Acid-base composition of mice blood during the progression of toxic pulmonary edema

BACKGROUND: Modeling toxic pulmonary edema for the purpose of studying the effectiveness of drugs is associated with difficulties in model validation and objectification of drug effectiveness criteria. To confirm the significance of changes in pulmonary coefficients and visual changes in lung tissue, acid-base balance and blood gas analysis are often used to objectify emerging gas exchange disorders.

AIM: To investigate the acid-base composition and blood gases in mice during the progression of toxic pulmonary edema caused by inhalational phosgene exposure.

MATERIAL AND METHODS: Toxic pulmonary edema was induced by exposing mice to phosgene at a dose corresponding to LCt₅₀ in an inhalation chamber. Blood samples were analyzed for acid-base balance and gas parameters, including partial oxygen pressure (pO₂), partial carbon dioxide pressure (pCO₂), total hemoglobin (tHb), oxyhemoglobin (O₂Hb), carboxyhemoglobin (COHb), methemoglobin (MetHb), reduced hemoglobin (RHb), oxygen saturation (sO₂), oxygen concentration (O₂ct), oxygen capacity (O₂cap), partial oxygen pressure at 50 % saturation (P₅₀), total carbon dioxide (tCO₂), true and standard bicarbonate (HCO_3–, SBC), actual and standard base excess (BE_b, BE_ecf), anion gap, lactate, and concentrations of sodium, potassium, chloride, and ionized calcium. Measurements were performed using a gas analyzer at 30 minutes, 3 hours, and 24 hours after exposure initiation.

RESULTS: Significant shifts in blood gas composition and acid-base balance were observed 3 hours after pulmonary edema initiation. These included decreased acid-base balance, reduced oxyhemoglobin levels, lowered oxygen saturation, and elevated partial carbon dioxide pressure, indicating respiratory insufficiency and compensated respiratory acidosis. Major changes in acid-base parameters were observed after 24 hours, with normalization of pH accompanied by increases in true and standard bicarbonate levels, as well as total carbon dioxide content. Changes in actual and standard base excess were observed, reflecting a reduction in base deficit. Electrolyte levels remained unchanged in all experimental groups throughout all observation periods.

CONCLUSIONS: The study elucidated the progression of respiratory hypoxia during toxic pulmonary edema and confirmed that respiratory hypoxia serves as a key pathogenic link, leading to significant disruptions in energy metabolism during the progression of pulmonary edema.