchange

To study the difference of changes on apoptosis, necrosis and respiratory burst of the polymorphonuclear neutrophils (PMN) in endotoxemia rat model. LPS (O(55)B(5), 5 mg/kg) was injected into abdominal cavity of 20 random normal Wistar rat. 2, 4, 8 and 12 hours after injection, the changes of apoptosis, necrosis and respiratory burst of the rats between PMN from the peripheral blood and from the bronchoalveolar lavage fluid were observed using the flow cytometer. At the same time, 5 uninjected rats were taken as control. The results demonstrated that the quantity proportions of apoptosis of PMN between the peripheral blood PMN and the bronchoalveolar lavage fluid PMN in rat's endotoxemia were similar. However, comparison with the uninjected LPS rat, the necrosis of peripheral blood PMN obviously increased and the respiratory burst capacity was clearly inhibited. Contrarily, the necrosis of bronchoalveolar lavage fluid PMN obviously decreased and the respiratory burst obviously increased in the injecting LPS rat. It was concluded that the necrosis and apoptosis displayed differently between the pulmonary and peripheral blood PMNs in endotoxemia. Under state of inflammation, the surviving PMN in tissue increased and kept the activated state due to tissue injury.
Animals ; Apoptosis ; Bronchoalveolar Lavage Fluid ; cytology ; Endotoxemia ; blood ; Necrosis ; Neutrophils ; physiology ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Wistar ; Respiratory Burst

BACKGROUNDHigh positive end-expiratory pressure (PEEP) and low tidal volume (VT) ventilation is thought to be a protective ventilation strategy. It is hypothesized that the stabilization of collapsible alveoli during expiration contributes to lung protection. However, this hypothesis came from analysis of indirect indices like the analysis of the pressure-volume curve of the lung. The purpose of this study was to investigate isolated healthy and injured rat lungs by means of alveolar microscopy, in which combination of PEEP and VT is beneficial with respect to alveolar stability (I-E%).

METHODSAlveolar stability was investigated in isolated, non-perfused mechanically ventilated rat lungs. Injured lungs were compared with normal lungs. For both groups three PEEP settings (5, 10, 20 cmH2O) were combined with three VT settings (6, 10, 15 ml/kg) resulting in nine PEEP-VT combinations per group. Analysis was performed by alveolar microscopy.

RESULTSIn normal lungs alveolar stability persisted in all PEEP-VT combinations (I-E% (3.2 +/- 11.0)%). There was no significant difference using different settings (P > 0.01). In contrast, alveoli in injured lungs were extremely instable at PEEP levels of 5 cmH2O (mean I-E% 100%) and 10 cmH2O (mean I-E% (30.7 +/- 16.8)%); only at a PEEP of 20 cmH2O were alveoli stabilized (mean I-E% of (0.2 +/- 9.3)%).

CONCLUSIONSIn isolated healthy lungs alveolar stability is almost unaffected by different settings of PEEP and VT. In isolated injured lungs only a high PEEP level of 20 cmH2O resulted in stabilized alveoli whereas lower PEEP levels are associated with alveolar instability.

Animals ; Female ; Lung ; pathology ; Lung Injury ; pathology ; Microscopy ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Wistar ; Tidal Volume ; physiology

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by non-cardiogenic, acute and progressive respiratory failure mediated by a variety of injurious stimuli. ALI can progress to ARDS if an effective management is not taken. The mortality rate remains high due to the complex pathogenesis and ineffective management of ARDS. At present, effective treatment methods for ALI are not available and thus it is important to study the pathogenesis and early diagnosis of ALI. This article reviews some of the biomarkers associated with ALI, with a focus on early diagnosis and future studies.
Acute Lung Injury ; diagnosis ; pathology ; Biomarkers ; Cytokines ; physiology ; Early Diagnosis ; Endothelial Cells ; pathology ; Humans ; Lung ; pathology ; Pulmonary Alveoli ; pathology

OBJECTIVETo investigate the expression patterns of surfactant protein B (SP-B) and its role in the development of human fatal lung epithelial cells.

METHODSHuman fetal lung tissues were obtained from 37 fetuses of 10-34 weeks at abortion with parental consent and from two newborn infants who died of non-pulmonary causes. SP-B expression in the lung tissues was examined by immunohistochemistry.

RESULTSSP-B was detected in the cytoplasm of nonciliated columnar epithelial cells of the human fetal lung in as early as the 16th week of gestation. The positive reaction of SP-B was enhanced during canalicular stages and was more intense in the distal than in the proximal airway epithelium. From the 25th week to the prenatal stage, SP-B expression underwent no significant changes in the primitive alveolar stage, but increased remarkably after birth.

CONCLUSIONThe expression and secretion of SP-B reflects the maturation of the epithelial cells in human fatal lungs, and may closely associate with the survival ability of the newborn infants.

Cell Survival ; physiology ; Cells, Cultured ; Epithelial Cells ; cytology ; metabolism ; Fetus ; Humans ; Infant, Newborn ; Lung ; Pulmonary Alveoli ; cytology ; metabolism ; Pulmonary Surfactant-Associated Protein B ; biosynthesis ; physiology

BACKGROUNDp120 catenin (p120ctn) is an adheren junction protein that regulates barrier function, but its role has not been explored in alveolar edema induced by ventilation. We measured stretch-induced cell gap formation in MLE 12 cells due to the loss of p120. We hypothesized that alveolar permeability was increased by high lung inflation associated with alveolar epithelia cell tight junctions being destroyed, which resulted from the loss of p120.

METHODSCultured MLE12 cells were subjected to being stretched or un-stretched (control) and some cells were pretreated with pp2 (c-src inhibitor). After the end of stretching for 0, 1, 2, and 4 hours, the cells were lysed, and p120 expression and c-src activation was determined by Western blotting analysis. In vivo, SD rats were taken to different tidal volumes (Vt 7 ml/kg or 40 ml/kg, PEEP = 0, respiratory rate 30-40 betas/min) for 0, 1, 2, and 4 hour and some were pretreated with pp2, and alveolar edema was calculated.

RESULTSIt was found that p120 expression was reduced and c-src activation increased in a time-dependent and strain-dependent manner due to cyclic-stretch of the alveolar epithelial cells. These changes could be reversed by inhibition of c-src. We obtained similar changes in rats when they were subjected to large tidal volumes and the alveolar edema increased more than in rats in the low Vt group. Pretreated the rats with inhibition of c-src had less pulmonary edema induced by the high tidal volume ventilation.

CONCLUSIONSCyclic stretch MLE 12 cells induced the loss of p120 and may be the same reason by high tidal volume ventilation in rats can aggravate alveolar edema. Maintenance of p120 expression may be a novel therapeutic strategy for the prevention and treatment of ventilation induced lung injury (VILI).

Animals ; Blotting, Western ; Catenins ; physiology ; Cells, Cultured ; Mice ; Pulmonary Alveoli ; pathology ; Pulmonary Edema ; pathology ; Rats ; Rats, Sprague-Dawley ; Tidal Volume ; Ventilator-Induced Lung Injury ; pathology

Acute respiratory distress syndrome (ARDS) remains a poor prognosis in spite of the recent development of new therapeutic strategies. Cell-based therapy with stem cells has been considered as a promising way for the treatment of vital organ damage. Putative endogenous stem cells have been shown to be located within the adult lung in the basal layer of the upper airways, within or near pulmonary neuroendocrine cell rests, at the bronchoalveolar junction, as well as within the alveolar epithelium. These stem cells are hypothesized to be the source of lung regeneration and repair. But this mechanism seems to be insufficient after lung injury. There is increasing excitement over the last few years with the suggestion that exogenous stem cells may offer new treatment options for ARDS. Exogenous stem cells have the ability to differentiate and function as both airway and lung parenchymal epithelial cells in both in vitro and increasingly in vivo experiments. However, there is great controversy concerning the repair effect of adult stem cells in lung injury. This review evaluates the advances in endogenous respiratory stem cells, and assesses the evidence for the use of stem cells in the repair of lung injury.
Adult Stem Cells ; physiology ; transplantation ; Bone Marrow Transplantation ; Bronchi ; cytology ; Cell Fusion ; Epithelial Cells ; physiology ; Humans ; Pulmonary Alveoli ; cytology ; Respiratory Distress Syndrome, Adult ; therapy

PURPOSE: Hypoxemia during one-lung ventilation (OLV) remains a serious problem, particularly in the supine position. We investigated the effects of alveolar recruitment (AR) and positive end-expiratory pressure (PEEP) on oxygenation during OLV in the supine position. MATERIALS AND METHODS: Ninety-nine patients were randomly allocated to one of the following three groups: a control group (ventilation with a tidal volume of 8 mL/kg), a PEEP group (the same ventilatory pattern with a PEEP of 8 cm H2O), or an AR group (an AR maneuver immediately before OLV followed by a PEEP of 8 cm H2O). The tidal volume was reduced to 6 mL/kg during OLV in all groups. Blood gas analyses, respiratory variables, and hemodynamic variables were recorded 15 min into TLV (TLVbaseline), 15 and 30 min after OLV (OLV15 and OLV30), and 10 min after re-establishing TLV (TLVend). RESULTS: Ultimately, 92 patients were analyzed. In the AR group, the arterial oxygen tension was higher at TLVend, and the physiologic dead space was lower at OLV15 and TLVend than in the control group. The mean airway pressure and dynamic lung compliance were higher in the PEEP and AR groups than in the control group at OLV15, OLV30, and TLVend. No significant differences in hemodynamic variables were found among the three groups throughout the study period. CONCLUSION: Recruitment of both lungs with subsequent PEEP before OLV improved arterial oxygenation and ventilatory efficiency during video-assisted thoracic surgery requiring OLV in the supine position.
Adult ; Aged ; Anoxia ; Female ; Humans ; Lung/physiopathology ; Lung Compliance/physiology ; Male ; Middle Aged ; One-Lung Ventilation/*methods ; Oxygen/*blood ; Positive-Pressure Respiration/*methods ; Pulmonary Alveoli/*physiology ; Pulmonary Gas Exchange ; Respiratory Mechanics/*physiology ; *Supine Position ; Thoracic Surgery, Video-Assisted ; Tidal Volume