Postinflammatory changes of the diaphragmatic stomata

Michailova, K.

doi:10.1016/s0940-9602(01)80168-0

Cited by 18 publications

(15 citation statements)

References 33 publications

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“…The intercellular spaces as preferable sites for the exocytosis of LB confirm the hypothesis for a safe defense against the frictional damage, and as a barrier to both protein leakage and pathogen invasion by spanning cell junctions (Whitaker et al 1982;Hills 2000). The validity of this conception is justified by the larger particles visible by SEM in the vicinity of effective diaphragmatic openings-stomata, which showed a significant increase in number and dimensions after peritonitis, according to our previous results (Michailova et al 2001B). We suggest that a larger number of the intercellular contacts between the cubic mesothelial cells, especially by the activated cells, ensure numerous places for exocytosis of the LB like other lamellar formations, compared to the non-activated mesothelial cells.…”

Section: Discussionsupporting

confidence: 69%

Mesothelial lamellar bodies in norm and experimental conditions. Transmission and scanning electron microscopic observations on the peritoneum, pleura and pericardium

Michailova

2004

Anat Embryol

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The ultrastructural characteristics of the mesothelial intracellular and extracellular lamellar bodies (LB) in norm, and especially in pathological conditions are still unknown. After routine fixation procedure, material from organs in the three serous cavities of Wistar rats, as control group were compared with animals following experimental hemothorax (EH) and experimental peritonitis (EP), using transmission and scanning electron microscopy (TEM, SEM). Different membrane-bound profiles, short strip-like structures and single LB characterize the control group. Five days after EH small groups of LB were observed. Single balloon-like profiles, numerous particles and larger groups of LB with wide varieties in size, form and membrane structure characterize the 8th day after EH. Thin and concentric membranes build single LB the 5th day of EP. Eight days after the same treatment, groups of LB, complex structures with several multilamellar centers, strip-like structures with rough granulo-filamentous material and uninterrupted covering over wide areas were observed. We conclude that constant components in the untreated rats are different membrane profiles, as initial lamellar formations and single typical LB with predominant intracellular position. The preferable sites for exocytosis of LB are the intercellular spaces. The present data demonstrate simultaneous findings of the two main groups of formations by using routine fixation in the control group and in the treated animals. The first represent LB as well as other round profiles, observed by TEM and particles, observed by SEM, which are widespread and probably have a basic role. The second ones are strip-like structures and its SEM-equivalents, i.e. uninterrupted covering. TEM-profiles and their SEM-images show significant organ differences and in some cases lack of correspondence between both electron microscopic techniques in the same treatment. Significant enlargement of the number of LB and the length of the strip-like structures characterize the mesothelium after pathologic conditions. LB with considerable differences in the structure and larger particles over the microvillous border predominate after EH. Strip-like profiles, continuous covering and smaller groups of LB with similar morphology and preferable submesothelial position characterize the mesothelium after EP.

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Section: Discussionsupporting

confidence: 69%

Mesothelial lamellar bodies in norm and experimental conditions. Transmission and scanning electron microscopic observations on the peritoneum, pleura and pericardium

Michailova

2004

Anat Embryol

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“…The increased peritoneal or pleural fluid loads were used in order to study the effect of a Δ P TD change on the diaphragmatic tracer distribution. No signs of local or systemic inflammation developed in our acute short‐term experiments, in which, unlike what observed in clinical stages of pleural effusion or ascitis (Michailova, 2001), the permeability of the pleural and peritoneal mesothelia and of the lymphatic endothelium are presumably still normal. Therefore, we believe the present experimental approach is best suited for following dextran progression into the diaphragmatic lymphatics down an imposed pressure gradient.…”

Section: Discussioncontrasting

confidence: 50%

Regional recruitment of rat diaphragmatic lymphatics in response to increased pleural or peritoneal fluid load

Moriondo¹,

Grimaldi

Sciacca³

et al. 2007

The Journal of Physiology

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The specific role of the diaphragmatic tendinous and muscular tissues in sustaining lymph formation and propulsion in the diaphragm was studied in 24 anaesthetized spontaneously breathing supine rats. Three experimental protocols were used: (a) control; (b) peritoneal ascitis, induced through an intraperitoneal injection of 100 ml kg −1 of iso-oncotic saline; and (c) pleural effusion, induced through an intrapleural injection of 6.6 ml kg −1 saline solution. A group of animals (n = 12) was instrumented to measure the hydraulic transdiaphragmatic pressure gradient between the pleural and peritoneal cavities in the three protocols. In the other group (n = 12), the injected iso-oncotic saline was enriched with 2% fluorescent dextrans (molecular mass = 70 kDa); at 30 min from the injections these animals were suppressed and their diaphragm excised and processed for confocal microscopy analysis. In control conditions, in spite of a favourable peritoneal-to-pleural pressure gradient, the majority of the tracer absorbed into the diaphragmatic lymphatic system converges towards the deeper collecting lymphatic ducts. This suggests that diaphragmatic lymph formation mostly depends upon pressure gradients developing between the serosal cavities and the lymphatic vessel lumen. In addition, the tracer distributes to lymph vessels located in the muscular diaphragmatic tissue, suggesting that active muscle contraction, rather than passive tendon stretch, more efficiently enhances local diaphragmatic lymph flow. Vice versa, a prevailing recruitment of the lymphatics of the tendinous diaphragmatic regions was observed in peritoneal ascitis and pleural effusion, suggesting a functional adaptation of the diaphragmatic network to increased draining requirements.

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“…The peritoneal and pleural surfaces of the diaphragm are both lined by mesothelial cells, and beneath this layer lies a network of lymphatics (42)(43)(44). On the peritoneal side, small openings (stomata) connect the peritoneal cavity with these diaphragmatic lymphatics, and tracer studies have revealed that substances injected intraperitoneally are capable of attaining the lymphatics as well as connective tissue spaces of the diaphragm (42).…”

Section: Preferential Weakness Of the Diaphragmmentioning

confidence: 99%

Preferential Diaphragmatic Weakness during Sustained Pseudomonas aeruginosa Lung Infection

Divangahi

Matecki

Dudley

et al. 2004

Am J Respir Crit Care Med

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Infection with Pseudomonas aeruginosa plays a major role in the pulmonary inflammation and injury associated with cystic fibrosis. Lung inflammation may also lead to more widespread systemic effects on other organs. We tested the following hypotheses: (1) ongoing P. aeruginosa lung infection produces diaphragmatic and limb muscle weakness and (2) such muscle dysfunction is directly correlated with the level of pulmonary inflammation. Chronic bronchopulmonary infection with mucoid P. aeruginosa was induced in C57BL/6 mice. At Day 2 after infection, diaphragmatic force was decreased (37%) only in mice infected with a high dose of 1 x 10(6) cfu, whereas by Day 7 after infection, diaphragmatic force was similarly reduced (36%) even at a fivefold lower inoculating dose. No significant correlations were found between diaphragmatic weakness and pulmonary inflammation, as assessed by the number of neutrophils, macrophages, and lymphocytes in bronchoalveolar lavage fluid. Moreover, in marked contrast to the diaphragm, no effects of P. aeruginosa infection on contractile function were observed in prototypical slow- and fast-twitch hindlimb muscles. We conclude that sustained lung infection with P. aeruginosa induces preferential weakness of the diaphragm, which is not directly correlated with the degree of pulmonary inflammation induced under these conditions.

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Postinflammatory changes of the diaphragmatic stomata

Cited by 18 publications

References 33 publications

Mesothelial lamellar bodies in norm and experimental conditions. Transmission and scanning electron microscopic observations on the peritoneum, pleura and pericardium

Mesothelial lamellar bodies in norm and experimental conditions. Transmission and scanning electron microscopic observations on the peritoneum, pleura and pericardium

Regional recruitment of rat diaphragmatic lymphatics in response to increased pleural or peritoneal fluid load

Preferential Diaphragmatic Weakness during Sustained Pseudomonas aeruginosa Lung Infection

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