FIGURE 5.

Effects of nomacopan treatment early after blast injury on MAP, CH50, and blood chemistry changes in a clinically relevant rat model of traumatic haemorrhagic shock. (a) Experimental design; (b) changes of MAP were monitored via the carotid artery using the BIOPAC system. During the shock and resuscitation period, the MAP was recorded every 5 min. Data are presented as mean ± SEM; (c) haemolytic TCA of sera was measured by CH50 and normalized to baseline level, which was a pre‐blast injury; the percentages of baseline are shown; (d) PaO₂/FiO₂ ratio (PFR) following injuries. The PFR was calculated at each time point based on the artery i‐STAT data. A PFR of less than 300 (dashed line) suggests acute respiratory distress syndrome (ARDS). E‐G, the blood chemistry of lactate, BE/BD, and K⁺ in injured and treated animals were measured by I‐stat and presented. Data shown are means ± SEM from groups of rats, sizes (n) as indicated. *P < 0.05, significant effect of NOM; unpaired t‐test with Welch's correction; †P < 0.05, significantly different as indicated; two‐way ANOVA. Abbreviations: BOP = blast overpressure; B + H = blast + haemorrhagic shock; NOM = nomacopan given to injured rats; MAP = mean arterial pressure; EOS = end of the study