Vesicular Transport across Pulmonary Capillary Endothelium in the Fluorocarbon Exchange Transfused Rat

2015 ◽  
pp. 59-66
Author(s):  
E. E. Schneeberger
Keyword(s):  
Vesicular Transport ◽  
Capillary Endothelium ◽  
Pulmonary Capillary

scholarly journals Pulmonary Capillary Endothelium-Bound Angiotensin-Converting Enzyme Activity in Acute Lung Injury

Circulation ◽  
2000 ◽  
Vol 102 (16) ◽  
pp. 2011-2018 ◽  
Author(s):  
Stylianos E. Orfanos ◽  
Apostolos Armaganidis ◽  
Constantinos Glynos ◽  
Ekaterini Psevdi ◽  
Panagiotis Kaltsas ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Angiotensin Converting Enzyme ◽  
Capillary Endothelium ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme Activity ◽  
Pulmonary Capillary

A morphometric study of the lungs of different sized bats: correlations between structure and function of the chiropteran lung

1991 ◽  
Vol 333 (1266) ◽  
pp. 31-50 ◽  
Keyword(s):  
Surface Area ◽  
Body Mass ◽  
Lung Volume ◽  
Capillary Blood ◽  
The Body ◽  
Capillary Endothelium ◽  
Diffusing Capacity ◽  
Blood Gas ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Blood

1. The lungs of four species of bats, Phyllostomus hastatus (PH, mean body mass, 98 g), Pteropus lylei (PL,456 g), Pteropus alecto (PA, 667 g), and Pteropus poliocephalus (PP, 928 g) were analysed by morphometric methods. These data increase fivefold the range of body masses for which bat lung data are available, and allow more representative allometric equations to be formulated for bats. 2. Lung volume ranged from 4.9 cm 3 for PH to 39 cm 3 for PP. The volume density of the lung parenchyma (i.e. the volume proportion of the parenchyma in the lung) ranged from 94% in PP to 89% in PH. Of the components of the parenchyma, the alveoli composed 89% and the blood capillaries about 5% . 3. The surface area of the alveoli exceeded that of the blood—gas (tissue) barrier and that of the capillary endothelium whereas the surface area of the red blood cells as well as that of the capillary endothelium was greater than that of the tissue barrier. PH had the thinnest tissue barrier (0.1204 μm) and PP had the thickest (0.3033 μm). 4. The body mass specific volume of the lung, that of the volume of pulmonary capillary blood, the surface area of the blood-gas (tissue) barrier, the diffusing capacity of the tissue barrier, and the total morphometric pulmonary diffusing capacity in PH all substantially exceeded the corresponding values of the pteropid species (i.e. PL, PA and PP). This conforms with the smaller body mass and hence higher unit mass oxygen consumption of PH, a feature reflected in the functionally superior gas exchange performance of its lungs. 5. Morphometrically, the lungs of different species of bats exhibit remarkable differences which cannot always be correlated with body mass, mode of flight and phylogeny. Conclusive explanations of these pulmonary structural disparities in different species of bats must await additional physiological and flight biomechanical studies. 6. While the slope, the scaling factor (b), of the allometric equation fitted to bat lung volume data (b = 0.82) exceeds the value for flight Vo 2max , (b = 0.70), those for the surface area of the blood-gas (tissue) barrier (b = 0.74), the pulmonary capillary blood volume (b = 0.74), and the total morphometric lung diffusing capacity for oxygen (b = 0.69) all correspond closely to the Vo 2max , value. 7 Allometric comparisons of the morphometric pulmonary parameters of bats, birds and non-flying mammals reveal that superiority of the bat lung over that of the non-flying mammal. However, the bat parameters relative to those of non-flying mammals deteriorate towards the higher body size range, because of the generally steeper slopes of the equations for non-flying mammals. Allometric comparisons also reveal that small-size bats have, in general, better adapted lungs than birds of equivalent size but at the higher body mass scale, bats are generally inferior to birds.

Influence of carbon dioxide kinetics on pulmonary carbon dioxide exchange

1993 ◽  
Vol 74 (2) ◽  
pp. 715-721 ◽  
Author(s):  
H. J. Schunemann ◽  
R. A. Klocke
Keyword(s):  
Carbon Dioxide ◽  
Indicator Dilution ◽  
Inert Gas ◽  
Capillary Endothelium ◽  
Carbon Dioxide Exchange ◽  
Pulmonary Capillary ◽  
Dilution Experiments ◽  
Isolated Lungs ◽  
Kinetics Of ◽  
Co2 Excretion

In the absence of erythrocytes, carbonic anhydrase (CA) localized to the pulmonary capillary endothelium catalyzes the dehydration of bicarbonate to CO2. We studied the effects of lung CA and the reactions of CO2 on CO2 excretion in isolated lungs perfused with buffer. In indicator-dilution experiments, recoveries of dissolved CO2 and acetylene (C2H2) in the venous effluent were delayed significantly compared with a vascular indicator because the gases were distributed in both the vascular and alveolar volumes. In a second group of experiments, the kinetics of CO2 excretion were monitored with a plethysmographic method after injection of a bolus containing dissolved CO2 or bicarbonate. Exchange was compared with excretion of dissolved C2H2. The rate of excretion of dissolved CO2 and C2H2 was identical, indicating that CO2 is exchanged in the same manner as an inert gas. When bicarbonate was injected, CO2 excretion lagged behind C2H2 excretion by approximately 0.3 s. Inhibition of lung CA with acetazolamide reduced the quantity of CO2 exchanged to one-fourth of control and decreased the delay in exchange by one-half.

Pulmonary injury in rats following continuous exposure to 60% O2 for 7 days

1981 ◽  
Vol 51 (5) ◽  
pp. 1220-1231 ◽  
Author(s):  
G. Hayatdavoudi ◽  
J. J. O'Neil ◽  
B. E. Barry ◽  
B. A. Freeman ◽  
J. D. Crapo
Keyword(s):  
Lung Compliance ◽  
Capillary Endothelium ◽  
Continuous Exposure ◽  
Pulmonary Injury ◽  
Lung Capacity ◽  
Perivascular Edema ◽  
Air Volume ◽  
Pulmonary Capillary ◽  
Morphometric Analyses ◽  
Glucose 6 Phosphate Dehydrogenase

Morphological, biochemical, and physiological studies were done on rats exposed to 60% O2 for 7 days. This exposure did not induce O2 tolerance but instead caused a significant decrease in survival time of animals subsequently exposed to pure O2. The activity of lung superoxide dismutases and glucose-6-phosphate dehydrogenase were unchanged after exposure to 60% O2. A decrease in lung compliance was suggested by changes in the total lung capacity and in the pressure-volume curves of excised lungs. Ventilation of these animals with large tidal excursion resulted in pulmonary edema. Morphometric analyses revealed a significant decrease in alveolar air volume and an increase in the number of alveolar macrophages. The most significant lesions involved the pulmonary vascular bed. The volume and thickness of the capillary endothelium was decreased. There were focal areas of pericapillary fluid accumulations, and a number of the smaller vessels had perivascular edema. These findings suggest that significant pulmonary injury occurs in rats exposed to 60% O2 and that the primary site of injury is the pulmonary capillary endothelium.

scholarly journals Η επίδραση της χορήγησης αντιπηκτικής αγωγής στην πνευμονική κυκλοφορία ασθενών με σήψη και ασθενών με οξεία πνευμονική βλάβη (ALI)

2013 ◽  
Author(s):  
Αικατερίνη Καζιάνη
Keyword(s):  
Lung Injury ◽  
Angiotensin Converting Enzyme ◽  
Capillary Endothelium ◽  
Converting Enzyme ◽  
Pulmonary Capillary

H σοβαρή σήψη και η σηπτικής αιτιολογίας οξεία πνευμονική βλάβη (Αcute Lung Injury/ARDS) σχετίζονται με σοβαρή ενδοθηλιακή βλάβη, η οποία οδηγεί σε διαταραχή της μικροκυκλοφορίας και εν τέλει σε οργανική δυσλειτουργία. Η ανθρώπινη ενεργοποιημένη πρωτεΐνη C (rhAPC), η οποία χαρακτηρίζεται από ενδοθηλιοπροστατευτική δράση χορηγούταν μέχρι προσφάτως, σύμφωνα με τις διεθνείς οδηγίες του Surviving Sepsis Guidelines ως θεραπεία διάσωσης σε ασθενείς με σοβαρή σήψη. Στη σήψη, η πρώιμη διάγνωση της ενδοθηλιακής δυσλειτουργίας, που αποτελεί δείκτη οργανικής δυσλειτουργίας, θα μπορούσε να συντελέσει στην έγκαιρη θεραπευτική παρέμβαση. Αν και πολυάριθμες κλινικές και βιοχημικές παράμετροι έχουν ελεγχθεί ως πιθανοί βιοδείκτες στη σήψη, κανείς δεν έχει αποδειχθεί αξιόπιστος και κλινικά εύχρηστος. H δραστικότητα του συνδεδεμένου με το πνευμονικό ενδοθήλιο (Pulmonary Capillary Endothelium Bound - PCEB) αγγειομετατρεπτικού ενζύμου (Angiotensin Converting Enzyme - ACE) έχει δειχθεί ότι συνιστά έναν άμεσο και ευαίσθητο δείκτη της πνευμονικής ενδοθηλιακής δυσλειτουργίας, σε οξείες και χρόνιες παθήσεις του πνεύμονα.Στην παρούσα μελέτη εκτιμήθηκε η δραστικότητα του PCEB-ACE σε δεκαεννέα (19) ασθενείς με σηπτικής αιτιολογίας οξεία πνευμονική βλάβη. Με την εφαρμογή της μεθόδου αραίωσης του δείκτη, εκτιμήθηκε ο ποσοστιαίος μεταβολισμός (%Μ) και η υδρόλυση (v) του συνθετικού, βιολογικά μη δραστικού και απολύτως ειδικού υποστρώματος του ACE, 3H-benzoyl-Phe-Ala-Pro (BPAP) στη διάρκεια μιας μόνο διέλευσης από την πνευμονική κυκλοφορία, υπό συνθήκες πρώτης τάξης αντίδρασης, ενώ υπολογίστηκε και ο δείκτης της λειτουργικής τριχοειδικής επιφάνειας (FCSA), πριν και κατά τη διάρκεια της χορήγησης rhAPC. Διαπιστώθηκε σημαντικά μειωμένη δραστικότητα του PCEB=ACE, στους ασθενείς με σηπτικής αιτιολογίας ARDS, ενώ δε φάνηκε αυτή να επηρεάζεται από τη χορήγηση της rhAPC. Επιπλέον, σοβαρότερη διαταραχή στη δραστικότητα του ενζύμου φάνηκε να σχετίζεται με κακή έκβαση (θάνατος στις 28 ημέρες). Οι δείκτες δραστικότητας του ACE ήταν στατιστικά σημαντικά μειωμένοι στους μη επιζήσαντες σε σύγκριση με τους επιζήσαντες (ο %M του BPAP διακυμάνθηκε από 32.7±3.4% στην αρχική μέτρηση έως 25.6±2.9% στο τέλος της μελέτης στους επιζήσαντες, ενώ στους μη επιζήσαντες από 20.8±2.8% έως 15.5±5%, αντίστοιχα (p=0.044), ενώ η υδρόλυση (v) διακυμάνθηκε από 0.41±0.06 στην αρχική μέτρηση έως 0.30±0.04 στο τέλος της μελέτης στους επιζήσαντες, ενώ στους μη επιζήσαντες από 0.24±0.04 σε 0.18±0.06, αντίστοιχα (p=0.049). Συμπερασματικά οι δείκτες της δραστικότητας του PCEB-ACE θα μπορούσαν να χρησιμεύσουν για την πρώιμη ανίχνευση της ενδοθηλιακής δυσλειτουργίας στη σήψη με σκοπό την έγκαιρη θεραπευτική παρέμβαση.

The bloodless rat: a new model for macromolecular transport studies across lung endothelium

1982 ◽  
Vol 242 (5) ◽  
pp. H890-H899
Author(s):  
E. E. Schneeberger ◽  
B. A. Neary
Keyword(s):  
Fold Increase ◽  
Capillary Endothelium ◽  
Numerical Density ◽  
Experimental Conditions ◽  
Rat Serum ◽  
Ether Anesthesia ◽  
Macromolecular Transport ◽  
Transport Studies ◽  
Pulmonary Capillary ◽  
Fluorocarbon Emulsion

To examine the effect of circulating proteins on the passage of intravenously injected native ferritin across pulmonary capillary endothelium, rats were exchange transfused with FC-43 fluorocarbon emulsion (FCE) under ether anesthesia. Protein concentration was reduced to less than 1.1 mg/ml by exchange transfusion, followed by FCE containing 15, 30, or 60 mg/ml of lyophilized rat serum protein (LRSP). Two minutes after ferritin injection lungs were prepared for ultrastructural morphometry. The diameter and numerical density of vesicles remained unchanged under all experimental conditions; however, at 0.6 mg/ml of circulating protein there was a 5- and 10-fold increase, respectively in percent vesicle (%VL) and basement membrane labeling (BML) by ferritin. This was reversible; at 60 mg/ml of circulating protein %VL and BML was indistinguishable from controls. Following a reduction of circulating protein to less than 1.1 mg/ml, the addition of 15 mg/ml LRSP reduced %VL but had no effect on BML. This suggests that in addition to shuttling vesicles there may be a second mechanism for the transport of ferritin, possibly involving transendothelial chains of vesicles.

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