Effect of superior vena caval hypertension on alloxan-induced lung injury in dogs

1990 ◽  
Vol 68 (2) ◽  
pp. 478-483 ◽  
Author(s):  
F. Ando ◽  
M. Arakawa ◽  
K. Kambara ◽  
H. Miyazaki ◽  
T. Segawa ◽  
...  
Keyword(s):  
Time Course ◽  
Low Dose ◽  
Superior Vena ◽  
Gravimetric Method ◽  
Base Line ◽  
Lung Water ◽  
Superior Vena Caval ◽  
Anesthetized Dogs ◽  
Water Accumulation ◽  
Permeability State

To investigate how fast and to what extent superior vena caval hypertension (SVCH) increases lung water in acute increased-permeability state, we studied the time course of lung water accumulation for 3 h in anesthetized dogs under different treatments: 1) controls without intervention (5 dogs), 2) SVCH alone (5 dogs), 3) mild lung microvascular injury induced by low-dose alloxan (75 mg/kg) alone (5 dogs), and 4) SVCH coupled with low-dose alloxan (5 dogs). Neither low-dose alloxan alone nor SVCH alone [superior vena caval pressure (Psvc) = 11.0 +/- 3.1 (SD) mmHg] increased lung water significantly. The SVCH coupled with low-dose alloxan (Psvc = 11.3 +/- 2.7 mmHg) doubled extravascular lung thermal volume measured by the thermal-dye dilution technique within 1 h (5.3 +/- 0.9 ml/kg at base line and 10.9 +/- 4.7 ml/kg at 1 h), then remained unchanged (12.5 +/- 5.7 ml/kg at 3 h). This increase in lung water was confirmed by gravimetric method (5.69 +/- 1.71 g/g blood-free dry wt). We conclude that SVCH is one of the factors that may promote lung water accumulation in increased-permeability state.

Type of lung injury influences the thermal-dye estimation of extravascular lung water

1984 ◽  
Vol 57 (3) ◽  
pp. 680-685 ◽  
Author(s):  
P. V. Carlile ◽  
B. A. Gray
Keyword(s):  
Lung Injury ◽  
Extravascular Lung Water ◽  
Base Line ◽  
Shunt Fraction ◽  
Lung Water ◽  
Animal Group ◽  
Group I ◽  
Injury Group ◽  
Anesthetized Dogs ◽  
Group Ii

To determine the effect of the type of lung injury on the thermodilution estimation of extravascular lung water, we produced pulmonary edema in 25 anesthetized dogs by injection of alloxan or alpha-naphthylthiourea (ANTU) into the pulmonary circulation or by instillation of hydrochloric acid (HCI) into the airway. HCl injury was bilateral, unilateral with tidal volume equal in each lung, or unilateral with equal airway pressure. Extravascular thermal volume (ETV) was measured at base line and 4 h after lung injury, and the final measurement was compared with the postmortem determination of extravascular lung mass (ELM). In 11 of 15 animals with HCl injury final ETV was less than the base-line measurement. The ratio of final ETV to ELM for all HCl animal (group I) averaged 0.31 +/- 0.14, which was different from the value for animals with alloxan or ANTU injury (group II), 1.04 +/- 0.14 (P less than 0.01). Extravascular lung water per gram of blood-free dry tissue was not different for the two groups (8.1 +/- 1.2 and 8.7 +/- 2.6 for I and II, respectively), indicating equally severe lung injury; however, shunt fraction was less in group I (P less than 0.01). ETV/ELM correlated with the shunt fraction for group I (r = 0.70) but not for group II (r = 0.32). These findings indicate that ETV underestimates lung water after HCl injury due to the redistribution of pulmonary blood flow away from edematous areas.

Superior vena caval pressure elevation causes pleural effusion formation in sheep

1988 ◽  
Vol 255 (3) ◽  
pp. H492-H495 ◽  
Author(s):  
S. J. Allen ◽  
G. A. Laine ◽  
R. E. Drake ◽  
J. C. Gabel
Keyword(s):  
Cardiac Output ◽  
Pleural Effusion ◽  
Protein Concentration ◽  
Superior Vena ◽  
Recovery Period ◽  
Balloon Catheter ◽  
Vena Cava ◽  
Base Line ◽  
Superior Vena Caval ◽  
Plasma Protein Concentration

The effect of superior vena caval pressure (SVCP) elevation on the formation of pleural effusions (PE) was studied in sheep. Through a right thoracotomy, a Silastic cuff was placed around the superior vena cava. Catheters for monitoring SVCP and pulmonary artery pressure (PAP) were also placed. After a 1- to 3-wk recovery period, we measured the SVCP, PAP, cardiac output, and plasma protein concentration (Cp). We then elevated the SVCP to various levels from base line [5.3 +/- 2.6 (SD) mmHg] to 33 mmHg. The cardiac output, PAP, and Cp were remeasured 1–2 h and 24 h after SVCP elevation. At the end of the 24-h period, the animals were killed. The PE volume and pleural fluid protein concentration (Cpl) were measured, and the Cpl/Cp was calculated. PE generally did not occur until the SVCP was elevated above 15 mmHg. To study the effect of the thoracotomy on the subsequent pleural effusion, we studied six additional sheep in which we did not perform a thoracotomy. In these animals, the SVCP was elevated to between 5 and 28 mmHg for 24 h by use of a 16-Fr balloon catheter placed via a left external jugular vein and a right carotid-external jugular shunt. We found that the PE volume, for a given SVCP elevation, was similar to that present in sheep that received a thoracotomy. For all sheep the volume of PE was related to SVCP by the equation PE (ml) = 0.24e0.26SVCP, r = 0.85. In the sheep without a thoracotomy, Cpl/Cp rose with increasing volume of PE. Our data demonstrate that elevation of SVCP greater than 15 mmHg for 24 h results in the formation of PE. The rise in Cpl/Cp with PE volume suggests that filtration through the pleural vessels is not the major contributor to PE formation.

Edema development and recovery in neurogenic pulmonary edema

1994 ◽  
Vol 77 (3) ◽  
pp. 1155-1163 ◽  
Author(s):  
M. B. Maron ◽  
P. H. Holcomb ◽  
C. A. Dawson ◽  
D. A. Rickaby ◽  
A. V. Clough ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Time Course ◽  
Indicator Dilution ◽  
Right Atrial ◽  
Neurogenic Pulmonary Edema ◽  
Gravimetric Analysis ◽  
Lung Water ◽  
Anesthetized Dogs ◽  
Acute Increase ◽  
System Activation

We determined the time course of changes in extravascular lung water (EVLW) that occur after massive sympathetic activation produced by intracisternal veratrine administration in chloralose-anesthetized dogs. Three groups of dogs were studied. In the first group (n = 9), acute increases in EVLW (occurring within minutes) were determined both by measuring extravascular thermal volume and by gravimetric analysis. In the second (n = 6) and third (n = 7) groups, changes in EVLW were followed for 2–3 h after veratrine administration. Extravascular thermal volume was measured in the second group. In the third group, right atrial injections of a vascular indicator (125I-labeled serum albumin) and an extravascular indicator (3HOH) were made while blood was sampled from the pulmonary artery (PA) and left atrium, and EVLW was determined by deconvolution of the left atrial and PA concentration-time curves. Indicator-dilution and gravimetric EVLW increased acutely only in dogs in which PA pressure exceeded 60 Torr, with two- to four-fold increases in EVLW being observed in dogs that developed the highest PA pressures (maximum 94 Torr). Thus, severe edema can develop rapidly after massive sympathetic nervous system activation but requires extreme degrees of pulmonary hypertension. In several dogs after the acute increase in EVLW associated with the pulmonary hypertension, the indicator-dilution EVLW decreased with time. These decreases appear to effect clearance of edema fluid rather than alterations in perfusion.

Edema affects intra-alveolar fluid pressures and interdependence in dog lungs

1981 ◽  
Vol 51 (4) ◽  
pp. 911-921 ◽  
Author(s):  
J. C. Parker ◽  
R. C. Allison ◽  
A. E. Taylor
Keyword(s):  
Time Course ◽  
Recovery Period ◽  
Positive Pressure ◽  
Base Line ◽  
Alveolar Wall ◽  
Lung Water ◽  
Lung Inflation ◽  
Volume Segment ◽  
The Mean ◽  
Line Pressure

The pressures in occluded, fluid-filled segments of lung were measured in closed-chest supine dogs ventilated with positive pressure at a constant tidal volume. Segment fluid pressures decreased in response to lung inflation and were used with esophageal and airway pressures to calculate an index of bronchiolar-parenchymal interdependence. Animals were subjected to three sequential 5% body wt infusions of Tyrode's solution followed by a 20- to 30 min-recovery period after each infusion. The interdependence index decreased significantly following each infusion, with infusions as small as 1% body wt producing a detectable decrease. The mean pressures in the Tyrode's solution-filled segments generally increased in response to the infusions, but the time course of the response was variable. The base-line pressure in Tyrode's solution-filled segments was -4.8 +/- 2.4 cmH2O. This increased to -1.1 +/- 2.7 cmH2O after a total of 15% body wt had been infused. At the same time, extravascular lung water increased by approximately 17%. Thus negative collapse pressures in the occluded segments were opposed by mechanical stresses transmitted through alveolar wall attachments. This counterbalancing stress was consistently reduced by both increased tissue hydration and increased pulmonary vascular pressure.

Increased cardiac output increases shunt: role of pulmonary edema and perfusion

1985 ◽  
Vol 59 (4) ◽  
pp. 1313-1321 ◽  
Author(s):  
P. H. Breen ◽  
P. T. Schumacker ◽  
J. Sandoval ◽  
I. Mayers ◽  
L. Oppenheimer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Edema ◽  
Base Line ◽  
Lung Water ◽  
Arteriovenous Fistulas ◽  
Anesthetized Dogs ◽  
The Right

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6–29%, O2 technique) and extravascular thermal volume (ETV, 2.6–7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.

Effect of negative-pressure ventilation on lung water in permeability pulmonary edema

1989 ◽  
Vol 66 (5) ◽  
pp. 2223-2230 ◽  
Author(s):  
M. Skaburskis ◽  
R. P. Michel ◽  
A. Gatensby ◽  
A. Zidulka
Keyword(s):  
Cardiac Output ◽  
Pulmonary Edema ◽  
Positive Pressure Ventilation ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Lung Water ◽  
Anesthetized Dogs ◽  
Water Accumulation ◽  
Permeability Pulmonary Edema ◽  
Continuous Positive Pressure

We have previously shown (Am. Rev. Respir. Dis. 136: 886–891, 1987) improved cardiac output in dogs with pulmonary edema ventilated with external continuous negative chest pressure ventilation (CNPV) using negative end-expiratory pressure (NEEP), compared with continuous positive-pressure ventilation (CPPV) using equivalent positive end-expiratory pressure (PEEP). The present study examined the effect on lung water of CNPV compared with CPPV to determine whether the increased venous return created by NEEP worsened pulmonary edema in dogs with acute lung injury. Oleic acid (0.06 ml/kg) was administered to 27 anesthetized dogs. Supine animals were then divided into three groups and ventilated for 6 h. The first group (n = 10) was treated with intermittent positive-pressure ventilation (IPPV) alone; the second (n = 9) received CNPV with 10 cmH2O NEEP; the third (n = 8) received CPPV with 10 cmH2O PEEP. CNPV and CPPV produced similar improvements in oxygenation over IPPV. However, cardiac output was significantly depressed by CPPV, but not by CNPV, when compared with IPPV. Although there were no differences in extravascular lung water (Qwl/dQl) between CNPV and CPPV, both significantly increased Qwl/dQl compared with IPPV (7.81 +/- 0.21 and 7.87 +/- 0.31 vs. 6.71 +/- 0.25, respectively, P less than 0.01 in both instances). CNPV and CPPV, but not IPPV, enhanced lung water accumulation in the perihilar areas where interstitial pressures may be most negative at higher lung volumes.

Changes in collateral ventilation with increased vascular pressure and edema formation

1982 ◽  
Vol 53 (1) ◽  
pp. 70-74 ◽  
Author(s):  
D. L. Emery ◽  
B. Shown ◽  
G. Batra ◽  
M. H. Gee
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Base Line ◽  
Lung Water ◽  
Edema Formation ◽  
Rate Of Increase ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Lung Water Content ◽  
Collateral Ventilation

To test the hypothesis that development of hemodynamic edema results in decreased collateral ventilation, we rapidly volume-expanded anesthetized dogs with volumes equivalent to 10 (n = 5) and 15% (n = 5) of body weight. We measured collateral resistance (Rcoll), pulmonary arterial pressure, and left ventricular end-diastolic pressure before, during, and for 1–2 h after the infusion. Lungs were subsequently processed for microscopic examination and measurement of extravascular lung water content. During the infusion, Rcoll increased modestly independent of the fluid-infusion rate or the rate of increase in vascular pressures. After the infusion, Rcoll continued to increase to maximum levels 2–33 times base line even though pressures decreased dramatically. At the end of the experiment, Rcoll returned to base line in one dog and was 3–15 times base line in the other dogs. These changes bore no relationship to the severity of edema formation. Until alveolar flooding occurs, accumulation of lung interstitial fluid and changes in collateral ventilation appear to be coincident events rather than causally related variables.

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