scholarly journals Mechanical ventilation-induced alterations of intracellular surfactant pool and blood–gas barrier in healthy and pre-injured lungs

2020 ◽  
Author(s):  
Jeanne-Marie Krischer ◽  
Karolin Albert ◽  
Alexander Pfaffenroth ◽  
Elena Lopez-Rodriguez ◽  
Clemens Ruppert ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Blood Gas ◽  
Control Groups ◽  
Gas Barrier ◽  
Alveolar Epithelial ◽  
Alveolar Surfactant ◽  
Healthy Control ◽  
Mean Size ◽  
The Mean ◽  
Injury Progression

AbstractMechanical ventilation triggers the manifestation of lung injury and pre-injured lungs are more susceptible. Ventilation-induced abnormalities of alveolar surfactant are involved in injury progression. The effects of mechanical ventilation on the surfactant system might be different in healthy compared to pre-injured lungs. In the present study, we investigated the effects of different positive end-expiratory pressure (PEEP) ventilations on the structure of the blood–gas barrier, the ultrastructure of alveolar epithelial type II (AE2) cells and the intracellular surfactant pool (= lamellar bodies, LB). Rats were randomized into bleomycin-pre-injured or healthy control groups. One day later, rats were either not ventilated, or ventilated with PEEP = 1 or 5 cmH2O and a tidal volume of 10 ml/kg bodyweight for 3 h. Left lungs were subjected to design-based stereology, right lungs to measurements of surfactant proteins (SP−) B and C expression. In pre-injured lungs without ventilation, the expression of SP-C was reduced by bleomycin; while, there were fewer and larger LB compared to healthy lungs. PEEP = 1 cmH2O ventilation of bleomycin-injured lungs was linked with the thickest blood–gas barrier due to increased septal interstitial volumes. In healthy lungs, increasing PEEP levels reduced mean AE2 cell size and volume of LB per AE2 cell; while in pre-injured lungs, volumes of AE2 cells and LB per cell remained stable across PEEPs. Instead, in pre-injured lungs, increasing PEEP levels increased the number and decreased the mean size of LB. In conclusion, mechanical ventilation-induced alterations in LB ultrastructure differ between healthy and pre-injured lungs. PEEP = 1 cmH2O but not PEEP = 5 cmH2O ventilation aggravated septal interstitial abnormalities after bleomycin challenge.

Maximal rowing has an acute effect on the blood-gas barrier in elite athletes

2003 ◽  
Vol 95 (3) ◽  
pp. 1076-1082 ◽  
Author(s):  
Birgitte Hanel ◽  
Ian Law ◽  
Jann Mortensen
Keyword(s):  
Acute Effect ◽  
Diethylenetriaminepentaacetic Acid ◽  
Blood Gas ◽  
Ventilation Distribution ◽  
Interstitial Edema ◽  
Gas Barrier ◽  
Alveolar Epithelial ◽  
Pulmonary Clearance ◽  
Elite Rowers ◽  
Initial Measurement

The purpose of the study was to evaluate the effects of maximal exercise on the integrity of the alveolar epithelial membrane using the clearance rate of aerosolized 99mTc-labeled diethylenetriaminepentaacetic acid as an index for the permeability of the lung blood-gas barrier. Ten elite rowers (24.3 ± 4.6 yr of age) completed two 20-min pulmonary clearance measurements immediately after and 2 h after 6 min of all-out rowing (initial and late, respectively). All subjects participated in resting control measurements on a separate day. For each 20-min measurement, lung clearance was calculated for 0-7 and 10-20 min. Furthermore, scintigrams were processed from the initial and late measurements of diethylenetriaminepentaacetic acid clearance. Compared with control levels, the pulmonary clearance measurement after rowing was increased from 1.2 ± 0.5 to 2.4 ± 1.0%/min (SD) at 0-7 min ( P < 0.01) and from 0.8 ± 0.3 to 1.5 ± 0.4%/min at 10-20 min ( P < 0.0005), returning to resting levels within 2 h. In 6 of 10 subjects, ventilation distribution on the lung scintigrams was inhomogeneous at the initial measurement. The study demonstrates an acute increased pulmonary clearance after maximal rowing. The ventilation defects identified on the lung scintigrams may represent transient interstitial edema secondary to increased blood-gas barrier permeability induced by mechanical stress.

Allometry of the mammalian intracellular pulmonary surfactant system

2010 ◽  
Vol 109 (6) ◽  
pp. 1662-1669 ◽  
Author(s):  
André Wirkes ◽  
Kristina Jung ◽  
Matthias Ochs ◽  
Christian Mühlfeld
Keyword(s):  
Surface Area ◽  
Pulmonary Surfactant ◽  
Human Lung ◽  
Mammalian Species ◽  
Weighted Mean ◽  
Electron Microscopic ◽  
Alveolar Epithelial ◽  
Interspecific Variations ◽  
Mean Size ◽  
The Mean

Alveolar epithelial (AE) surface area is closely correlated with body mass (BM) in mammals. The AE is covered by a surfactant layer produced by alveolar epithelial type II (AE2) cells. We hypothesized that the total number of AE2 cells and the volume of intracellular surfactant-storing lamellar bodies (Lb) are correlated with BM with a similar slope as AE surface area. We used light and electron microscopic stereology to estimate the number and mean volume of AE2 cells and the total volume of Lb in 12 mammalian species ranging from 2 to 3 g (Etruscan shrew) to 400–500 kg (horse) BM. The mean size of Lb was evaluated using the volume-weighted mean volume and the volume-to-surface ratio of Lb. The mean volume of AE2 cells was 500–600 μm3 in most species, but was higher in Etruscan shrew, guinea pig, and human lung. The mean volume of Lb per AE2 cell was 80–100 μm3 in most species, with the same exceptions as above. However, the total number of AE2 cells and the total volume of Lb were closely correlated with BM and exhibited an allometric relationship similar to the slope of AE surface area. The mean size of Lb was similar in all investigated species. In conclusion, the mean volume of AE2 cells and their Lb are independent of BM but show some interspecific variations. The adaptation of the intracellular surfactant pool size to BM is obtained by the variation of the number of AE2 cells in the lung.

scholarly journals Tear Osmolarity Changes Following External and Trans-Canalicular Dacryocystorhinostomy in Primary Acquired Nasolacrimal Duct Obstruction

2021 ◽  
Author(s):  
Ceren Gurez ◽  
Şenay Aşık Nacaroğlu ◽  
Ahu Yılmaz
Keyword(s):  
Nasolacrimal Duct ◽  
Control Group ◽  
Control Groups ◽  
External Group ◽  
Healthy Control ◽  
External Dacryocystorhinostomy ◽  
The Mean ◽  
Group 2 ◽  
And Control ◽  
Group 1

Abstract Purpose: The aim of this study is to evaluate the tear osmolarity(TO) in patients with epiphora caused by primary acquired nasolacrimal-duct obstructions(PANDOs), before and one month after an external dacryocystorhinostomy(E-DCR) and trans-canalicular laser-assisted endoscopic dacryocystorhinostomy(TLA-DCR).Material-Methods: Twenty eyes of 21 patients(16 women, 5 men) who suffered from epiphora and, 20 healthy eyes of the same subjects were included in this study. External(Group 1) or laser-assisted(Group 2) DCR were applied to all patients with PANDO.Results: The mean age of the subjects was 60.09±8.46 in Group 1, 57.50±9.41 in Group 2 and, 55.13±9.38 in healthy control subjects. The mean period for complaints of epiphora was 1.9±0.7 years. Nasolacrimal duct irrigation was successful in all patients at the first-month visit after surgery. Group 1 had a mean TO of 284.16±12.43 mOsm/l and, Group 2 had 286.70±10.46 mOsm/l before DCR, and this increased to 295.75±5.86 mOsm/l and, 298.70±8.76 mOsm/l one month after DCR, respectively. Preoperative TO values in both groups were significant hypoosmolar compared with the control group (292.27±9.65 mOsm/l). No significant differences were detected between postoperative and control group TO values.Conclusion: We found no significant osmolarity changes between surgery and control groups.

scholarly journals AB0055 SOLUBLE TREM-1 LEVELS IN FAMILIAL MEDITERRANEAN FEVER RELATED AA-AMYLOIDOSIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1329.2-1330
Author(s):  
S. Ugurlu ◽  
B. H. Egeli ◽  
I. M. Bolayirli ◽  
H. Ozdogan
Keyword(s):  
Familial Mediterranean Fever ◽  
Demographic Data ◽  
Enzyme Linked Immunosorbent Assay ◽  
Aa Amyloidosis ◽  
Control Groups ◽  
Tertiary Center ◽  
Healthy Control ◽  
Mediterranean Fever ◽  
The Mean

Background:Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) is a monocyte and neutrophil receptor functioning in innate immunity. TREM-1 produces proinflammatory cytokines and serves for neutrophil degranulation. TREM-1 activity is well known in the pathogenesis of sepsis; hence it can be also present in autoinflammatory diseases such as the most common monogenic one, Familial Mediterranean Fever (FMF).Objectives:The objective of this study is to measure soluble TREM-1 (sTREM-1) activity in severe FMF cases complicated with systemic AA-Amyloidosis.Methods:The cohort of the study includes regularly followed FMF related AA-Amyloidosis patients in a tertiary center outpatient rheumatology clinic. Soluble TREM-1 levels were measured using enzyme-linked immunosorbent assay (ELISA). In addition, demographic data, renal function tests, acute phase reactants, and medical prescription history was also noted and analyzed. None of the FMF diagnosed patients had an attack during the collection of the blood samples.Results:The patients were categorized into 4 groups: FMF related AA-Amyloidosis patients (A(+) FMF(+)), FMF unrelated AA-Amyloidosis (FMF(-) A(+)), FMF patients without Amyloidosis diagnosis (FMF(+) A (-)), and healthy controls (HC). The mean ages, TREM-1, C - reactive protein (CRP), and Creatinine levels of each group are shown in Table 1. TREM-1 levels were found to be significantly higher in A(+) FMF(+) group than FMF(+) A (-), and healthy control groups (p= 0.001 and 0.002). Nevertheless, this difference was not found in between A(+) FMF(+) and FMF(-) A(+) (p= 0.447). In addition, the TREM-1 levels of FMF(+) A (-), and healthy control groups were not different (0.532). In A(+) FMF(+) group, 36 patients used colchicine with the mean dose of 1.9±0.8 mg/day, 14 patients used anakinra, and 9 patients used canakinumab. In FMF(+) A (-) group all 20 patients used colchicine with the mean dose of 2.8±0.9 mg/day, 1 patient used anakinra, and 2 patients used canakinumab.Table 1.Clinical Features of Patients and TREM-1 levelsA(+) FMF(+)(n= 42)FMF(-) A(+)(n=5)FMF(+) A(-)(n=20)HC(n=20)Age43.9±12.954.8±1935.3±9.6435.4±6.57TREM-1735.3±566.51247.1±1349.2414.3±142.3439.2±104.6CRP11.1±14.251.3±98.325.8±541.8±1.7Creatinine1.6±1.83.28±4.170.7±0.150.7±0.15Conclusion:In conclusion, TREM-1 is a proinflammatory marker found significantly high in AA-amyloidosis patients regardless of their FMF diagnosis. TREM-1 may be useful in AA-amyloidosis follow-up and early diagnosis since currently there is a deficit of an early diagnostic marker of amyloidosis. This study is a cross-sectional one so it is hard to reach a conclusion on the effectiveness of TREM-1 during regular FMF follow-up for the secondary prevention of amyloidosis. However, the sensitivity of TREM-1 as a marker cannot be denied in amyloidosis.Disclosure of Interests:None declared

Effect of reducing alveolar surface tension on stress failure in pulmonary capillaries

1995 ◽  
Vol 79 (6) ◽  
pp. 2114-2121 ◽  
Author(s):  
Y. Namba ◽  
S. S. Kurdak ◽  
Z. Fu ◽  
O. Mathieu-Costello ◽  
J. B. West
Keyword(s):  
Surface Tension ◽  
Autologous Blood ◽  
Outer Boundary ◽  
Transmural Pressure ◽  
Basement Membranes ◽  
Blood Gas ◽  
Gas Barrier ◽  
Alveolar Epithelial ◽  
Pulmonary Capillaries ◽  
Alveolar Surface

We previously showed that when pulmonary capillaries are exposed to high transmural pressures, stress failure of the blood-gas barrier occurs. It has been suggested that the surface tension of the alveolar lining layer may protect against stress failure because at high transmural pressures the capillaries bulge into the alveolar spaces. To test this hypothesis, we abolished the gas-liquid surface tension of the alveoli by filling rabbit lungs with normal saline. The lungs were then perfused at capillary transmural pressures of 32.5 or 52.5 cmH2O for 1 min with autologous blood, the blood was washed out with a saline-dextran mixture (3 min), and the lungs were fixed for electron microscopy with buffered glutaraldehyde; all perfusions were done at the same pressure. The frequency of breaks was measured in the capillary endothelial layer, alveolar epithelial layer, and basement membranes, and the data were compared with those in air-filled lungs at the same capillary transmural pressure and lung volume. We found that the frequency of breaks in the endothelium was not significantly different between air and saline filling and that there were fewer breaks in the outer boundary of the epithelial cells. By contrast, after saline filling, a larger number of breaks were seen in the inner boundary of the epithelium. The frequency of disruptions of the inner boundary of the epithelium was closely correlated with the volume of edema fluid collected at the trachea during the perfusion. These breaks in the inner boundary of the epithelium had not previously been seen in air-filled lungs exposed to the same pressures. The results suggest that abolishing the surface tension of the alveolar lining layer removes support from parts of the blood-gas barrier when the capillaries are subjected to a high transmural pressure but that not all portions of the barrier are subjected to the same forces.

Ultrastructural appearances of pulmonary capillaries at high transmural pressures

1991 ◽  
Vol 71 (2) ◽  
pp. 573-582 ◽  
Author(s):  
K. Tsukimoto ◽  
O. Mathieu-Costello ◽  
R. Prediletto ◽  
A. R. Elliott ◽  
J. B. West
Keyword(s):  
Autologous Blood ◽  
Alveolar Epithelium ◽  
Basement Membranes ◽  
Capillary Endothelium ◽  
Blood Gas ◽  
Gas Barrier ◽  
Pulmonary Capillaries ◽  
The Mean ◽  
Cell Lining

Electronmicroscopic appearances of pulmonary capillaries were studied in rabbit lungs perfused in situ when the capillary transmural pressure (Ptm) was systematically raised from 12.5 to 72.5 +/- 2.5 cmH2O. The animals were anesthetized and exsanguinated, and after the chest was opened, the pulmonary artery and left atrium were cannulated and attached to reservoirs. The lungs were perfused with autologous blood for 1 min, and this was followed by saline-dextran and then buffered glutaraldehyde to fix the lungs for electron microscopy. Normal appearances were seen at 12.5 cmH2O Ptm. At 52.5 and 72.5 cmH2O Ptm, striking discontinuities of the capillary endothelium and alveolar epithelium were seen. A few disruptions were seen at 32.5 cmH2O Ptm (mostly in one animal), but the number of breaks per millimeter cell lining increased markedly up to 72.5 cmH20 Ptm, where the mean frequency was 27.8 +/- 8.6 and 13.6 +/- 1.4 (SE) breaks/mm for endothelium and epithelium, respectively. In some instances, all layers of the blood-gas barrier were disrupted and erythrocytes could be seen moving into the alveolar spaces. In about half the endothelial and epithelial breaks, the basement membranes remained intact. The average break lengths for both endothelium and epithelium did not change significantly with pressure. The width of the blood-gas barrier increased at 52.5 and 72.5 cmH2O Ptm as a result of widening of the interstitium caused by edema. The cause of the disruptions is believed to be stress failure of the capillary wall. The results show that high capillary hydrostatic pressures cause major changes in the ultrastructure of the walls of the capillaries, leading to a high-permeability form of edema.

Vitamin D Treatment in Patients with Hashimoto’s Thyroiditis may Decrease the Development of Hypothyroidism

2016 ◽  
Vol 86 (1-2) ◽  
pp. 9-17 ◽  
Author(s):  
Bekir Ucan ◽  
Mustafa Sahin ◽  
Muyesser Sayki Arslan ◽  
Nujen Colak Bozkurt ◽  
Muhammed Kizilgul ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Hashimoto’S Thyroiditis ◽  
Healthy Control Group ◽  
Hashimoto's Thyroiditis ◽  
Control Group ◽  
Endocrine Society ◽  
Thyroid Autoantibody ◽  
Healthy Control ◽  
The Mean

Abstract.The relationship between Hashimoto’s thyroiditis and vitamin D has been demonstrated in several studies. The aim of the present study was to evaluate vitamin D concentrations in patients with Hashimoto’s thyroiditis, the effect of vitamin D therapy on the course of disease, and to determine changes in thyroid autoantibody status and cardiovascular risk after vitamin D therapy. We included 75 patients with Hashimoto’s thyroiditis and 43 healthy individuals. Vitamin D deficiency is defined as a 25-hydroxy vitamin D (25(OH)D3) concentration less than 20ng/mL. Vitamin D deficient patients were given 50.000 units of 25(OH)D3 weekly for eight weeks in accordance with the Endocrine Society guidelines. All evaluations were repeated after 2 months of treatment. Patients with Hashimoto’s thyroiditis had significantly lower vitamin D concentrations compared with the controls (9.37±0.69 ng/mL vs 11.95±1.01 ng/mL, p < 0.05, respectively). Thyroid autoantibodies were significantly decreased by vitamin D replacement treatment in patients with euthyroid Hashimoto’s thyroiditis. Also, HDL cholesterol concentrations improved in the euthyroid Hashimoto group after treatment. The mean free thyroxine (fT4) concentrations were 0.89±0.02 ng/dL in patients with Hashimoto’s thyroiditis and 1.07±0.03 ng/dL in the healthy control group (p < 0.001). The mean thyroid volumes were 7.71±0.44 mL in patients with Hashimoto’s thyroiditis and 5.46±0.63 mL in the healthy control group (p < 0.01). Vitamin D deficiency is frequent in Hashimoto’s thyroiditis and treatment of patients with this condition with Vitamin D may slow down the course of development of hypothyroidism and also decrease cardiovascular risks in these patients. Vitamin D measurement and replacement may be critical in these patients.

The Clinical Usefulness of the Platelet Aggregation Test for the Diagnosis of Heparin-Induced Thrombocytopenia

1993 ◽  
Vol 69 (04) ◽  
pp. 344-350 ◽  
Author(s):  
B H Chong ◽  
J Burgess ◽  
F Ismail
Keyword(s):  
Platelet Aggregation ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Point System ◽  
Control Groups ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Concentration ◽  
Release Test ◽  
The Mean ◽  
Normal Controls

SummaryThe platelet aggregation test is widely used for the diagnosis of heparin-induced thrombocytopenia (HIT), a potentially serious complication of heparin therapy. We have evaluated its sensitivity and specificity in comparison with those of the 14C-serotonin release test. The sensitivity of the platelet aggregation test was found to vary with the heparin concentration and the donor of the platelets used in the test. The optimal heparin concentrations were between 0.1 and 1.0 U/ml. Using these heparin concentrations, the mean sensitivity varied from 39% (with the least reactive platelets) to 81% (with the most reactive platelets). In comparison, the sensitivity of the release test ranged from 65% to 94%. The specificities of the platelet aggregation test were 82%, 90% and 100% for the following control groups: (1) non-thrombocytopenic patients given heparin, (2) patients with thrombocytopenia due to other causes, and (3) normal controls not given heparin, respectively. The corresponding specificities for the release test was 94%, 90% and 100%. The specificities can be further increased to 100% for all controls with the adoption of a two-point system which defines a positive result as one in which platelet aggregation occurs with a low heparin concentration (0.5 U/ml) but not with 100 U heparin/ml. For optimal results, a two-point platelet aggregation test should be performed with heparin concentrations of 0.5 and 100 U/ml and using platelets of more reactive donors.

The Quantitation of Platelet Aggregation Induced by Four Compounds: A Study in Relation to Myocardial Infarction

1966 ◽  
Vol 16 (03/04) ◽  
pp. 752-767 ◽  
Author(s):  
J. R O’Brien ◽  
F. C Path ◽  
Joan B. Heywood ◽  
J. A Heady
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Myocardial Infarct ◽  
Control Groups ◽  
The Mean ◽  
Platelet Shape

SummaryMethods for measuring and comparing day to day differences in the response of platelet aggregation in platelet-rich plasma to added ADP, 5-H.T., adrenaline and collagen are reported. Platelet aggregation induced by ADP, 5-H.T. and adrenaline was studied in patients with acute myocardial infarction and in others 3 months to 5 years after an infarct; some were receiving anti-coagulants and others not: these three groups were compared with three control groups. The mean platelet shape was rounder and the response to ADP and to 5-H.T. and one parameter of the response to adrenaline was significantly greater in all groups of patients with myocardial infarct taken together than in the controls. The platelet-rich plasma from patients with recent infarction were most responsive to ADP and 5-H.T. immediately after the infarct. Anti-coagulants had no effect on these tests. However, there was wide variation within the individuals and much overlap between groups, and these tests can only reliably distinguish between groups and not between individuals. The significance of these findings is discussed.

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