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Ibuprofen Pre‐Treatment Increases Biomarkers of Heat Stroke Severity and Attenuates Fever during Recovery in Conscious Rats
Author(s) -
Audet Gerald N,
Duran Rocio M,
Ward Jermaine A,
Leon Lisa R
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1243.2
Subject(s) - medicine , stroke (engine) , ibuprofen , population , blood pressure , heart rate , anesthesia , pharmacology , antipyretic , cardiology , analgesic , mechanical engineering , environmental health , engineering
Heat stroke (HS) is a significant environmental threat to both military and civilian populations. We have shown previously in aconscious rodent model that non‐steroidalanti‐inflammatory drugs (NSAIDs) compound HS induced organ damage. Ibuprofen (IB) is one of the top prescribed NSAIDs globally and there are over 450,000 prescriptions for IB in US War fighter population alone, which does not include non‐prescription use. Yet, the effects of IB on HS morbidity have never been investigated. In the current study, we examined what effect a single pre‐dosage of IB has on physiological parameters during HS recovery in a new exertional heat stroke (EHS) rodent model. Fischer 344 rats were implanted with radio telemetry devices that continuously monitor core temperature (T c ),heart rate (HR), and mean arterial blood pressure (MAP). Rats were given either a single dose(62mg/Kg) of IB or vehicle (V, gum arabic) via oral gavage immediately prior to heating. Rats were then forced run(2–8m/min custom interval program) on a specialized heat‐specific running wheelat an ambient temperature of 37°C until cardiovascular crisis/compensatory failure (HR 608 ± 2 BPM; MAP 179 ± 1 mmHg). Rats were sacrificed at 5 days and organs were harvested for molecular and histological analysis. We found that those animals receiving IB had significantly higher temperatures at a given time point during heating (30 min sheating: IB 40.4 ± 0.1, V 40.0 ± 1 P<0.01; 45mins heating: IB 41.6 ± 0.1, V 41.2 ± 0.1 P<0.05), suggesting a decrease in cooling performance during running. IB increased the incidence of physiological biomarkers of severity; IB was the only group with hypothermia after heating (T c <37 °C, persisting through 24hrs), and had a significantly decreased MAP at 12 hours (IB= 102 ± 5, V= 119 ± 2, P<0.01). In those IB animals that did not experience hypothermia (60%), IB blunted the normal, mild, hyperthermic response found through 12hrs (IB Avg 37.8°C vs V38.4°C), suggesting for the first time that hyperthermia after EHS is a true febrile response. IB had no effect on control animals (those that were unheated). In conclusion, IB may be decreasing performance during heating, inducing increased morbidity during EHS recovery, and could be altering protective physiologic responses. Author views not official US Army or DoD policy.