Rat |
Shock tube (358 kPa, duration 10 ms), head only exposure with body armor protection |
GFAP, neuron specific enolase (NSE), and UCH-L1 increased in blood |
(64) |
Pig |
Shock tube, 20–40 psi |
Increased serum levels of S100B, MBP, NSE, and NF-H 6 h to 2 weeks following injury |
(116) |
Rat |
Shock tube, 20.6 psi whole body exposure combined with 1 week stress (predator scent exposure combined with unpredictable stress) |
2 months after blast/stress exposure elevated serum levels of cortisol, creatine kinase-BB, neurofilament-H (NF-H), neuron specific enolase (NSE), glial fibrillary acidic protein (GFAP), and vascular endothelial cell growth factor (VEGF). |
(43) |
Rat |
Shock tube, 20.63 psi |
51 days post-blast exposure, elevated CRP, MCP-1, cortisol, NSE, neurofilament-H, tau, claudin 5, and S100β in serum, elevations normalized by daily treatment with non-steroidal anti-inflammatory drug minocycline for four consecutive days after blast exposure |
(69) |
Rat |
Shock tube, 230–380 kPa on axis composite blast (blast wave plus pressure jet, duration 3–5 ms) or off axis (blast wave only, duration 50–100 μs) exposures |
Increased serum GFAP 1–7 days after primary and composite blast, markers of vascular/endothelial inflammation integrin α/β, soluble intercellular adhesion molecule-1, and L-selectin increased in serum within 6 h after primary and composite blast persisting for 7 days, systemic IL-1, IL-10, and fractalkine raised predominantly after primary blast exposure |
(48) |
Rat |
Shock tube, one or five 138 kPa exposures |
Serum VEGF, NSE, neurofilament H, and GFAP elevated in single and multiply injured animals at 22 days post-exposure |
(70) |
Rat |
Shock tube, 117 kPa, duration 7.5 ms |
Decreased IL-1a at 3 h, decreased macrophage colony stimulating factor (m-CSF) at 24 h, increased EPO at 48 h, decreased IL-1a, IL-1ss, IL-6, IL-10, EPO, and increased VEGF and m-CSF at 72 h, no changes in TNF-α at any time point |
(117) |
Rat |
Shock tube 120 kPa, positive pressure duration ~3 ms |
Plasma C5b-9 elevated by ELISA at 3 h and 24 h after blast but not 72 to 168 h |
(49) |
Rat |
Shock tube, 138 kPa, single or repeated (5 total administered on consecutive days) |
Changes in arterial oxygen saturation levels and heart rates of single-injured and multiply injured rats throughout observation period of 42 days, elevation of plasma biomarkers at 42 days (HNE, HIF-1α, ceruloplasmin, VEGF, von Willebrand factor, neurofilament H, GFAP, myelin basic protein, MMP-8, formyl peptide receptor 1, p38 mitogen-activated protein kinase, and chemokine receptor 5) in one or more groups |
(118) |
Mouse |
Shock tube, single 10, 15, or 21 psi exposures, repeat 3 × 21 psi delivered with 1–30 min intervals between exposures, whole body or head restricted exposure with a vest covering whole body except the head |
Plasma aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and creatine kinase increased as early as 1 h after blast exposure remaining elevated up to 6 h in an overpressure dose-dependent manner, returning close to normal levels at 24 h, head-only blast exposure with body protection showed no increase in the enzyme activities. |
(104) |
Mouse |
Shock tube, 20.6 psi three times with 1–30 min intervals between exposures |
Increased platelet activation at 4 h after repeated blast exposures, platelet serotonin decreased at 4 h after blast with a concurrent increase in plasma serotonin levels, blood and plasma myeloperoxidase enzyme activity and expression increased in repeated blast exposed mice at multiple time-points |
(53) |
Rat |
Head-directed blast with body armor delivered as (1) moderate “composite” blast with strong head acceleration or (2) moderate primary blast, without head acceleration, 230–380 kPa |
Thrombin generation in blood increased in both forms of blast, integrin alpha/beta and sICAM-1 levels elevated after both composite and primary blast at 6 h, 1 d, and 7 d, sE-selectin exhibited near normal levels after composite blast but increased at 7 d after primary blast, MMP-2, MMP-8, and MMP-13 rose slightly after composite blast and increased two-to-fourfold after primary blast |
(105) |
Rat |
Shock tube, single 120 kPa whole body exposure |
Increased IL-1β, erythropoietin, TNF-α, and IL-10 in the serum at 3 h, reaching peak at 24 h and returning to normal at 48 h |
(58) |
Rat |
Shock tube, five exposures administered as progressively higher exposures from 15.54–19.41 psi (107.14–133.83 kPa, durations 9.01–10.6 ms) at rate of one per 30 min with chest protection |
Two days post-exposure elevation in plasma of 4-HNE, HIF-1α, ceruloplasmin, VEGF, von Willebrand factor, aquaporin 1 and 4, fetal liver kinase 1 (FLK1/VEGF receptor 2), claudin 5, integrin α 6, TIMP1, TIMP4, Gal-1, p38 mitogen-activated protein kinase, MIP1, chemokine receptor 5, MCP1, cytokine-induced neutrophil chemoattractant 1 (CINC1), fibrinogen, CRP, N-formyl peptide receptor, GFAP, OX44, S100β, neuron-specific enolase, neurofilament H, creatine kinase-brain type, and tau |
(79) |
Rat |
Exposure to pentaerythritol tetranitrate explosive, (2,4,6-trinitrotoluene equivalent = 15.6 mg, “moderate” blast or = 27.0 mg “severe” blast) using a spherical exploder fixed over the head |
After either moderate or severe injury serum levels of tau, GFAP and TNF-α increased at 8 h, reaching peak at 24 h and remaining elevated at six days (last time-point tested), serum malondialdehyde levels increased at 3 and 6 days |
(106) |