Analysis of pulmonary microvascular permeability after smoke inhalation

Abstract

We estimated the reflection (sigma) and filtration coefficients (Kf) in a chronic sheep lung lymphatic preparation after smoke inhalation. Group I (n = 7) sheep were insufflated with cotton smoke and group II animals (n = 5) with room air. After inhalation injury, the lung lymph flow increased nearly four times the baseline value by 24 h after injury. There was a concomitant reduction of sigma (0.81 +/- 0.02 to 0.64 +/- 0.02) and elevation of Kf (0.020 +/- 0.002 to 0.042 +/- 0.009 ml.min-1.mmHg-1); pulmonary capillary pressure was also elevated (13 +/- 1 to 17 +/- 1 mmHg). By 48 h postinjury, sigma and Kf returned toward baseline but pulmonary capillary pressure was still elevated. We determined that 34% of the increase in capillary filtration was attributable to increased capillary pressure and 66% to increased permeability 24 h after inhalation, but 48 h after injury, 75% of the increase in capillary filtration was attributable to increased capillary pressure and 25% to increased permeability. We conclude that the lung edema formation following smoke inhalation is the result of marked increases in both capillary pressure and permeability.

Burn and smoke inhalation injury in sheep depletes vitamin E: Kinetic studies using deuterated tocopherols

“…The tissue injury included an increase in pulmonary vascular permeability to both fluid and protein (11). Although the exact mechanism of the acute lung injury in thermal damage is not completely understood, we have shown that ROS play a critical role in this pathological process (12).…”

Combined burn and smoke inhalation injury impairs ovine hypoxic pulmonary vasoconstriction*

“…Although we did not determine transvascular fluid flux, we have previously shown that there is a marked increase in pulmonary lymph flow and a reduced reflection coefficient in both smoke alone and the combined injury (19,45).…”

Inhalational and Acute Lung Injury

“…We determined that the filtration coefficient rose from 0.020 Ô 0.002 mL/min/mm Hg to 0.042 Ô 0.009 mL/min/mm Hg (37). Using a paradigm developed by Taylor et al (29), we determined that 24 h after injury, 66% of the pulmonary microvascular fluid flux was the result of increases in small and large molecular permeability, whereas 34% was the result of increases pulmonary microvascular pressure (37).…”

“…We used pneumatic occluders placed on the pulmonary veins to raise microvascular pressure (36). With this technique, we determined that the reflection coefficient fell from 0.81 Ô 0.02 to 0.64 Ô 0.02 after injury (37).…”