Noninvasive evaluation of acute capillary permeability changes during high-volume ventilation in rats with and without hypercapnic acidosis.
OBJECTIVE
To evaluate whether hypercapnic acidosis attenuates acute alterations of pulmonary capillary permeability due to high lung stretch in rats using a simple, noninvasive, scintigraphic method.


METHODS
Prospective, randomized, controlled animal study.


METHODS
University research laboratory.


METHODS
Male adult Wistar rats weighing 291 +/- 7.5 g.


METHODS
Three groups of rats were studied: controls ventilated with a low (6 mL/kg body weight) tidal volume and rats ventilated with a high (38 mL/kg body weight) tidal volume under normocapnic (Paco(2) = 35.2 +/- 1.65 mm Hg) or hypercapnic (Paco(2) = 102.5 +/- 5.63 mm Hg) conditions.


RESULTS
Pulmonary capillary permeability alterations were assessed by monitoring the rate of (111)In-transferrin accumulation in lung tissue. Respiratory system pressure-volume curves were registered and analyzed. High tidal volume ventilation increased In-transferrin plasma to lung flux in such a way that I(111)In-transferrin behaved like a marker of water. The rate of initial (first 30 mins of high tidal volume ventilation) lung transferrin accumulation measured by scintigraphy (standardized lung/heart ratio) was steady, correlated with the percent decrease in respiratory system compliance (a marker of edema progression), and did not differ between normocapnic and hypercapnic groups (18.9 +/- 3.97 vs. 14.2 +/- 2.89%/hr, not significant). However, lung In-tranferrin accumulation rate was highly scattered due to variable interindividual mechanical properties of the respiratory system. This rate was correlated with initial values of volume of the upper inflection point of the pressure-volume curve (r = -.53, p < .001) and end-inspiratory pressure (r = .54, p < .001). Mechanical properties were similar in normocapnic and hypercapnic rats. There was no difference between In-transferrin accumulation rates in these rats when a stringent selection was made based on end-inspiratory pressure (28-32 cm H(2)O) or body weight (330-360 g).


CONCLUSIONS
Hypercapnic acidosis does not influence in vivo the acute increase in pulmonary capillary permeability due to high-volume ventilation.
Bouvet
François
F
IFR Claude Bernard, Faculté Xavier Bichat, Paris, France.
Dreyfuss
Didier
D
Lebtahi
Rachida
R
Martet
Geneviève
G
Le Guludec
Dominique
D
Saumon
Georges
G
D000142:Acidosis, Respiratory / Q000000981:diagnostic imaging* / Q000503:physiopathology; D000818:Animals; D002199:Capillary Permeability / Q000502:physiology*; D006612:High-Frequency Ventilation; D006935:Hypercapnia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D007205:Indium Radioisotopes; D008168:Lung / Q000098:blood supply*; D008170:Lung Compliance / Q000502:physiology; D008297:Male; D010100:Oxygen / Q000097:blood; D011654:Pulmonary Edema / Q000000981:diagnostic imaging / Q000503:physiopathology; D011877:Radionuclide Imaging; D051381:Rats; D017208:Rats, Wistar; D013990:Tidal Volume / Q000502:physiology*; D014168:Transferrin
D007205:Indium Radioisotopes; D014168:Transferrin; D010100:Oxygen