Sclerosis therapy of bronchial artery attenuates acute lung injury induced by burn and smoke inhalation injury in ovine model

Abstract

Introduction: In burned sheep, we showed more than a 10-fold increase in bronchial blood flow following smoke inhalation. It was previously reported that sclerosis of the bronchial artery prior to smoke exposure reduces the pathophysiology of the inhalation insult. We hypothesized that sclerosis of the bronchial artery after insult attenuates smoke/burn-induced acute lung injury.

Methods: Through an incision at the 4th intercostal space, a catheter was placed via the esophageal artery into the bronchial artery such that the bronchial blood flow remained intact. Acute lung injury was induced by a 40% total body surface area, 3rd degree cutaneous burn and smoke inhalation. Adult female sheep (n=18, 35.6±1.0 kg) were divided into three groups following the injury: (1) sclerosis group: 1h after injury, 4 mL of 70% ethanol was injected into bronchial artery via bronchial catheter, n=6; (2) control group: 1h after injury, an equal dose of saline was injected into bronchial artery via the bronchial catheter, n=6; (3) sham group: no injury and no treatment, n=6. The experiment was conducted in awake animals for 24 h.

Results: Bronchial blood flow, measured by microspheres, was significantly reduced after ethanol injection in the sclerosis group. Pulmonary function, evaluated by measurement of blood gas analysis, pulmonary mechanics, and pulmonary transvascular fluid flux, was severely impaired in the control group. However, pulmonary function was significantly improved by bronchial artery sclerosis.

Conclusion: The results of our study clearly demonstrate a crucial role of enhanced bronchial circulation in thermal injury-related morbidity. Decreasing bronchial circulation using pharmacological agents may be an effective strategy in management of burn patients with concomitant smoke inhalation injury.

Fig 1

Changes in airway blood flow after burn and smoke inhalation injury. Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).

Fig 2

Effects of bronchial artery sclerosis on pulmonary gas exchanges. Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).

Fig 3

Effects of bronchial artery sclerosis on pulmonary artery pressure (A) and pulmonary vascular resistance (B). Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).

Fig 4

Effects of bronchial artery sclerosis on peak (A) and pause (B) airway pressure. Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).

Fig 5

Effect of bronchial artery sclerosis on lung lymph flow (A) and lung pulmonary vascular permeability index (B). Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).

Fig 6

Photographs showing representative cast formation in trachea and bronchi in control animals at 24 h (A), cast formation in bronchia in control animals (B) and cast formation in trachea and bronchi in sclerosis animals at 24 h (C). Burn and smoke inhalation injury causes cast formation in airway (A, B). However, bronchial artery reduced the cast formation in bronchi (white circle) but not in trachea (C).

Fig 7

Effect of bronchial artery sclerosis on the bloodless lung wet to dry (A) and myeloperoxidase activity (B). Data are expressed as mean ± SEM. * Significant difference vs. sham group (p < 0.05); † Significant difference vs. control group (p < 0.05).