scholarly journals Effect of positive end-expiratory pressure on alveolar capillary perfusion

1988 ◽  
Vol 95 (4) ◽  
pp. 712-716 ◽  
Author(s):  
Gary F. Nieman ◽  
Andrew M. Paskanik ◽  
Carl E. Bredenberg
Keyword(s):  
Positive End Expiratory Pressure ◽  
Capillary Perfusion ◽  
Alveolar Capillary

Blood flow switching among pulmonary capillaries is decreased during high hematocrit

2004 ◽  
Vol 97 (2) ◽  
pp. 522-526 ◽  
Author(s):  
William A. Baumgartner ◽  
Amanda J. Peterson ◽  
Robert G. Presson ◽  
Nobuhiro Tanabe ◽  
Eric M. Jaryszak ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Average Distance ◽  
Substantial Part ◽  
Alveolar Wall ◽  
Capillary Perfusion ◽  
Capillary Networks ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Alveolar Capillary

Pulmonary capillary perfusion within a single alveolar wall continually switches among segments, even when large-vessel hemodynamics are constant. The mechanism is unknown. We hypothesize that the continually varying size of plasma gaps between individual red blood cells affects the likelihood of capillary segment closure and the probability of cells changing directions at the next capillary junction. We assumed that an increase in hematocrit would decrease the average distance between red blood cells, thereby decreasing the switching at each capillary junction. To test this idea, we observed 26 individual alveolar capillary networks by using videomicroscopy of excised canine lung lobes that were perfused first at normal hematocrit (31–43%) and then at increased hematocrit (51–62%). The number of switches decreased by 38% during increased hematocrit ( P < 0.01). These results support the idea that a substantial part of flow switching among pulmonary capillaries is caused by the particulate nature of blood passing through a complex network of tubes with continuously varying hematocrit.

SUPRAPHYSIOLOGIC TIDAL VENTILATION DOES NOT DECREASE ALVEOLAR CAPILLARY PERFUSION

1999 ◽  
Vol 27 (Supplement) ◽  
pp. A104
Author(s):  
Adam S Becker ◽  
Ulysse G McCann ◽  
Gary F Nieman ◽  
Brian J Park ◽  
Andrew M Paskanik ◽  
...  
Keyword(s):  
Capillary Perfusion ◽  
Tidal Ventilation ◽  
Alveolar Capillary

Alveolar function following surfactant deactivation

1981 ◽  
Vol 51 (4) ◽  
pp. 895-904 ◽  
Author(s):  
G. F. Nieman ◽  
C. E. Bredenberg ◽  
W. R. Clark ◽  
N. R. West
Keyword(s):  
Normal Saline ◽  
Tween 20 ◽  
Partial Recovery ◽  
Marked Variation ◽  
Capillary Perfusion ◽  
Surfactant Activity ◽  
Alveolar Stability ◽  
Ventilation Perfusion Ratio ◽  
Alveolar Capillary

In vivo cinemicroscopic studies of subpleural alveoli were conducted in dogs for 4 h after pulmonary lavage with 5% Tween 20 and after lavage with normal saline. Saline-lavaged alveoli showed little change in alveolar size during tidal ventilation, whereas Tween lavage resulted both in alveolar recruitment and marked variation in alveolar size from end expiration to peak inspiration, with total collapse frequently occurring by end expiration. Following Tween, alveolar stability decreased, but alveolar capillary perfusion increased. Marked recovery of stability by 4 h was noted in most alveoli. Wilhelmy balance studies on lung extracts showed a decrease in surfactant function 30 min after Tween and a partial recovery of surfactant activity after 4 h. This study provides in vivo evidence that normal surfactant function is critical to alveolar stability and that alveolar stability is markedly restored 4 h after acute deactivation or displacement by Tween. Surfactant deactivation and loss of alveolar stability are associated with increased alveolar capillary perfusion creating significant ventilation-perfusion ratio abnormalities.

Leukocyte effects on microcirculation in artificially perfused rat lungs

1989 ◽  
Vol 256 (4) ◽  
pp. H1117-H1126 ◽  
Author(s):  
M. Braide ◽  
H. Sonander ◽  
B. R. Johansson ◽  
U. Bagge
Keyword(s):  
Mononuclear Cells ◽  
Low Flow ◽  
Capillary Perfusion ◽  
Tracer Gas ◽  
Capillary Networks ◽  
Rat Lungs ◽  
Pulmonary Capillaries ◽  
A Cell ◽  
Complete Exclusion ◽  
Alveolar Capillary

Evidence indicates that leukocyte microvascular flow obstructions play an important role in no-reflow phenomena after ischemia and that leukocytes may cause significant disturbances of capillary perfusion in low flow states. In the present study, a cell-free colloid perfusion (20-60 ml.kg-1.min-1) of isolated ventilated rat lungs was interrupted by bolus injections of leukocytes in varying numbers. Leukocyte effects on flow resistance, tracer gas exchange, and micromorphology were evaluated. The vast majority of the infused leukocytes remained trapped in the lungs after repeated infusions regardless of the number of leukocytes given, although leukocyte trapping decreased at the higher flow rates. The functional and morphological analyses showed that the polymorphonuclear granulocytes had a greater tendency than the mononuclear cells to become permanently trapped in the pulmonary capillaries. The tracer gas analyses indicated that the trapped leukocytes were scattered in the alveolar capillary networks and did not cause complete exclusion of flow from the affected alveoli. This was probably due to the anatomy of the pulmonary microvasculature, with its abundancy in interconnecting pathways.

Stability of alveolar capillary opening pressures

1994 ◽  
Vol 77 (4) ◽  
pp. 1630-1637 ◽  
Author(s):  
R. G. Presson ◽  
O. Okada ◽  
C. C. Hanger ◽  
P. S. Godbey ◽  
J. A. Graham ◽  
...  
Keyword(s):  
Video Microscopy ◽  
Capillary Perfusion ◽  
Experimental Conditions ◽  
Pump Flow ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
The Stability ◽  
Alveolar Capillary

Little is known about the stability of the process by which pulmonary capillaries open. To investigate this process, pulmonary capillary perfusion patterns in isolated pump-perfused canine lobes were studied using video microscopy. After pump flow was set to perfuse one-half of the capillaries, the pump was turned off and all of the capillaries emptied. Turning the pump back on reopened the capillaries. The on-off cycle was repeated six times. If the same capillaries were perfused during each observation, it would demonstrate that there were stable and significant differences between individual capillary opening pressures, causing consistent recruitment of those capillaries with the lowest opening pressures. Alternatively, variable perfusion patterns would result if capillary opening pressures changed between observations, if the differences in opening pressures between capillary segments were negligible, or if experimental conditions changed between cycles. The perfusion pattern was more reproducible than expected by chance alone, which indicated the existence of stable differences among alveolar capillary opening pressures.

Ultrastructural Studies of Bovine Respiratory Disease Complex

1975 ◽  
Vol 33 ◽  
pp. 428-429
Author(s):  
James C.S. Kim
Keyword(s):  
Michigan State University ◽  
State University ◽  
Diagnostic Laboratory ◽  
Ultrastructural Studies ◽  
Bovine Respiratory Diseases ◽  
Etiologic Agents ◽  
Diagnostic Difficulties ◽  
The Subject ◽  
Capillary Walls ◽  
Alveolar Capillary

Bovine respiratory diseases cause serious economic loses and present diagnostic difficulties due to the variety of etiologic agents, predisposing conditions, parasites, viruses, bacteria and mycoplasma, and may be multiple or complicated. Several agents which have been isolated from the abnormal lungs are still the subject of controversy and uncertainty. These include adenoviruses, rhinoviruses, syncytial viruses, herpesviruses, picornaviruses, mycoplasma, chlamydiae and Haemophilus somnus.Previously, we have studied four typical cases of bovine pneumonia obtained from the Michigan State University Veterinary Diagnostic Laboratory to elucidate this complex syndrome by electron microscopy. More recently, additional cases examined reveal electron opaque immune deposits which were demonstrable on the alveolar capillary walls, laminae of alveolar capillaries, subenthothelium and interstitium in four out of 10 cases. In other tissue collected, unlike other previous studies, bacterial organisms have been found in association with acute suppurative bronchopneumonia.

Thrombin Stimulated Platelet Accumulation on Protein Coated Glass Capillaries: Role of Adhesive Platelet α-Granule Proteins

1989 ◽  
Vol 62 (03) ◽  
pp. 989-995 ◽  
Author(s):  
Juliette N Mulvihill ◽  
J Andrew Davies ◽  
Florence Toti ◽  
Jean-Marie Freyssinet ◽  
Jean-Pierre Cazenave
Keyword(s):  
Human Platelets ◽  
Capillary Perfusion ◽  
Coated Glass ◽  
Bovine Collagen ◽  
Glass Capillaries ◽  
Human Thrombin ◽  
Platelet Accumulation ◽  
Granule Proteins ◽  
Von Willebrand

SummaryThe generation of trace amounts of thrombin at artificial surfaces in contact with blood is likely to be a contributing factor in thrombosis on biomaterials. Using an in vitro capillary perfusion system, platelet accumulation on glass surfaces, uncoated or precoated with purified bovine collagen or human plasma proteins, was determined in the presence or absence of preadsorbed purified human thrombin. Static adsorption for 15 min at 22° C from solutions of thrombin 100 NIH units (33 μg)/ml gave surface concentrations in the range 0.019-0.101 μg/cm2. Protein coated capillaries, thrombin treated or untreated, were perfused for 2 min at 37° C with suspensions of washed 111In-labeled human platelets in Tyrode's-albumin buffer containing 40% washed red blood cells, under conditions of controlled, non pulsatile laminar flow (50 s−1 or 2,000 s−1). Platelet accumulation was increased in the presence of surface adsorbed thrombin on uncoated and albumin or fibrinogen coated glass but little affected on fibronectin or collagen coated glass. On von Willebrand factor (vWF) coated glass, thrombin enhancement was observed only at high shear forces. In experiments using antibodies against human platelet α-granule proteins, thrombin stimulated platelet deposition in uncoated glass capillaries was inhibited at 2,000 s−1 by anti-vWF and to a lesser extent by anti-fibrinogen but not by antithrombospondin antibodies.

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