Key result
Inhaled nitric oxide selectively reversed pulmonary hypertension and decreased lung compliance induced by cell-free hemoglobin.
Why the study?
Does inhaled nitric oxide reverse pulmonary hypertension and decreased lung compliance induced by cell-free hemoglobin in a pig model?
Does inhaled nitric oxide reverse pulmonary hypertension and decreased lung compliance induced by cell-free hemoglobin in a pig model?
p-value: p=<0.05
Inhaled nitric oxide selectively reverses pulmonary hypertension and decreased lung compliance induced by cell-free hemoglobin blood substitutes in a pig model.
Does not support clinical use of inhaled nitric oxide for blood substitutes; leaves open translation from pig models to human trials.
BACKGROUND: In order to test the hypothesis that inhaled nitric oxide (NO) reverses the pulmonary hypertension induced by alphaalpha-diaspirin crosslinked hemoglobin (alphaalphaHb), were studied anesthetized pigs that were administered with a total dose of 200 mg/kg of 10% alphaalphaHb. Inhaled NO (5 ppm) was administered for 10 min, and then discontinued for 10 min. This cycle was then repeated with 10 ppm inhaled NO. RESULTS: alphaalphaHb caused pulmonary arterial pressure (PAP) to increase from 27 +/- 1.7 to 40 +/- 3.0 mmHg (P<0.05) and dynamic lung compliance to decrease from 29+/- 1.5 to 23+/- 1.6 ml/cmH2O (P < 0.05). After both doses of inhaled NO, but particularly 10 ppm, PAP was reduced (P < 0.05) and lung compliance increased (P < 0.05) from the alphaalphaHb levels. When inhaled NO was discontinued PAP again increased and lung compliance decreased to levels significantly different from baseline (P < 0.05). CONCLUSION: We conclude that cell-free hemoglobin-induced pulmonary hypertension and decreased lung compliance can be selectively counteracted by inhaled NO.
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Figueiredo et al. (1998) studied Cell-free hemoglobin-induced pulmonary hypertension (n=5). Inhaled nitric oxide vs. Baseline / ααHb infusion was evaluated on Pulmonary arterial pressure (PAP) (p=<0.05). Inhaled nitric oxide selectively reversed pulmonary hypertension and decreased lung compliance induced by cell-free hemoglobin.
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