PULMONARY GAS EXCHANGE DURING INDUCTION OF PULMONARY EDEMA IN ANESTHETIZED DOGS

1965 ◽  
Vol 9 (6) ◽  
pp. 544???545 ◽  
Author(s):  
S. I. SAID ◽  
J. W. LONGACHER ◽  
R. K. DAVIS ◽  
C. M. BANERJEE ◽  
W. M. DAVIS ◽  
...  
1964 ◽  
Vol 19 (3) ◽  
pp. 403-407 ◽  
Author(s):  
Sami I. Said ◽  
Joseph W. Longacher ◽  
Ronald K. Davis ◽  
Chandra M. Banerjee ◽  
William M. Davis ◽  
...  

We examined pulmonary gas exchange in 19 anesthetized dogs during the induction of acute pulmonary edema by intravenous infusion of dextran in saline. We monitored pulmonary capillary pressure by a left atrial catheter, and arterial blood Po2 by an indwelling electrode. PaOO2 remained near normal until just before pulmonary edema was grossly apparent, when it fell precipitously; left atrial pressure mounted to a peak and then declined. The apparent “steady-state” DlCO was reduced as much as 61%, but the dominant cause of hypoxemia was an increased venous admixture (shunt flow) on O2 breathing. Since the shunt was reversible by forcible inflation of the lungs, induced pulmonary edema was probably associated with closure of alveolar units. pulmonary venous admixture (shunt flow) and diffusing capacity; alveolar closure; arterial blood oxygen; tension in vivo; hypoxemia Submitted on August 14, 1963


1991 ◽  
Vol 260 (4) ◽  
pp. H1080-H1086 ◽  
Author(s):  
S. Brimioulle ◽  
J. L. Vachiery ◽  
P. Lejeune ◽  
M. Leeman ◽  
C. Melot ◽  
...  

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.


1991 ◽  
Vol 71 (1) ◽  
pp. 252-258 ◽  
Author(s):  
K. B. Domino ◽  
B. L. Eisenstein ◽  
F. W. Cheney ◽  
M. P. Hlastala

We studied the independent influence of changes in perfusion on pulmonary gas exchange in the left lower lobe (LLL) of anesthetized dogs. Blood flow to the LLL (QLLL) was raised 50% (increased QLLL) or reduced 50% (decreased QLLL) from baseline by partial occlusion of the right or left pulmonary artery, respectively. Minute ventilation and alveolar PCO2 of the LLL remained constant throughout the study. We determined ventilation-perfusion distributions of the LLL using the multiple inert gas elimination technique. Increased QLLL impaired LLL pulmonary gas exchange. All dispersion indexes and all arterial-alveolar difference areas increased (P less than 0.01). Decreased QLLL increased the log standard deviation of the perfusion distribution (P less than 0.05) and reduced the log standard deviation of the ventilation distribution (P less than 0.01) but did not affect the dispersion indexes or alveolar-arterial difference areas. We conclude that ventilation-perfusion heterogeneity is increased by independent changes in perfusion from normal baseline blood flow, even when ventilation and alveolar gas composition remain constant.


1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


Respiration ◽  
1978 ◽  
Vol 35 (3) ◽  
pp. 136-147 ◽  
Author(s):  
P. Jebavý ◽  
J. Fabián ◽  
M. Henzlová ◽  
A. Belán

1992 ◽  
Vol 9 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Th. Wanke ◽  
D. Formanek ◽  
M. Auinger ◽  
H. Zwick ◽  
K. Irsigler

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