Pathogenesis of Gastric Particulate Lung Injury

Abstract

Experimental aspiration pneumonitis studies in general have focused on the pathogenesis of the acidic component of the lung injury, although the injury produced by the particulate component of gastric contents largely has been ignored. The present study compares the inflammatory potential of small gastric particles to acidic lung injury and examines their interaction. Washed and filtered rat gastric food particles, 2-30 mu were resuspended in saline/HCl, pH = 5.3 or 1.25 at different particle densities and instilled intratracheally into anesthetized rats. Nonlethal lung injury was assessed at different times postaspiration by measuring changes in lung permeability and histology. Maximal survival after lung injury in this model occurred at a particle concentration of 40 mg/mL and at a volume of 1.5 mL/kg. Under these conditions, the alveolar capillary leak was less severe during the first 4 h after injury than that seen with a maximal nonlethal acidic injury (1.5 mL/kg, pH = 1.25). However, after 4 h postinjury the alveolar capillary leak increased to levels that were no different from the acidic injury. When the small gastric food particles were suspended in saline/HCl, pH = 1.25, the alveolar capillary leak was increased synergistically. Intratracheal instillation of inert, 10 mu (glass) particles, 40 mg/mL at 1.5 mL/kg, did not result in an increase in lung injury or interact additively or synergistically with acidic saline. Histologically, the small gastric particle injured lungs were associated with focal inflammatory changes as the acidic damage was diffuse.(ABSTRACT TRUNCATED AT 250 WORDS)

NADPH Oxidase and Nrf2 Regulate Gastric Aspiration–Induced Inflammation and Acute Lung Injury

“…Mice were fluid-resuscitated with 1 ml normal saline injected subcutaneously into the ventral neck and allowed to recover in room air with food and water ad lib . Particles were derived from gastric filtrates, as previously described (28, 30). The particle preparation procedure removes gastric enzymes and bile salts and results in a mixture of gastric particles that ranged in size from 2 – 30 μm in diameter.…”

Low pH Environmental Stress Inhibits LPS and LTA-Stimulated Proinflammatory Cytokine Production in Rat Alveolar Macrophages

“…Although gastric components are highly variable with varying proportions of gastric particles, acidity, and bacterial load, it appears that the extent of pulmonary injury is directly related to the aspirate volume, acidity, and composition [3, 4]. In rat models of gastric aspiration injury, intratracheal administration of acidified solution (pH of 1.25) results in an early direct corrosive irritation to the airway epithelium followed by a delayed inflammatory response (4–6 hours after exposure) characterized by neutrophil activation and extravasation into the air spaces and elaboration of proinflammatory mediators and chemotactic cytokines [3, 5, 6].…”

Assessment of Pre-Gastroscopy Fasting Period Using Ultrasonography

“…Animal experiments demonstrate that the mortality in pulmonary aspiration depends on the pH and the amount of fluid regurgitated. Whereas a small volume with low pH might be fatal, higher volumes of fluid with higher pH values might be tolerated without serious adverse event [12,13]. The authors therefore assessed if recent ingestion of fluids might contribute to increased acidity of the gastric fluid upon subsequent endoscopy and therefore increase the risk of acid aspiration.…”