New Isolated Lung Method

1967 ◽  
Vol 8 (6) ◽  
pp. 736-736
Author(s):  
C. Heymans ◽  
A. Delaunois
Keyword(s):  
1979 ◽  
Vol 47 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
D. S. Simon ◽  
J. F. Murray ◽  
N. C. Staub

We evaluated the attenuation of the 122 keV gamma ray of cobalt-57 across the thorax of anesthetized dogs as a method for following the time course of lung water changes in acute pulmonary edema induced by either increased microvascular permeability or increased microvascular hydrostatic pressure. The gamma rays traversed the thorax centered on the seventh rib laterally where the lung mass in the beam path was greatest. Calibration measurements in isolated lung lobes demonstrated the high sensitivity and inherent accuracy of the method over a wide range of lung water contents. In control dogs reproducibility averaged +/-3%. Increased permeability edema led to large rapid increases in the transthoracic gamma ray attenuation (TGA), while increased pressure caused an immediate, modest increase in TGA (vascular congestion) followed by a slow further increase over 2 h. There was a fairly good correlation between the increase in extravascular lung water and the change in TGA. The method is simple, safe, and noninvasive and appears to be useful for following the time course of lung water accumulation in generalized lung edema in anesthetized animals.


1989 ◽  
Vol 257 (2) ◽  
pp. H415-H422 ◽  
Author(s):  
B. R. Walker ◽  
J. Haynes ◽  
H. L. Wang ◽  
N. F. Voelkel

Experiments were performed to determine the pulmonary vascular responses to exogenous or endogenous arginine vasopressin (AVP) in rats. Both in vitro and in vivo approaches were used to examine the direct pulmonary vasoactive properties of AVP and how those properties affect pulmonary hemodynamics in the intact animal. In conscious, unrestrained rats, constant infusion of AVP (4.0 mU.kg-1.min-1 iv) resulted in a fall in mean pulmonary artery pressure (PAP), although systemic pressure was increased. Coincident with the fall in PAP were similar reductions in cardiac output and heart rate. Similarly, bolus administration of AVP reduced PAP, and this effect was augmented during hypoxia. Another series of experiments examined the effect of endogenous AVP released by arterial hypoxemia on pulmonary hemodynamics in conscious rats. Administration of a specific V1-vasopressinergic antagonist had no effect on the PAP response to hypoxia; however, systemic resistance tended to fall following V1-antagonism. To determine the vasoactive properties of AVP independent of these changes in blood flow, a series of experiments were performed on isolated, perfused rat lungs. Injection of 25, 200, or 2,000 mU of AVP into the circulation of the isolated lung was without effect under normoxic conditions. In contrast, 25 mU AVP elicited reproducible pulmonary vasodilation when injected during ongoing hypoxic pulmonary vasoconstriction. This vasodilatory response was unaffected by meclofenamate or by the platelet-activating factor receptor antagonist SRI 63-441, but was blocked by a specific V1-vasopressinergic antagonist. We conclude that although AVP exerts profound systemic vasoconstriction, the pulmonary circulation appears relatively unaffected by exogenous or endogenous AVP in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 93 (4) ◽  
pp. 791-802 ◽  
Author(s):  
Hidde Bult ◽  
Jose J. Heiremans ◽  
Arnold G. Herman ◽  
Christiane M.A. Malcorps ◽  
Frank A.M. Peeters

1993 ◽  
Vol 7 (4) ◽  
pp. 359-364 ◽  
Author(s):  
B. Nemery ◽  
P.H.M. Hoet
Keyword(s):  

1993 ◽  
Vol 75 (4) ◽  
pp. 1525-1528 ◽  
Author(s):  
S. Ganesan ◽  
S. J. Lai-Fook

Previous measurements in isolated lung showed that alveolar liquid pressure was near the pleural pressure at a lung volume near functional residual capacity (FRC). In this study we verified that alveolar liquid pressure in vivo was similar to that of the isolated lung. In anesthetized paralyzed rabbits (3#x2013;4 kg, n = 9) ventilated with 100% O2 in the left lateral position, we made a pleural window between the fifth and sixth ribs near midchest by removing tissue down to the parietal pleura. Window height was 6 cm above the base of the lung. During apnea, alveolar liquid and pleural pressures were measured by puncturing through the pleural window with micropipettes connected to a servo-nulling pressure-measuring system. Pressures were measured at airway pressures of 0 (FRC) and 10 cmH2O both in vivo and postmortem. In vivo, alveolar liquid and pleural pressures relative to ambient pressure averaged -2.3 +/- 1.4 (SD) and -1.8 +/- 0.9 cmH2O at FRC and increased to 3.3 +/- 1.8 and 1.8 +/- 1.6 cmH2O after inflation to an airway pressure of 10 cmH2O, respectively. Similar values were obtained postmortem. These results were similar to previous measurements in the isolated lung.


2012 ◽  
Vol 7 (10) ◽  
pp. 1567-1573 ◽  
Author(s):  
Bram Balduyck ◽  
Jana Van Thielen ◽  
Anouschka Cogen ◽  
Willem Den Hengst ◽  
Jeroen Hendriks ◽  
...  

1992 ◽  
Vol 73 (6) ◽  
pp. 2440-2447 ◽  
Author(s):  
P. A. Vincent ◽  
P. B. Kreienberg ◽  
F. L. Minnear ◽  
T. M. Saba ◽  
D. R. Bell

Fluid conductance and protein permeability have been studied in isolated perfused lung models of pulmonary edema. However, previous studies have not investigated changes of both fluid conductance and protein permeability in the same isolated lung preparation after injury. Arachidonic acid (AA) metabolites are involved in the inflammatory processes that lead to the development of pulmonary edema. The hemodynamic effects of AA have been well established; however, controversy exists concerning the ability of AA to alter the permeability of the pulmonary microvasculature to fluid and protein. The purpose of this study was to simultaneously determine whether transvascular fluid conductance and protein permeability are increased in isolated perfused rabbit lungs with pulmonary edema induced by AA. Indomethacin (80 microM) was added to the perfusate to inhibit the hemodynamic effects of AA and produce a pressure-independent model of pulmonary edema. Fluid conductance was assessed by determination of the capillary filtration coefficient (Kf), and protein permeability was evaluated by measurement of 125I-albumin clearance. The injection of AA (3 mg/200 ml of perfusate) into the pulmonary arterial catheter resulted in an increase in lung weight over the remaining 30-min experimental period. Kf (microliter.s-1 x cmH2O-1 x g dry lung-1) was increased (P < 0.05) in AA-treated lungs at 10 and 30 min post-AA injection when compared with control lungs and baseline values (determined 10 min before AA injection). Albumin clearance was also greater (P < 0.05) in lungs that received AA. 125I-albumin clearance was measured at different rates of fluid flux produced by elevation of venous pressure.(ABSTRACT TRUNCATED AT 250 WORDS)


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