Hyperbaric oxygen therapy may overcome nitric oxide blockage during cyanide intoxication.

PURPOSE: To determine the effects of a blockade of nitric oxide (NO) synthesis on hyperbaric oxygen (HBO2) therapy during cyanide (CN) intoxication. METHODS: 39 anesthetized female Sprague-Dawley rats were exposed to CN intoxication (5.4 mg/kg intra-arterially) with or without previous nitric oxide synthase (NOS) inhibition by L-NG-nitroarginine methyl ester (L-NAME) injection (40 mg/kg intraperitoneally). Subsequently, either HBO2 therapy (284 kPa/90 minutes), normobaric oxygen therapy (100% oxygen/90 minutes) or nothing was administered. Intracerebral microdialysis was used to measure the interstitial brain concentration of lactate, glucose, glycerol and lactate/pyruvate ratios. RESULTS: L-NAME potentiated CN intoxication by higher maximum and prolonged lactate (in mM: 0. 5 ± 0.3 vs. 0.7 ± 0.4, P ⟨ 0.005) concentrations compared with solely CN-intoxicated rats. The same trend was found for mean glucose, glycerol and lactate/pyruvate ratio levels. During HBO2 treatment a sustained reduction occurred in mean lactate levels (in mM: 0.5 ± 0.5 vs. 0.7 ± 0.4, P ⟨ 0.01) regardless of NOS blockade by L-NAME. The same trend was found for mean glucose and glycerol levels. CONCLUSION: The results suggest that blocking NOS using L-NAME can worsen acute CN intoxication. HBO2 treatment can partially overcome this block and continue to ameliorate CN intoxication.

SuPAR correlates with mortality and clinical severity in patients with necrotizing soft-tissue infections: results from a prospective, observational cohort study.

Necrotizing soft tissue infections (NSTI) have a 90-day mortality rate of 18-22%. Tools are needed for estimating the prognosis and severity of NSTI upon admission. We evaluated soluble urokinase-type plasminogen activator receptor (suPAR) levels at admission as a prognostic marker of NSTI severity and mortality. In a prospective, observational cohort study, suPAR was measured in 200 NSTI patients. We compared admission suPAR levels in survivors and non-survivors, patients with septic shock and non-shock, amputation and non-amputation, correlations with Simplified Acute Physiology Score II (SAPS II) and the Sequential Organ Failure Assessment (SOFA) score. Admission suPAR levels were higher in septic shock vs. non-septic shock patients (9.2 vs. 5.8 ng/mL, p-value < 0.001) and non-survivors vs. survivors (11 vs. 6.1 ng/mL, p-value < 0.001) and correlated with SAPS II (r = 0.52, p < 0.001) and SOFA score (r = 0.64, p < 0.001). Elevated suPAR upon admission was associated with 90-day mortality (log-rank test p < 0.001), however not after adjustment for age, sex, and SOFA score. The AUC for suPAR and 90-day mortality was 0.77. We found that suPAR is a promising candidate for prognosis and severity in patients with NSTI.