Distribution of diaphragmatic lymphatic stomata

Negrini, Daniela; Mukenge, Sylvain; Fabbro, Massimo Del; Gonano, C.; Miserocchi, G.

doi:10.1152/jappl.1991.70.4.1544

Cited by 65 publications

(53 citation statements)

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“…Subsequent experiments confirmed that there were indeed physical channels existing in the mediastinal pleura of rats, implying that the anatomy of rat mediastinal pleura is different from that of human beings. Although stomas on the costal pleura and the diaphragm have been identified and confirmed previously [15,16] , there was previously no report on stomas on the mediastinal pleura, which is a thin membrane. Through light microscopy, we could observe stomas on the mediastinal pleura, as shown in Figure 7C-7D.…”

Section: Wwwchinapharcom Qin Zh Et Almentioning

confidence: 65%

Intrapleural delivery of mesenchymal stem cells: a novel potential treatment for pleural diseases

Qin

Jian

et al. 2011

Acta Pharmacol Sin

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Aim: To develop a method to deliver mesenchymal stem cells (MSCs) into the pleural cavity for the treatment of pleural diseases. Methods: MSCs were isolated from rat bone marrow of rats and labeled with 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI) or green fluorescent protein (GFP) using a lentiviral vector. Eighteen Sprague-Dawley (SD) rats were inoculated intrapleurally with 1×10 6 MSCs-DAPI. The distribution of the fluorescent cells was observed using fluorescent microscopy for the following 30 d. Another 12 rats inoculated intrapleurally with 1×10 6 MSCs-GFP were observed for 14 d. Results: The isolated cells were typical MSC phenotypes and could differentiate into adipocytes, osteoblasts, and chondroblasts in vitro. Microscopic analysis revealed that the labeled cells adhered to the surface of the pleural cavity. The highest number of the labeled cells was found to be adhered to all specimens from the mediastinal pleura, but no labeled cells were detected in the lung parenchyma or other tissues/organs, such as the liver, kidney, spleen, and mesenterium. Incidentally, stomas were found in the mediastinal pleura. The recovered MSCs-GFP from the pleural cavity retained their ability to adhere and proliferate. Conclusion: We have established a novel method for intrapleural delivery of MSCs. The distribution of intrapleurally delivered MSCs was found to be limited to the pleurae and the pleural cavity, thereby providing us with a new approach to further investigation of the therapeutic roles of MSCs in pleural diseases.

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Section: Wwwchinapharcom Qin Zh Et Almentioning

confidence: 65%

Intrapleural delivery of mesenchymal stem cells: a novel potential treatment for pleural diseases

Qin

Jian

et al. 2011

Acta Pharmacol Sin

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“…The lymphatics provide drainage of the interstitial spaces but also of the pleural cavity, as they open directly on the parietal pleura (lymphatic stomata). Stomata, in rabbits and sheep [8][9][10][11], are frequently grouped in clusters and connect to an extensive network of submesothelial lacunae [11,12]. They range in density from 100 stomata·cm -2 on the intercostal surface to 8,000·cm -2 on the diaphragm and their diameter averages 1 µm (range <1-~40 µm) in size.…”

Section: The Pleural Compartmentsmentioning

confidence: 99%

Physiology and pathophysiology of pleural fluid turnover

Miserocchi¹

1997

Eur Respir J

Self Cite

248

128

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Number 1 in this SeriesA review on pleural space is certainly most welcome, for the simple reason that on opening a textbook of physiology the concepts concerning pleural fluid turnover date back to 1927 [1]. The same comment, in fact, applies in general to microvascular water and solute exchange. This appears particularly misleading, considering the major advances achieved in the field over the last 70 yrs. Around the turn of the 19th century, STARLING and TUBBY [2] interpreted microvascular fluid and solute exchange as resulting from the balance between hydraulic and colloidosmotic pressures. This concept is still valid today, but the complete formulation of transmicrovascular exchange has become much more complex because water crosses biological membranes more easily than large solutes (namely, plasma proteins) do [3]. In fact, different equations describe water and solute fluxes [4].As a result, the general model of transcapillary fluid exchange still taught to students, based on fluid filtration at the arteriolar end of the capillary bed and reabsorption at the venular end, appears rather simplistic. Due to the different permeability to water and solutes, one could predict on a mathematical basis that such a model would lead to a progressive increase in interstitial protein concentration over time [3,4], a condition that cannot be confirmed experimentally.Similarly, the old hypothesis claiming that pleural fluid filters at parietal level and is reabsorbed through the visceral pleura [1] would imply that pleural liquid protein concentration would keep increasing with age, but again there are no indications that this occurs. The existence of partial restriction to the movement of large solutes, compared to that of water molecules, posed scientists the major problem of explaining how interstitial volume and protein concentration are kept fairly steady. Ideologically, this led to re-evaluation of lymphatics as the major route for interstitial fluid drainage. In fact, since lymphatics do not sieve proteins, they leave the interstitial protein concentration unaltered the latter depending only upon the sieving properties of the filtering membrane. Accordingly, the description of interstitial fluid homeostasis under steady state conditions is now being explained as a balance between capillary filtration and lymphatic absorption. Major validation of this model has come from the accumulating experimental data over the past 30 yrs concerning interstitial tissues [4] and serous spaces [5]. Interestingly, since the pioneering, work of STARLING and TUBBY [2] the pleural space has been used as a useful experimental model to study the interaction between microvascular filtration and lymphatic drainage.This article presents an integrated view of pleural fluid turnover, based on data gathered from experimental studies on animals over the last 15 yrs. The situation in man is, unfortunately, still poorly defined; yet, where possible, Under physiological conditions, the lung interstitium and the pleural space behave as function...

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“…During PD, however, only a minor portion (20 to 30%) of the total fluid and solute reabsorption seems to occur by the lymphatics (4 -7). True lymphatic absorption from the PC occurs from the peritoneal tissues and also via the lymphatic lacunae in the diaphragm (22,23). The latter have the ability to remove small particles up to the size of 10 m, thus even erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

Acute Peritoneal Dialysis in Rats Results in a Marked Reduction of Interstitial Colloid Osmotic Pressure

Rosengren

Rippe²,

Tenstad

et al. 2004

Journal of the American Society of Nephrology

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Abstract. The aim of this study was to investigate whether the interstitial colloid osmotic pressure (COP i ) of peritoneum is of importance for peritoneal fluid reabsorption during peritoneal dialysis (PD). For testing this hypothesis, a method to isolate interstitial fluid from the peritoneal membrane and to measure the interstitial COP i in the normal peritoneum and directly after the initiation of PD needed to be developed and validated. Eighteen female rats were anesthetized subcutaneously in the neck region with fentanyl-midazolam (1:1). Nylon wicks were implanted postmortem by means of a plastic catheter in the tissue just underneath the peritoneal surface. The characteristics of this fluid were compared with that isolated from wicks that were implanted in intermuscular spaces in hindlimb muscle and back subcutis. All wicks were removed after 20 min and centrifuged. The wick fluid was collected and analyzed in a colloid osmometer constructed for submicroliter samples, and interstitial fluid COP was compared with that of plasma. PD was initiated by injecting 20 ml of 3.86% glucose-containing PD fluid (Dianeal) into the peritoneal cavity, over a dwell time of 4 h. Control rats received no PD. The ratio of COP i to that of plasma (COP p ) during control was 0.65 Ϯ 0.05 in peritoneum, 0.53 Ϯ 0.04 in muscle, and 0.59 Ϯ 0.05 in skin. After a PD dwell, the ratio was 0.29 Ϯ 0.03 in peritoneum, 0.54 Ϯ 0.08 in muscle, and 0.41 Ϯ 0.06 in skin. Thus, the COP ratio in peritoneum fell by 55% (P ϭ 0.014) and in skin by 30% (P ϭ 0.03), whereas the COP ratio in muscle was unchanged. The results suggest that acute PD results in a marked fall of the COP i in the peritoneal membrane, shifting the Starling equilibrium toward an absorptive state. The effect was restricted to the peritoneal membrane and, to some extent, the skin. It is speculated that the increase in peritoneal hydrostatic pressure after PD causes an increase in interstitial tissue volume, with primarily a dilution of interstitial colloids.

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Distribution of diaphragmatic lymphatic stomata

Cited by 65 publications

References 0 publications

Intrapleural delivery of mesenchymal stem cells: a novel potential treatment for pleural diseases

Intrapleural delivery of mesenchymal stem cells: a novel potential treatment for pleural diseases

Physiology and pathophysiology of pleural fluid turnover

Acute Peritoneal Dialysis in Rats Results in a Marked Reduction of Interstitial Colloid Osmotic Pressure

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