Pathogenesis of Gastric Particulate Lung Injury: A Comparison and Interaction with Acidic Pneumonitis

• Published in: Anesthesia and analgesia Vol. 77; no. 4; pp. 754 - 760
• Main Authors: Knight, Paul R., Rutter, Timothy, Tait, Alan R., Coleman, Elizabeth, Johnson, Kent
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD International Anesthesia Research Society 01.10.1993; Lippincott
• Subjects: Acids; Anesthesia; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Food; Local anesthesia. Pain (treatment); Male; Medical sciences; Pneumonia, Aspiration - chemically induced; Pneumonia, Aspiration - etiology; Pneumonia, Aspiration - mortality; Rats; Specific Pathogen-Free Organisms; Lung disease; Stomach; Rat; Respiratory disease; Pathogenesis; Rodentia; General anesthesia; Trauma; Particle; Vertebrata; Mammalia; Acids; Aspiration pneumonia; Animal; pH; Complication; Foreign body
• ISSN: 0003-2999; 1526-7598
• DOI: 10.1213/00000539-199310000-00017

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 μ 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 μ (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. Although rats that received both particulate and acidic material had a much more severe lung injury than with either of these substances alone, particulate injury also induced chronic inflammation with the formation of early granuloma at 48 h postaspiration. This confirms the synergistic effects of a combined acidic and particulate injury on alveolar capillary leakage. These data suggest a critical and interactive role for both acid and small particulate components in the pathogenesis of gastric aspiration pneumonitis.