Effect of ablated bronchial blood flow on survival rate and pulmonary function after burn and smoke inhalation in sheep

Summary

The bronchial circulation plays a significant role in the pathophysiological changes of burn and smoke-inhalation injury. Bronchial blood flow markedly increases immediately after inhalational injury. This study examines whether the ablation of the bronchial artery attenuates pathophysiological changes and improves survival after burn and smoke-inhalational injury in an ovine model. Acute lung injury was induced by 40% total body surface-area third-degree cutaneous burn and cotton smoke inhalation (48 breaths of cotton smoke, <40 °C) under deep anaesthesia. Twelve adult female sheep were divided into two groups: (1) sham (injured, non-ablated bronchial artery, n = 6); (2) ablation (injured, ablated bronchial artery, n = 6). Ablation of the bronchial artery was performed 72 h before the injury. The experiment was continued for 96 h. Burn and smoke-inhalation injury significantly increased regional blood flow in the bronchi. Ablation of the bronchial artery significantly reduced acute regional blood flow increases in the proximal and distal bronchi. All animals in the ablation group survived to 96 h. Four of these were successfully weaned off the ventilator. Three animals of the sham group met standardised euthanasia criteria at 60 h, while another met the criteria at 78 h. The lung wet-to-dry weight ratio, histology score and myeloperoxidase (MPO) activity were significantly increased by the insult, but ablation of the bronchial artery attenuated these changes. Burn and smoke-inhalation injury induced a significant increase in bronchial blood flow and accelerated airway obstruction, pulmonary vascular changes, pulmonary oedema and pulmonary dysfunction. Ablated bronchial circulation attenuated these pathophysiological changes.

Introduction

Severe burn is very traumatic, especially when the injury is associated with smoke inhalation. This combination greatly increases morbidity and mortality [1], [2]. After smoke inhalation, there is a rapid appearance of hyperaemia in the upper airway of humans and sheep [3], [4], [5]. Hyperaemia of the airway is the most effective way of diagnosing smoke inhalation [6]. Pulmonary oedema has been directly related to smoke-inhalational injury, as evidenced by an increase in extravascular lung water and lung lymph flow after inhalational injury [7], [8], [9], [10], [11]. Smoke inhalation has also been shown to cause an increase in microvascular permeability to protein in the pulmonary and bronchial circulations [8], [9], [10], [12].

These physiological alterations in the pulmonary microvasculature are delayed in onset, and the peak of increased microvascular permeability was observed around 24 h after injury [13]. In contrast, there is a marked increase in bronchial blood flow immediately after inhalational injury [3], [14]. Because the increased bronchial blood flow largely enters the pulmonary vasculature through pre-capillary anastomoses with the pulmonary microcirculation [15], [16], [17], it has been suggested that the bronchial circulation plays a significant role in the spread of injury from the airway of the lung to the parenchyma [11], [18]. Reduction of the bronchial artery circulation reduced lung oedema formation after inhalation in the anaesthetised canine model [11] and in a conscious sheep model [10], [18]. For this, we performed 96-h survival experiments and analysed the regional tissue blood flow. The present study was undertaken to provide a detailed analysis of pulmonary function at 96 h after injury and to estimate the 96-h survival rate. We hypothesised that ablation of the bronchial artery would not only reduce pulmonary injury following combination burn and inhalational injury, but would also allow survival to 96 h with weaning from ventilatory support.