Jianpu Wang

Administration of aerosolized terbutaline and budesonide reduces chlorine gas-induced acute lung injury.

BACKGROUND The pathophysiology and treatment of chlorine gas-induced acute lung injury is poorly characterized and based on anecdotal data. This study aimed to assess the effects of aerosolized beta-2 adrenergic agonist and corticosteroid therapy on chlorine gas-induced lung injury. METHODS Anesthetized, ventilated pigs were exposed to chlorine gas (400 parts per million for 20 minutes), then assigned randomly 30 minutes later to receive aerosolized terbutaline, budesonide, terbutaline followed by budesonide or placebo (6 pigs in each group). Hemodynamics, gas exchange, and lung mechanics were evaluated for another 5 hours. RESULTS All the animals demonstrated an immediate increase in airway and pulmonary artery pressure as well as sharp drops in arterial oxygen tension (PaO2) and lung compliance (CL). Recovery of PaO2 and CL was greatest in the terbutaline plus budesonide group, but therapy with terbutaline and budesonide alone also was associated with significant improvement in PaO2 and CL, as compared with placebo. CONCLUSIONS Treatment of acute chlorine gas lung injury with aerosolized terbutaline followed by aerosolized budesonide improved lung function. Combined treatment was more effective than treatment with either drug alone.

Inhaled and intravenous corticosteroids both attenuate chlorine gas-induced lung injury in pigs

Background:  The accidental release of chlorine gas is a constant threat in urban areas. The purpose of this randomized, blinded, controlled experiment was to examine the effects of post‐injury administration of inhaled or intravenous corticosteroid in chlorine gas‐injured pigs followed for 23 h.

Effects of prone and supine posture on cardiopulmonary function after experimental chlorine gas lung injury

Background: Chlorine gas may induce severe acute lung injury. Improvement of pulmonary gas exchange in patients and animals with acute lung injury nursed in the prone position was observed in recent years. The purpose of this study was to evaluate the effects of prone and supine positions on pulmonary and cardiovascular functions following experimental chlorine gas lung injury.

Effects of endothelin receptor antagonism on acute lung injury induced by chlorine gas

Objective:To test the hypothesis that the endothelin system is involved in chlorine gas-induced lung injury. Design:Experimental study. Setting:Academic research laboratory. Subjects:Twenty-four domestic juvenile pigs. Interventions:Anesthetized, ventilated pigs were exposed to chlorine gas (400 parts per million in air) for 20 mins and then randomly allocated to four groups (n = 6 in each group). The tezosentan pretreatment group received the dual endothelin receptor antagonist tezosentan 20 mins before and hyperoxic gas (Fio2 0.6) after chlorine gas exposure. The tezosentan postinjury treatment group received hyperoxic gas after chlorine gas exposure and tezosentan 60 mins later. Animals in the oxygen group received hyperoxic gas after chlorine gas exposure. Pigs in the fourth group (air) were ventilated with room air (Fio2 0.21) throughout the experiment. Measurements and Main Results:Hemodynamics, gas exchange, lung mechanics, and plasma endothelin-1 were evaluated for 6 hrs. Chlorine gas exposure induced an increase in circulating endothelin-1 by 90% (p < .05). The acute chlorine gas-induced rise in pulmonary vascular resistance was partly blocked by tezosentan pretreatment (p < .001). Tezosentan postinjury treatment also decreased pulmonary vascular resistance to levels significantly lower than in the air and oxygen groups (p < .001). Recovery of peak airway pressure was better in the tezosentan-treated groups than in the air group. There were significant linear relationships between circulating endothelin-1 and pulmonary vascular resistance (r2 = .47, p < .001) and endothelin-1 and peak airway pressure (r2 = .41, p < .001). These relationships were modified by tezosentan. Conclusions:Tezosentan modified chlorine gas-induced pulmonary dysfunction, indicating that the endothelin system is involved in this mode of acute lung injury.

Establishment of a teaching animal model for sonographic diagnosis of trauma.

BACKGROUND Ultrasound is widely accepted as a valuable diagnostic tool for detecting intra-abdominal and intrathoracic bleeding in trauma patients. Nevertheless, many doctors are reluctant to use it because they do not have sufficient training. This study aimed to define intra-abdominal and intrathoracic fluid volumes that can be detected by sonography and their relation to fluid width in pigs to establish a clinically relevant animal model for teaching and training. METHODS Different volumes of normal saline were infused into the abdomen (50-2,000 mL) and chest (25-250 mL) in five anesthetized pigs. The maximum width of fluid as detected by ultrasound was recorded. The right upper quadrant, left upper quadrant, pelvis, and right paracolic section of the abdomen and right pleural cavity were studied. An experienced radiologist performed the studies. The effects on respiratory and cardiovascular functions were evaluated. RESULTS The sonographic findings in the pig were similar to those in humans. Up to 50 mL of intra-abdominal fluid and up to 25 mL of intrathoracic fluid could be detected by ultrasound. There was a significant correlation between the volume infused and the fluid width detected. The respiratory and cardiovascular monitoring of the animals showed that the infused intrathoracic volumes mimicked a survivable hemothorax. CONCLUSION The pig may serve as an excellent clinically relevant model with which to teach surgeons detection of different volumes of intra-abdominal and intrathoracic fluids. The value of this model as an educational tool has yet to be tested.

Chlorine gas inhalation: mechanisms of injury and treatment

Chlorine is a highly reactive gas that is used in large quantities throughout modern society. Accidental release of chlorine gas with exposure of large numbers of people is a constant threat to urban areas. The toxicity of chlorine is related almost entirely to effects in the respiratory system. The treatment of victims exposed to chlorine gas is mainly symptomatic including supplemental oxygen and antitussive medication. Administration of nebulized β2‐agonists is supported by recent experimental studies, and early treatment with inhalational or systemic corticosteroids is supported by case reports and experimental data. Systematic experimental studies and pre‐arranged treatment protocols are needed to advance the evidence base of therapy for chlorine gas lung injury.