Reappraisal of extravascular lung thermal volume as a measure of pulmonary edema

1980 ◽  
Vol 48 (1) ◽  
pp. 120-129 ◽  
Author(s):  
W. H. Noble ◽  
J. C. Kay ◽  
K. H. Maret ◽  
G. Caskanette
Keyword(s):  
Pulmonary Edema ◽  
Chest Wall ◽  
Transit Time ◽  
Mean Transit Time ◽  
Pulmonary Arteries ◽  
Pericardial Fluid ◽  
Left Heart ◽  
Lung Water ◽  
Tissue Weight ◽  
Arteries And Veins

Previous papers have evaluated extravascular thermal volume of the lung (ETVL) as a measure of lung water by using median transit time (tmed) rather than the correct mean transit time (tmean). Calculation of ETVL using tmean (ETVLmean) and tmed (ETVLmed) gave an excellent relationship, ETVLmean = 1.48 ETVLmed - 0.74 (r = 0.99). This allowed us to calculate a new ratio of ETVLmean to PETW = 1.55 +/- 0.17, WHERE PETW is the postmortem value of pulmonary extravascular tissue weight. Thermistors were placed in dogs to determine the contribution of chest wall, pleural and pericardial fluid, left heart, bronchi, and lung gas to the ETVL measurement. We found ETVLmean greater than PETW because of thermal distributioninto left heart (18 +/- 2% of ETVL), bronchi (estimate 7% of ETVL), pulmonary arteries and veins (estimate 7% of ETVL), and perhaps a small portion of chest wall. We could not detect any portion of lung gas or pleural or pericardial effusions as a part of the ETVL measurement. When the distribution into left heart, bronchi, pulmonary arteries, and veins is removed ETVLmean/PETW = 1.07.

Lung water measurements with the mean transit time approach

1985 ◽  
Vol 59 (3) ◽  
pp. 673-683 ◽  
Author(s):  
R. M. Effros
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Tissue Perfusion ◽  
Time Data ◽  
Lung Water ◽  
Thermal Signal ◽  
The Mean ◽  
Points Of View ◽  
Vascular Obstruction ◽  
Pulmonary Vascular Obstruction

The potential usefulness and limitations of the double-indicator mean transit time approach for measuring lung water are evaluated from both theoretical and empirical points of view. It is concluded that poor tissue perfusion is the most serious factor that can compromise the reliability of this approach. Replacement of the conventional water isotopes with a thermal signal enhances indicator delivery to ischemic areas but the diffusion of heat is not sufficiently rapid to permit measurements of water in macroscopic collections of fluid which remain unperfused. The frequency of pulmonary vascular obstruction in patients with pulmonary edema related to lung injury suggests that interpretation of transit time data will be complicated by uncertainties concerning perfusion. Thermal-dye measurements of lung water may prove more helpful in situations where pulmonary blood flow remains relatively uniform.

Oxygen radicals participate in alloxan-induced pulmonary EDEMA

1990 ◽  
Vol 48 (3) ◽  
pp. 298-299
Author(s):  
Tomoo Kawada ◽  
Michio Arakawa ◽  
Kenjiro Kambara ◽  
Takashi Segawa ◽  
Fumio Ando ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Oxygen Radicals ◽  
Bolus Injection ◽  
Physiological Saline ◽  
Baseline Period ◽  
Alveolar Epithelial Cells ◽  
Control Group ◽  
Intervention Period ◽  
Lung Water ◽  
Electron Microscopic

We know that alloxan causes increased-permeability pulmonary edema and that alloxan generates oxygen radicals (H2O2, O2−, ·OH) in blood. Therefore, we hypothesize that alloxan-generated oxygen radicals damage pulmonary capillary endothelial cells, and, possibly, alveolar epithelial cells as well. We examined whether oxygen radical scavengers, such as catalase or dimethylsulfoxide (DMSO), protected against alloxaninduced pulmonary edema.Five dogs in each following group were anesthetized: control group: physiological saline (20ml/kg/h); alloxan group: physiological saline + alloxan (75mg/kg) bolus injection at the beginning of the experiment; catalase group: physiological saline + catalase (150,000u/kg) bolus injection before injection of alloxan; DMSO group: physiological saline + DMSO (0.4mg/kg) bolus injection before alloxan. All dogs had 30-min baseline period and 3-h intervention period. Hemodynamics and circulating substances were measured at the specific points of time. At the end of intervention period, the dogs were killed and had the lungs removed for electron microscopic study and lung water measurement with direct destructive method.

Cerebral vascular mean transit time determined by PET and DSC-MRI

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S676-S676
Author(s):  
Masanobu Ibaraki ◽  
Hiroshi Ito ◽  
Eku Shimosegawa ◽  
Hideto Toyoshima ◽  
Keiichi Ishigame ◽  
...  
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Dsc Mri ◽  
Cerebral Vascular

Measurement of pulmonary edema in intact dogs by transthoracic gamma-ray attenuation

1979 ◽  
Vol 47 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
D. S. Simon ◽  
J. F. Murray ◽  
N. C. Staub
Keyword(s):  
Pulmonary Edema ◽  
Time Course ◽  
Gamma Ray ◽  
High Sensitivity ◽  
Lung Edema ◽  
Lung Water ◽  
Vascular Congestion ◽  
Isolated Lung ◽  
Wide Range ◽  
Gamma Ray Attenuation

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.

scholarly journals Effect of fulvine on pulmonary arteries and veins of the rat

Thorax ◽  
1974 ◽  
Vol 29 (5) ◽  
pp. 522-529 ◽  
Author(s):  
C. A. Wagenvoort ◽  
N. Wagenvoort ◽  
H. J. Dijk
Keyword(s):  
Pulmonary Arteries ◽  
Arteries And Veins

Reproducibility of mean transit time for maximal myocardial flow assessment by videodensitometry

1990 ◽  
Vol 6 (2) ◽  
pp. 101-108 ◽  
Author(s):  
Nico H. J. Pijls ◽  
Gerard J. H. Uijen ◽  
Truus Pijnenburg ◽  
Karel van Leeuwen ◽  
Wim R. M. Aengevaeren ◽  
...  
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Myocardial Flow

scholarly journals Serial Quantitative Computed Tomography Perfusion in Aneurysmal Subarachnoid Hemorrhage

2016 ◽  
Vol 43 (3) ◽  
pp. 375-380 ◽  
Author(s):  
Cheemun Lum ◽  
Matthew J. Hogan ◽  
John Sinclair ◽  
Shane English ◽  
Howard Lesiuk ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Transit Time ◽  
Cerebral Artery ◽  
Computed Tomography Angiography ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Mean Transit Time ◽  
Arterial Diameter ◽  
Computed Tomography Perfusion

AbstractPurpose: Computed tomography perfusion (CTP) has been performed to predict which patients with aneurysmal subarachnoid hemorrhage are at risk of developing delayed cerebral ischemia (DCI). Patients with severe arterial narrowing may have significant reduction in perfusion. However, many patients have less severe arterial narrowing. There is a paucity of literature evaluating perfusion changes which occur with mild to moderate narrowing. The purpose of our study was to investigate serial whole-brain CTP/computed tomography angiography in aneurysm-related subarachnoid hemorrhage (aSAH) patients with mild to moderate angiographic narrowing. Methods: We retrospectively studied 18 aSAH patients who had baseline and follow-up whole-brain CTP/computed tomography angiography. Thirty-one regions of interest/hemisphere at six levels were grouped by vascular territory. Arterial diameters were measured at the circle of Willis. The correlation between arterial diameter and change in CTP values, change in CTP in with and without DCI, and response to intra-arterial vasodilator therapy in DCI patients was evaluated. Results: There was correlation among the overall average cerebral blood flow (CBF; R=0.49, p<0.04), mean transit time (R=–0.48, p=0.04), and angiographic narrowing. In individual arterial territories, there was correlation between changes in CBF and arterial diameter in the middle cerebral artery (R=0.53, p=0.03), posterior cerebral artery (R=0.5, p=0.03), and anterior cerebral artery (R=0.54, p=0.02) territories. Prolonged mean transit time was correlated with arterial diameter narrowing in the middle cerebral artery territory (R=0.52, p=0.03). Patients with DCI tended to have serial worsening of CBF compared with those without DCI (p=0.055). Conclusions: Our preliminary study demonstrates there is a correlation between mild to moderate angiographic narrowing and serial changes in perfusion in patients with aSAH. Patients developing DCI tended to have progressively worsening CBF compared with those not developing DCI.

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