Nitric oxide production after acute, unilateral hydrochloric acid-induced lung injury in a canine model

Objective: To determine if acute unilateral lung injury induces only local or systemic inflammatory effects by measuring the production of nitric oxid e (NO) and its metabolites (nitrites and nitrates) in the injured and the c ontralateral lung and the blood initially and 4 hrs after injury. Design: Unilateral hydrochloric acid instillation in split lung intubated s ubject studied over time. Setting: Animal physiology laboratory. Subjects: Five mongrel dogs. Interventions: Instillation of 10 mL of 0.1 N hydrochloric acid into one lu ng via a plastic catheter. Bronchoalveolar lavage (BAL) was done at 4 hrs. Measurements and Main Results: Unilateral acid instillation did not alter s ystemic blood pressure or cardiac output, nor did it induce arterial hypoxe mia. The BAL nitrite and nitrate level on the side of injury was higher tha n the control side (3.6 +/- 1.36 vs. 1.5 +/- 1.58 mM, p < .05), and serum n itrites and nitrates levels also decreased from the levels before acid inst illation levels (p < .05). Exhaled NO levels were measured only in three an imals. The levels increased acutely on hydrochloric acid instillation from only the injured lung and returned to baseline over several minutes. Howeve r, the level of exhaled NO from the injured lung failed to increase 4 hrs a fter injury, despite the increase in BAL nitrites and nitrates. Conclusions: Acute unilateral lung injury in the dog results in increased N O production that is compartmentalized to the injured lung. The increase in exhaled NO after injury is transient and does not allow one to monitor the progress of lung injury.