We have developed a model including three serial compliant compartments (arterial, capillary, and venous) separated by two resistances (arterial and venous) for interpreting in vivo single pulmonary arterial or venous occlusion pressure profiles and double occlusion. We formalized and solved the corresponding system of equations. We showed that in this model 1) pulmonary capillary pressure (Pc) profile after arterial or venous occlusion has an S shape, 2) the estimation of Pc by zero time extrapolation of the slow component of the arterial occlusion profile (Pcao) always overestimates Pc, 3) symmetrically such an estimation on the venous occlusion profile (Pcvo) always underestimates Pc, 4) double occlusion pressure (Pcdo) differs from Pc. We evaluated the impact of varying parameter values in the model with parameter sets drawn either from the literature or from arbitrary arterial and venous pressures, being respectively 20 and 5 mmHg. Resulting Pcao-Pc differences ranged from 0.4 to 5.4 mmHg and resulting Pcvo-Pc differences ranged from -0.3 to -5.0 mmHg. Pcdo-Pc was positive or negative, its absolute value in general being negligible (< 1.1 mmHg).

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This study was designed to investigate the pathogenesis of chlorine gas (Cl 2 ) induced acute lung injury and oedema.Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl 2 (n=7) for 10 min.Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl 2 -exposed lungs, the fluid filtration rate increased from -0.228±0.25 to 1.823±1.23 mL·min -1 ·100 g -1 (p<0.001) and the filtration coefficient increased from 0.091±0.01 to 0.259±0.07 mL·min -1 ·cmH 2 O -1 ·100 g -1 (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6±1.6 in the Cl 2 group and 4.0±0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid.Although the alveolar flooding by oedema is explained, in part, by the Cl 2 -induced epithelial injury, our results suggest that Cl 2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.

C Ca ap pi il ll la ar ry y p pr re es ss su ur re e e es st ti im ma at te es s f fr ro om m a ar rt te er ri ia al l a an nd d v ve en no ou us s o oc cc cl lu us si io on n i in n i in nt ta ac ct t d do og g l lu un ng g ABSTRACT: We performed pulmonary venous occlusions in order to check the validity of the pulmonary capillary pressure measurements obtained using pulmonary arterial occlusion in the intact animal.The venous and arterial postocclusion pressure profiles were recorded using balloon catheters introduced, respectively, into a left lower lobe vein and into a right pulmonary artery in the anaesthetized open-chest dog.The pressure profiles were fitted by a biexponential function with an early exponential and a late exponential presenting, respectively, a short and a long time constant. We used the zero-time extrapolation of the late slow exponential to obtain an arterial (Pc,ao) and a venous (Pc,vo) estimate of the pulmonary capillary pressure. Each P c,ao and P c,vo made it possible to calculate a fractional arterial or venous pressure gradient when referenced to the arteriovenous pressure gradient measured during the occlusion process. In nine dogs, when referenced to the whole lung, the arterial, middle and venous fractional pressure gradients were 37±11, 10±6, and 53±12%, respectively.As the middle fractional pressure gradient is low, we conclude that pulmonary capillary pressure estimates from arterial occlusion are close to the venous occlusion estimates of capillary pressure in the intact dog lung.