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Abstract
To examine whether the critical closing pressure (Pcrit) of the pulmonary vasculature
is dependent upon vasomotor tone, we measured Pcrit in six dog lobes before and after
the administration of vasodilators. We evaluated the pressure-flow (P-Q) relationship
in zone 2 flow conditions in situ perfused dog lobe (control period). We calculated
Pcrit as the mean extrapolated zero-flow pressure intercepts for the P-Q relationship.
We also used arterial and venous occlusions under zone 3 conditions to partition pulmonary
vascular resistance into arterial, middle and venous segment resistances. We then
repeated all measurements following administration of papaverine (150 micrograms/ml)
and sodium nitroprusside (200 micrograms/min) into the venous reservoir (vasodilator
period). Resistance in all three vascular segments was significantly reduced during
vasodilator conditions. Pcrit decreased from 3.68 +/- 0.76 cm H2O to 2.53 +/- 0.92
cm H2O during control and vasodilator periods respectively (P less than 0.05). The
slopes of the P-Q relationships were similar during both conditions. Our data support
a model in which vasomotor tone normally sets Pcrit but in which the pulmonary vasculature
can exhibit the phenomenon of critical closure even with vasomotor tone pharmacologically
ablated.