Individuals with spinal cord injury (SCI) exhibit reduced lung volumes and flow rates as a result of respiratory muscle weakness. These features have not, however, been investigated in relation to the combined effects of injury level and posture. Changes in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV(1)), FEV(1)/FVC, forced expiratory flow at 50% vital capacity (FEF(50)), inspiratory capacity (IC), and expiratory reserve volume (ERV) were assessed by injury level in the seated and supine positions in 74 individuals with SCI. The main findings were 1) FVC, FEV(1), and IC increased with descending SCI level down to T(10), below which they tended to level off; 2) supine values of FVC and FEV(1) tended to be larger in the supine compared with the seated posture down to injury level T(1), caudad to which they were less than when seated; 3) IC increased proportionately more down to injury level L(1), below which it declined slightly and plateaued; 4) ERV was measurable even at high cervical injuries, was generally smaller in the supine position, reached peak values in both positions at T(10) injury level, and then rapidly declined at lower levels; 5) when subjects were separated according to current, former, and never smokers, only formerly smoking paraplegic individuals demonstrated spirometric values significantly less than paraplegic individuals who never smoked. Changes in spirometric measurements in SCI are dependent on injury level and posture. These findings support the concept that the increase in vital capacity in supine position is related to the effect of gravity on abdominal contents and increase in IC.

Rationale We propose renin angiotensin system (RAS) peptides are critical in wound reparative processes such as in acute respiratory distress syndrome (ARDS). Their role in predicting clinical outcomes in ARDS has been unexplored; thus, we used a targeted metabolomics approach to investigate them as potential predictors of outcomes. Methods Thirty-nine ARDS patients were enrolled within 24 hours of ARDS diagnosis. Plasma RAS peptide levels were quantified at study entry and 24, 48 and 72 hours using a liquid chromatography-mass spectrometry based metabolomics assay. RAS peptide concentrations were compared between survivors and non-survivors, and were correlated with clinical and pulmonary measures. Measurements and main results Angiotensin I (Ang-I or A(1–10)) levels were significantly higher in non-survivors at study entry and 72 hours. ARDS survival was associated with lower A(1–10) concentration (OR 0.36, 95% CI 0.18–0.72, p = 0.004) but higher A(1–9) concentration (OR 2.24, 95% CI 1.15–4.39, p = 0.018), a biologically active metabolite of A(1–10) and an agonist of angiotensin II receptor type 2. Survivors had significantly higher median A(1–9)/A(1–10) and A(1–7)/A(1–10) ratios than the non-survivors (p = 0.001). Increased A(1–9)/A(1–10) ratio suggests that angiotensin converting enzyme II (ACE2) activity is higher in patients who survived their ARDS insult while an increase in A(1–7)/A(1–10) ratio suggests that ACE activity is also higher in survivors. Conclusion A(1–10) accumulation and reduced A(1–9) concentration in the non-survivor group suggest that ACE2 activities may be reduced in patients succumbing to ARDS. Plasma levels of both A(1–10) and A(1–9) and their ratio may serve as useful biomarkers for prognosis in ARDS patients.

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