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Table 1 Time changes in systemic hemodynamics, metabolism, and inflammation

From: Time course of nitric oxide synthases, nitrosative stress, and poly(ADP ribosylation) in an ovine sepsis model

   Time after injury (hours)
  Control 4 8 12 18 24
MAP, mmHg 105 ± 1 108 ± 10 87 ± 4a 81 ± 4a 76 ± 11b 63 ± 2c
CO, L/min 3.8 ± 0.2 5.4 ± 0.4 5.4 ± 0.1 6.6 ± 0.6a 6.9 ± 0.5a 7.1 ± 0.3b
apH, -log10 [H+] 7.50 ± 0.02 7.60 ± 0.03 7.50 ± 0.07 7.51 ± 0.02 7.37 ± 0.04a 7.29 ± 0.06a
aBE, mmol/L 2.1 ± 0.8 3.9 ± 1.9 -0.4 ± 2.0 0.3 ± 1.3 -3.2 ± 1.8 -3.6 ± 2.0a
PaCO2, mmHg 31 ± 0.0 30 ± 2 32 ± 4 30 ± 1 34 ± 2 38 ± 3a
BCT, °C 39.6 ± 0.1 40.7 ± 0.7 41.0 ± 0.2 40.6 ± 0.1a 40.1 ± 0.4a 39.2 ± 0.5
WBC, K/μL 6.7 ± 1.4 3.2 ± 1.0a 1.8 ± 0.6b 2.2 ± 0.6b 1.8 ± 0.5b 1.1 ± 0.2c
  1. Values recorded before sacrifice of animals with sham injury (control) and at different time points after induction of sepsis following acute lung injury. Each group includes four animals.
  2. aBE, arterial base excess; apH, arterial pH; BCT, body core temperature; CO, cardiac output; MAP, mean arterial pressure; PaCO2, partial arterial carbon dioxide pressure; WBC, white blood cells. a P < 0.05, b P < 0.01, c P < 0.001 vs. control group.