In order to partition pulmonary vascular resistance in its arterial (Ra), venous (Rv) and capillary (Rcap) components, we applied the method of arterial and venous occlusions (Hakim et al., J Appl Physiol 52: 710-715, 1982) in 7 anesthetized (Chloralose 50 mg/ 100g i.p.), tracheotomized, positive pressure ventilated rats. The thorax was opened, and two catheters were inserted into the pulmonary artery and left atrium through two small incisions performed on the right and left ventricular walls respectively. The catheters were firmly kept in place by a single binding passed in the atria-ventricula solcum. Hydraulic resistance of the catheters (Req) was separately measured and subtracted from results, which hence represent intrinsic values. The lungs were perfused with eparinized Emagel at a fixed flow rate of 5 ml/min, and pulmonary artery pressure was monitored and recorded on paper. Left atrium pressure was mantained near athmospheric. Three to five arterial and venous occlusions were performed for each rat, and the pressure drops due to arterial and venous resistances were measured. The resistance of the highly distensible middle component, which most likely includes capillaries, and small arterioles and venules, was quantified by subtraction of Ra and Rv from total vascular resistance (R). Pulmonary vascular compliance (C) was also measured analyzing the rise of intravascular pressure during venous occlusion and maintained perfusion (see Hakim et al.). Results were as follows:

a) the mean values of R, Ra, Rv, Rcap resulted 5.7±0.8, 2.05±0.4, 1.26±0.16, 2.4±0.9 cmH₂O/ml sec^-1 respectively, while C resulted 0.048 ml/ cm H₂O.

b) Ra, Rv, Rcap represent about 36%, 22% and 42% of R respectively.

R values resulted rather high, probably because of the low flow we used in order to avoid the risk of pulmonary edema, and of the low lung volume. Some degree of hypoxic vasoconstriction also may not be excluded.

These data are rather similar to those previously published (Rubini, Europ J Appl Physiol 93: 435-439, 2005), and show that the higher resistance in the pulmonary vascular tree is attributable to the middle segment. This is different from what previusly observed in tha isolated dog lung lobe.