Effect of edema and hemodynamic changes on extravascular thermal volume of the lung

1984 ◽  
Vol 56 (4) ◽  
pp. 878-890 ◽  
Author(s):  
B. A. Gray ◽  
R. C. Beckett ◽  
R. C. Allison ◽  
D. R. McCaffree ◽  
R. M. Smith ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Mean Transit Time ◽  
Hemodynamic Changes ◽  
Pulmonary Hemodynamics ◽  
Indocyanine Green Dye ◽  
Pulmonary Arterial ◽  
The Mean ◽  
The Difference ◽  
Acute Changes ◽  
Thermal Dilution

The extravascular thermal volume of the lung (ETV) has been measured in dogs as the difference between mean transit time (t) volumes for heat and indocyanine green dye across the pulmonary circulation, calculated as the product of thermal dilution cardiac output (CO) and the difference in t for aortic indicator-dilution curves generated by right and left atrial injections. ETV measurements were compared with the extravascular lung mass (ELM): in 21 normal dogs, ETV/ELM = 1.11 +/- 0.14 (SD); in 17 dogs with hydrostatic pulmonary edema (up to 21 g/kg), ETV/ELM = 0.90 +/- 0.11; and in 27 dogs with alloxan pulmonary edema (up to 51 g/kg); ETV/ELM = 0.93 +/- 0.13. For all 65 dogs the mean ETVELM was 0.98 +/- 0.15, and the liner regression was ETV (ml/kg) = 0.90 ELM (g/kg) + 0.86 +/- 2.25 (SEE; r = 0.96). Calculations based on measurements of lung specific heat predict that ETV/ELM should equal 0.984. With acute changes in pulmonary hemodynamics, ETV was reduced by reductions in pulmonary arterial pressure (Ppa) sufficient to produce zone 1 conditions at the top of the lung. However, ETV was not affected by increases in CO (mean = 50%) produced by nitroprusside or by increases in Ppa and pulmonary blood volume (mean = 27%) produced by partial mitral valve obstruction. Distortion of the thermal dilution curve due to position of the arterial thermistor appears to be the greatest source of variability and overestimation. Simultaneous measurements from pairs of thermistors differed by 14% (range 0.4–50%).

Elevated intracranial pressure increases pulmonary vascular permeability to protein

1989 ◽  
Vol 67 (3) ◽  
pp. 1185-1191 ◽  
Author(s):  
M. D. McClellan ◽  
I. M. Dauber ◽  
J. V. Weil
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Pulmonary Edema ◽  
Vascular Permeability ◽  
Elevated Intracranial Pressure ◽  
Hemodynamic Changes ◽  
Pulmonary Vascular Permeability ◽  
Pulmonary Arterial ◽  
Protein Permeability

The syndrome of neurogenic pulmonary edema raises the question of whether there are neurological influences on pulmonary vascular permeability. Previous experimental models commonly produced severe hemodynamic alterations, complicating the distinction of increased permeability from increased hydrostatic forces in the formation of the pulmonary edema. Accordingly, we employed a milder central nervous system insult and measured the pulmonary vascular protein extravasation rate, which is a sensitive and specific indicator of altered protein permeability. After elevating intracranial pressure via cisternal saline infusion in anesthetized dogs, we used a dual isotope method to measure the protein leak index. This elevated intracranial pressure resulted in a nearly three-fold rise in the protein leak index (54.1 +/- 7.5 vs. 20.2 +/- 0.9). This central nervous system insult was associated with only mild increases in pulmonary arterial pressures and cardiac output. However, when we reproduced these hemodynamic changes with left atrial balloon inflation or isoproterenol infusion, we observed no effect on the protein leak index compared with control. Although the pulmonary arterial wedge pressure with intracranial pressure remained <10 mmHg, increases in the extravascular lung water were demonstrated. The results suggest the existence of neurological influences on pulmonary vascular protein permeability. We conclude that neurological insults result in increase pulmonary vascular permeability to protein and subsequent edema formation, which could not be accounted for by hemodynamic changes alone.

Transit time dispersion in the pulmonary arterial tree

1998 ◽  
Vol 85 (2) ◽  
pp. 565-574 ◽  
Author(s):  
Anne V. Clough ◽  
Steven T. Haworth ◽  
Christopher C. Hanger ◽  
Jerri Wang ◽  
David L. Roerig ◽  
...  
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Arterial Tree ◽  
Lung Lobe ◽  
Transit Times ◽  
Pulmonary Capillary ◽  
Time Dispersion ◽  
Pulmonary Arterial ◽  
The Difference ◽  
In Transit

Knowledge of the contributions of arterial and venous transit time dispersion to the pulmonary vascular transit time distribution is important for understanding lung function and for interpreting various kinds of data containing information about pulmonary function. Thus, to determine the dispersion of blood transit times occurring within the pulmonary arterial and venous trees, images of a bolus of contrast medium passing through the vasculature of pump-perfused dog lung lobes were acquired by using an X-ray microfocal angiography system. Time-absorbance curves from the lobar artery and vein and from selected locations within the intrapulmonary arterial tree were measured from the images. Overall dispersion within the lung lobe was determined from the difference in the first and second moments (mean transit time and variance, respectively) of the inlet arterial and outlet venous time-absorbance curves. Moments at selected locations within the arterial tree were also calculated and compared with those of the lobar artery curve. Transit times for the arterial pathways upstream from the smallest measured arteries (200-μm diameter) were less than ∼20% of the total lung lobe mean transit time. Transit time variance among these arterial pathways (interpathway dispersion) was less than ∼5% of the total variance imparted on the bolus as it passed through the lung lobe. On average, the dispersion that occurred along a given pathway (intrapathway dispersion) was negligible. Similar results were obtained for the venous tree. Taken together, the results suggest that most of the variation in transit time in the intrapulmonary vasculature occurs within the pulmonary capillary bed rather than in conducting arteries or veins.

Deconvolution Analysis of Renograms Obtained with Simultaneously Administered 99mTc-DTPAand 131l-Hippuran

1988 ◽  
Vol 27 (05) ◽  
pp. 188-194 ◽  
Author(s):  
V. Kempi
Keyword(s):  
Ureteral Obstruction ◽  
Mean Transit Time ◽  
Retention Function ◽  
Renal Handling ◽  
Deconvolution Analysis ◽  
Transit Times ◽  
The Matrix ◽  
Absolute Amplitude ◽  
The Mean ◽  
The Difference

Seventy patients were studied with a dual radionuclide technique. The conventional renograms and the blood curve were subjected to deconvolution analysis using the matrix algorithm method, and the following curve data calculated from the retention functions: absolute and relative amplitudes, minimum time of the retention function, maximum time of the retention function and mean transit time. The findings with the two radiopharmaceuticals 99mTc-DTPA and 131l-Hippuran were compared under normal and pathological conditions. The correlations between the data with 99mTc-DTPA and those with 131l-Hippuran were highly significant (p <0.01). So was the correlation between the absolute amplitude of the retention curve and the rate of uptake based on the corresponding renogram (p <0.01). Due to the difference in the renal handling of the two tracers, longer maximum times were obtained with 99mTc-DTPA. The mean transit times were also longer with 99mTc-DTPA, except in kidneys with parenchymal insufficiency. The highest amplitudes were found in normal kidneys, while the lowest values were observed in parenchymal insufficiency. In the group with acute ureteral obstruction, the mean transit times tended to be increased. The maximum times were even more increased. With both tracers it is possible to distinguish between the three groups of renal conditions studied here: Normal, parenchymal insufficiency, and acute ureteral obstruction.

CVF-induced decomplementation: effect on lung transvascular protein flux after thrombin

1987 ◽  
Vol 62 (3) ◽  
pp. 863-869 ◽  
Author(s):  
A. Johnson ◽  
S. K. Lo ◽  
F. B. Blumenstock ◽  
A. B. Malik
Keyword(s):  
Plasma Protein Concentration ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Hemolytic Complement Activity ◽  
The Mean ◽  
Lung Lymph ◽  
Made In ◽  
Protein Exchange

We examined the effects of cobra venom factor (CVF) on the changes in pulmonary hemodynamics and transvascular fluid and protein exchange following thrombin-induced pulmonary microembolism. Studies were made in unanesthetized sheep prepared with lung lymph fistulas. The animals received tranexamic acid (100 mg) to suppress fibrinolysis and were then challenged with an intravenous infusion of alpha-thrombin (80 U/kg). Control-thrombin challenged sheep were compared with the CVF-treated sheep challenged with the same thrombin dosage. CVF treatment (187 U X kg-1 X day-1 for 4 days) decreased the total hemolytic complement activity by 45% of control. Thrombin infusion in control sheep increased the mean pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), and lymph protein clearance (pulmonary lymph flow X lymph-to-plasma protein concentration ratio, Clym). Thrombin infusion in CVF-treated sheep produced smaller increments in Ppa, PVR, and Clym. Pulmonary lymph obtained from control-thrombin and CVF-thrombin sheep induced migration of granulocytes obtained from normal unchallenged sheep. The granulocytes obtained from CVF-treated sheep responded relatively less to the migratory and O-2-generating stimuli (i.e., zymosan-treated serum, pulmonary lymph from sheep after thrombin challenge, and plasma from sheep after CVF treatment) compared with normal granulocytes. The attenuation of the thrombin-induced increases in Ppa, PVR, and lung transvascular fluid and protein exchange by CVF treatment may be the result of impaired function of granulocytes.

Effect of Gram-Negative Endotoxin on Pulmonary Circulation

1958 ◽  
Vol 192 (2) ◽  
pp. 335-344 ◽  
Author(s):  
Hiroshi Kuida ◽  
Lerner B. Hinshaw ◽  
Robert P. Gilbert ◽  
Maurice B. Visscher
Keyword(s):  
Pulmonary Artery ◽  
Vascular Response ◽  
Weight Changes ◽  
Hemodynamic Changes ◽  
Lung Weight ◽  
Pulmonary Hemodynamics ◽  
Pump System ◽  
Absolute Increase ◽  
Consistent Increase ◽  
Pulmonary Arterial

Effects of endotoxin on the pulmonary hemodynamics of dogs and cats have been studied in intact animals, open chest animals with and without control of cardiac output by an extracorporeal venous reservoir—pump system, and in isolated perfused continuously weighed lungs. Pulmonary artery pressure increased without a rise in left atrial pressure in all preparations following the injection of endotoxin. Pulmonary artery wedge and small pulmonary vein pressures uniformly increased. Total pulmonary vascular, pulmonary arterial and pulmonary venous resistances were calculated in five perfused lungs. The absolute increase in pulmonary venous resistance was greater than in the arterial resistance in four of the five studies and was relatively greater in every instance. There was a consistent increase in lung weight associated with these hemodynamic changes. Analysis of the determinants of lung weight changes has provided evidence to support the conclusion that the pulmonary vascular response to endotoxin administration is characterized predominantly by constriction of pulmonary venules and/or small veins.

Pulmonary hemodynamics and gas exchange properties during progressive edema

1983 ◽  
Vol 55 (4) ◽  
pp. 1154-1159 ◽  
Author(s):  
Y. K. Ngeow ◽  
W. Mitzner
Keyword(s):  
Pulmonary Edema ◽  
Critical Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Outflow ◽  
Pulmonary Hemodynamics ◽  
Lung Inflation ◽  
Isolated Lung ◽  
Pulmonary Arterial ◽  
The Relationship ◽  
Lung Preparation

In this investigation we have studied the effect of increments of pulmonary edema on pulmonary hemodynamics, and physiological and hemodynamic shunt in an isolated lung preparation. Hemodynamic shunt was defined by the slope of the relationship between pulmonary arterial and airway pressures; when the slope decreases, there is a greater degree of shunt. Cardiovascular changes were analyzed using a Starling resistor model of the pulmonary circulation where the effective downstream pressure to flow as seen from the pulmonary artery exceeds the pulmonary venous outflow pressure. This effective downstream pressure is referred to as the critical pressure (Pc), and at low lung inflation the locus of this critical pressure is in extra-alveolar vessels. With 3-4 h of progressive edema to an average of 185% initial lobe weight we found a progressive rise in pulmonary arterial pressure (Ppa) from 12.1 to 21.5 cmH2O. About one-third of this increase in Ppa resulted from an increased Pc and the remainder resulted from an increased resistance upstream from the locus of Pc. These results are consistent with the hypothesis that the interstitial accumulation of fluid creates enough of an increase in interstitial pressure to compress extra-alveolar vessels. There was no significant correlation between the amount of edema and the measured physiologic shunt, but the hemodynamic shunt showed a highly significant correlation. The hemodynamic shunt theoretically measures the extent of obstructed airways and may be a useful index of the degree of pulmonary edema.

Hemodynamic Effects of Cardiovascular Medications in a Normovolemic and Hemorrhaged Yorkshire-cross Swine Model

2021 ◽  
Author(s):  
Jacob H Cole ◽  
Scott B Hughey ◽  
Phillip G Geiger ◽  
Kamala J Rapp-Santos ◽  
Gregory J Booth
Keyword(s):  
Swine Model ◽  
Vasoactive Agents ◽  
Hemodynamic Changes ◽  
Arterial Access ◽  
Study Protocols ◽  
Cardiovascular Medications ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Physiologic State ◽  
Vasoactive Medications

The Yorkshire-cross swine model is a valuable translational model commonly used to study cardiovascular physiologyand response to insult. Although the effects of vasoactive medications have been well described in healthy swine, the effects of these medications during hemorrhagic shock are less studied. In this study, we sought to expand the utility of the swine model by characterizing the hemodynamic changes that occurred after the administration of commonly available vasoactive medications during euvolemic and hypovolemic states. To this end, we anesthetized and established femoral arterial,central venous, and pulmonary arterial access in 15 juvenile Yorkshire-cross pigs. The pigs then received a series of rapidlymetabolized but highly vasoactive medications in a standard dosing sequence. After completion of this sequence, each pigunderwent a 30-mL/kg hemorrhage over 10 min, and the standard dosing sequence was repeated. We then used standard statisticaltechniques to compare the effects of these vasoactive medications on a variety of hemodynamic parameters betweenthe euvolemic and hemorrhagic states. All subjects completed the study protocol. The responses in the hemorrhagic state wereoften attenuated or even opposite of those in the euvolemic state. For example, phenylephrine decreased the mean arterialblood pressure during the euvolemic state but increased it in the hemorrhagic state. These results clarify previously poorlydefined responses to commonly used vasoactive agents during the hemorrhagic state in swine. Our findings also demonstratethe need to consider the complex and dynamic physiologic state of hemorrhage when anticipating the effects of vasoactivedrugs and planning study protocols.

Metabolism of [2-14C]Prostaglandin E1 on Passage Through the Pulmonary Circulation

1975 ◽  
Vol 53 (4) ◽  
pp. 610-615 ◽  
Author(s):  
Christopher A. Dawson ◽  
Bruce O. Cozzini ◽  
Andrew J. Lonigro
Keyword(s):  
Mean Transit Time ◽  
Sampling Period ◽  
Prostaglandin E ◽  
Indocyanine Green Dye ◽  
Multiple Indicator Dilution ◽  
Transit Times ◽  
Sequential Samples ◽  
Multiple Indicator ◽  
The Mean ◽  
Layer Chromatography

A multiple indicator dilution technique was used to study inactivation of [14C] prostaglandin E1 (PGE1) by isolated cat lungs. A bolus containing [2-14C]PGE1, indocyanine green dye and 3HOH was rapidly introduced into the blood entering the pulmonary artery. Sequential samples of the venous effluent were collected and analyzed for 3H, dye, and 14C. The 14C-labelled compounds were separated by thin-layer chromatography, and the quantity of PGE, and its metabolites contained in each sample was determined (radiochromatogram scanning). Recovery of the dye and 3H was complete within the sampling period. However, only 79% of the injected 14C emerged from the lung within this period, 36% as [14C]PGE1, and 43% as two less polar metabolites. The mean transit times (including connecting tubing) for the unmetabolized [14C]PGE1 and the dye were 9.1 and 8.7 s, respectively. The apparent mean transit times for 14C in the metabolites were considerably longer, 12.4 and 14.3 s. The 3HOH mean transit time was 10.7 s. These data are compatible with an extraluminal site for PGE1 metabolism.

Pulmonary microvascular response to LTB4: effects of perfusate composition

1988 ◽  
Vol 64 (5) ◽  
pp. 1989-1996 ◽  
Author(s):  
T. C. Noonan ◽  
W. M. Selig ◽  
K. E. Burhop ◽  
C. A. Burgess ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Protein Concentration ◽  
Autologous Blood ◽  
Endothelial Permeability ◽  
Leukotriene B4 ◽  
Albumin Concentration ◽  
Weight Changes ◽  
Lung Weight ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Arterial

We examined the effects of leukotriene B4 (LTB4) on pulmonary hemodynamics and vascular permeability using isolated perfused guinea pig lungs and cultured monolayers of pulmonary arterial endothelial cells. In lungs perfused with Ringer solution, containing 0.5 g/100 ml albumin (R-alb), LTB4 (4 micrograms) transiently increased pulmonary arterial pressure (Ppa) and capillary pressure (Pcap). Pulmonary edema developed within 70 min after LTB4 injection despite a normal Pcap. The LTB4 metabolite, 20-COOH-LTB4 (4 micrograms), did not induce hemodynamic and lung weight changes. In lungs perfused with autologous blood hematocrit = 12 +/- 1%; protein concentration = 1.5 +/- 0.2 g/100 ml), the increases in Ppa and Pcap were greater, and both pressures remained elevated. The lung weight did not increase in blood-perfused lungs. In lungs perfused with R-alb (1.5 g/100 ml albumin) to match the blood perfusate protein concentration, LTB4 induced similar hemodynamic changes as R-alb (0.5 g/100 ml) perfusate, but the additional albumin prevented the pulmonary edema. LTB4 (10(-11)-10(-6) M) with or without the addition of neutrophils to the monolayer did not increase endothelial 125I-albumin permeability. Therefore LTB4 induces pulmonary edema when the perfusate contains a low albumin concentration, but increasing the albumin concentration or adding blood cells prevents the edema. The edema is not due to increased endothelial permeability to protein and is independent of hemodynamic alterations. Protection at higher protein-concentration may be the result of LTB4 binding to albumin.

scholarly journals Effects of pulmonary vascular pressures and flow on airway and parenchymal mechanics in isolated rat lungs

2002 ◽  
Vol 92 (1) ◽  
pp. 169-178 ◽  
Author(s):  
Ferenc Peták ◽  
Walid Habre ◽  
Zoltán Hantos ◽  
Peter D. Sly ◽  
Denis R. Morel
Keyword(s):  
Mechanical Properties ◽  
Low Frequency ◽  
Pulmonary Hemodynamics ◽  
Airway Narrowing ◽  
Rat Lungs ◽  
Pulmonary Capillary ◽  
Primary Determinant ◽  
Normal Rat ◽  
Pulmonary Arterial ◽  
Acute Changes

Changes in pulmonary hemodynamics have been shown to alter the mechanical properties of the lungs, but the exact mechanisms are not clear. We therefore investigated the effects of alterations in pulmonary vascular pressure and flow (Q˙p) on the mechanical properties of the airways and the parenchyma by varying these parameters independently in three groups of isolated perfused normal rat lungs. The pulmonary capillary pressure (Pcest), estimated from the pulmonary arterial (Ppa) and left atrial pressure (Pla), was increased at constant Q˙p ( n = 7), orQ˙p was changed at Pcest = 10 mmHg ( n = 7) and at Pcest = 20 mmHg ( n = 6). In each condition, the airway resistance (Raw) and parenchymal damping (G) and elastance (H) were identified from the low-frequency pulmonary input impedance spectra. The results of measurements made under isogravimetric conditions were analyzed. The changes observed in the mechanical parameters were consistent with an altered Pla: monotonous increases in Raw were observed with increasing Pla, whereas G and H were minimal at Pla of ∼7–10 mmHg and increased at lower and higher Pla. The results indicate that Pla, and not Ppa or Q˙p, is the primary determinant of the mechanical condition of the lungs after acute changes in pulmonary hemodynamics: the parenchymal mechanics are impaired if Pla is lower or higher than physiological, whereas airway narrowing occurs at high Pla.

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