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At least 19 recordsLinked to original sources
PubMed2000

Retinoic acid receptor-beta: an endogenous inhibitor of the perinatal formation of pulmonary alveoli.

Pulmonary alveoli are formed, in part, by subdivision (septation) of the gas-exchange saccules of the immature lung. Septation is developmentally regulated, and failure to septate at the appropriate time is not followed by delayed spontaneous septation. We report retinoic acid receptor (RAR) beta knockout mice exhibit premature septation; in addition, they form alveoli twice as fast as wild-type mice during the period of septation but at the same rate as wild-type mice thereafter. Consistent with the perinatal effect of RARbeta knockout, RARbeta agonist treatment of newborn rats impairs septation. These results 1) identify RARbeta as the first recognized endogenous signaling that inhibits septation, 2) demonstrate premature onset of septation may be induced, and 3) show the molecular signaling regulating alveolus formation differs during and after the period of septation. Suppressing perinatal RARbeta signaling by RARbeta antagonists may offer a novel, nonsurgical, means of preventing, or remediating, failed septation in prematurely born children.

Animals↗
PubMed1995

Variants of shape of the pulmonary alveoli in corrosion casts in human lungs.

The shape of the pulmonary alveoli in pulmonary acini was investigated in corrosion casts and in translucent slices. Five types of the pulmonary alveoli in corrosion casts were distinguished. Most of them were spherical or saucer-shaped. In slices, made translucent in methyl salicylate, the pulmonary alveoli filled with the air were always spherical.

Adult↗
PubMedDate not supplied

Rupture of the pulmonary alveoli during general anesthesia.

The rupture of pulmonary alveoli during the induction of general anesthesia is a significant complication of general anesthesia that has been seldom reported in our literature. This article documents this occurrence in a patient scheduled for elective orthognathic surgery. The diagnosis and treatment are discussed.

Adult↗
PubMed1993

An improved mathematical model of hydrodynamical self-cleansing of pulmonary alveoli.

In the present paper we postulate a hydrodynamical mechanism of pulmonary alveoli cleansing and explain the role of the lung surfactant system in this phenomenon. Then a new, significantly refined mathematical model of the dynamics of the layer lining alveoli is derived and tested numerically in order to check theoretically whether the mechanism postulated can explain the phenomenon observed and to establish the influence of various physicochemical and physiological parameters on the rate of alveolar cleansing. The results obtained confirmed our hypothesis and two examples of the model verification were also shown.

Humans↗
PubMed1986

Biphasic mode of epithelial regeneration in murine pulmonary alveoli.

After administration to mice of butylated hydroxytoluene, the pulmonary alveolar epithelium adopts a biphasic pattern of regenerative proliferation. This hitherto-unnoticed pattern of epithelial repair in the lung was revealed by the investigation of stereologic parameters. The earliest evidence of epithelial injury involved the type I pneumocytes, whose necrosis and disappearance from the septal surface was shown by a lowered surface density (SV). Proliferation of the type II pneumocytes ensued: the volume density (VV) rose above normal soon after the onset of necrosis, only to decrease as the cells slowly differentiated into intermediate and then type I pneumocytes. A second peak of type II pneumocytes appeared as the denuding of septa persisted. This twofold proliferation was also shown by the numerical density count (NV). Differentiation into an intermediate pneumocyte was itself documented by the raised VV and SV values. These observations of a biphasic mode of proliferation of type II pneumocytes raise the question of an unsuspected, persistent action of the toxic agent within pulmonary alveoli and serve to document the homeostasis of epithelial regeneration.

Animals↗
PubMed1994

Actinobacillus pleuropneumoniae in gnotobiotic piglets: ultrastructural changes in the pulmonary alveoli with dose and time.

The ultrastructural changes in pulmonary alveoli produced by transtracheal inoculation of 10(6) and 10(8) CFU of Actinobacillus pleuropneumoniae serotype 5 in gnotobiotic piglets were studied after 1 and 4 h. At 1 h postinoculation (p.i.) with 10(6) or 10(8) CFU, no gross change in lung and no evidence of infiltration of cells into alveoli was observed. At 4 h p.i., at a dose of 10(6) CFU, a generalized red mottling occurred in the dorsal half of the caudal lobe, which revealed ultrastructural evidence of neutrophil infiltration into alveoli along with fibrin and a few erythrocytes. At 4 h p.i., at a dose of 10(8) CFU, there was a bilateral lung lesion characterized by a generalized mottling and congestion, within which we observed ultrastructural evidence of bacteria and cellular debris in the alveoli and fibrin clots and cellular necrosis in the alveolar septum. By using gnotobiotic piglets and visualizing the effects of bacterial inoculum on cellular ultrastructure of the lung, we have demonstrated that both dose and time play roles in the early pathogenesis of experimental porcine pleuropneumonia. The developing lesion in lungs of gnotobiotic piglets infected with pure cultures of A. pleuropneumoniae can be controlled experimentally. This experimental procedure can provide a base of reproducible, sequential, ultrastructural changes with which to compare the role of inflammatory mediators in the lung and the effects of drugs on immunologic events in the lung.

Actinobacillus Infections↗
PubMed2000

Dynamic ultrastructure of mouse pulmonary alveoli revealed by an in vivo cryotechnique in combination with freeze-substitution.

A morphological approach to cell dynamics is usually difficult, since routine preparative techniques for electron microscopy always induce artifacts due to cessation of the blood supply into organs. An in vivo cryotechnique followed by the freeze-substitution method probably reduces such problems. It was applied for examining the pulmonary alveoli of BALB/c mice in vivo. The following ultrastructural features were revealed. (1) A surfactant layer provided a continuous covering to the alveolar epithelium. (2) Pleural epithelial cells, alveolar cells and endothelial cells contained many small vesicles and pits. In the alveolar epithelium, they were often localised near microtubules. (3) Typical lamellar structures in large alveolar epithelial cells were rarely detected. (4) Circulating erythrocytes with various shapes were observed in branching blood capillaries. (5) A close association between erythrocytes and the endothelium was seen at the peripheral alveolar septum. Such ultrastructural arrangements may be appropriate for the physiological functions of the pulmonary alveoli, such as exchanges of gases or materials in vivo.

Animals↗
PubMed1985

How many pulmonary alveoli are supplied by a single arteriole and drained by a single venule?

A detailed measurement of histological specimens of the lungs of the cat shows that each terminal precapillary vessel (arteriole) supplies, on the average, 24.5 pulmonary alveoli; each terminal postcapillary vessel (venule) drains, on the average, 17.8 alveoli. These numbers link pulmonary alveolar blood flow in capillary sheets with the flow in pulmonary arteries and veins which are cylindrical tubes. They are key numbers needed for hemodynamic analysis. In the literature, these numbers are variously speculated to be 1 or smaller; thus our results correct, even though only for the cat, an important concept.

Animals↗
PubMed2004

The search for stem cells of the epithelium in pulmonary alveoli.

In recent years significant progress has been witnessed in the identification of stem cells, which have now also been identified in the lungs. The aim of this was to induce post-pneumonia alveolar regeneration to facilitate the identification of stem cells. The studies were performed on Buffalo strain rats. Pneumonia was induced in the animals by a sub-pleural injection of carragenin. On days 4, 5 and 10 of the experiment both the control and experimental animals received intraperitoneal injections of bromodeoxyuridine (BrdU). Twenty-four hours after the last BrdU injection the rats were sacrificed and samples of the lungs were taken for examination. In order to detect proliferating cells in the paraffin sections, BrdU incorporation was detected with monoclonal antibodies. In pilot experiments BrdU incorporation was demonstrated in individual alveolar cells of variable distribution and of variable intensity in the colour reaction. The results have confirmed the existence of stem cells in pulmonary alveoli but their closer characterisation requires further studies with other techniques to detect pulmonary stem cells.

Animals↗
PubMed1996

Formation of pulmonary alveoli and gas-exchange surface area: quantitation and regulation.

New morphometric procedures allow selection of alveoli for analysis in an unbiased manner and then to determine the volume of individual alveoli. The latter, together with the easily measured lung volume, allows the calculation of alveolar number. These new techniques have greatly increased the rigor of the study of the formation of alveoli and the manner in which this process is regulated. This review deals mainly with work based on these new morphometric methods that explore the regulation of the formation of alveoli and hence the size of the lung's gas-exchange surface area. We expect that continued application of these methods, buttressed with experiments at the cellular and molecular level, will result in a fundamental understanding of how the formation of alveoli and the size of the gas-exchange surface area is regulated. This new information holds the promise of translation into the induction of the formation of alveoli for therapeutic purposes.

Animals↗