Effect of hyaluronidase on interstitial pressure response to edema in air-inflated rabbit lung.

The response in perivascular interstitial pressure to water accumulation was measured in air-inflated isolated rabbit lungs. The blood vessels and trachea of isolated lungs were cannulated and the vascular cannulas were connected to a reservoir filled either with a 3% albumin in saline solution (control) or with hyaluronidase in the albumin solution (treated). The lungs were inflated to 5 cmH2O transpulmonary pressure and the vascular reservoir elevated to a height of 7-10 cm above the lung base. The reservoir was suspended by a load cell which measured liquid accumulation in the lung. As the lung gained weight, interstitial pressure was measured by the micropuncture technique in the interstitium surrounding a vein near the hilum of an upper lobe. In control lungs, interstitial pressure increased monotonically with time from a value slightly below 0 cmH2O (pleural pressure) to a value of approx. 3.0 cmH2O by 5 h. In treated lungs, interstitial pressure increased more slowly to a value of approx. 1.5 cmH2O by 5 h. Interstitial compliance, the change in weight gain divided by the change in interstitial pressure, was 1.2 g.(g lobe wt)-1.cmH2O-1 for the control lungs and 2.9 for the treated lungs. A two-compartment electrical analog model representing the perivascular interstitium and alveolar liquid space was developed to simulate the data. The analysis indicated that in the control lungs, perivascular interstitial conductance and compliance were 5-fold and 15-fold smaller than those of the alveolar liquid space, respectively. The slower rise in interstitial pressure with water accumulation in the treated lungs was attributed to an increased compliance of the alveolar liquid space. The effect of hyaluronidase on the alveolar liquid space was to increase its compliance 2.4-fold with little change in its fluid resistance.