Heat Stress Causes Persistent Multisystemic Dysfunction

Abstract Heat stress (HS) causes multisystemic dysfunction and negatively impacts animal production. That the deleterious effects on production persist after HS abates raises the possibility of continuing injury and pathology that is not remediated by reestablishing euthermia. We hypothesized that a single bout of HS would cause immediate and persistent heart, liver, and kidney injury. To test this hypothesis, we collected blood from 3 month-old crossbred pigs (n = 12; 8 barrows, 4 gilts) under thermoneutral (TN; Pre) conditions (20.6 ± 0.2 ºC), following a 24 h HS (37.4 ± 0.2 ºC, 24hP), and 3 mo following HS (3mP). Skeletal muscle and cardiac muscle injury were apparent as creatine kinase (P < 0.05), myoglobin (P < 0.05), cardiac troponin I (cTnI; P < 0.05) and NT-proBNP (P < 0.05) were increased in 24hP compared with Pre, and elevations in NT-proBNP in 3mP raise the possibility of lasting cardiac injury. Additionally, cTnI and NT-proBNP were greater in gilts than barrows as a main effect of sex (P < 0.05). Increased creatinine, Mg, and blood urea nitrogen (BUN) in 24hP, and chronic elevations in creatinine, Cl, Mg, Na, Ca, bicarbonate, and BUN and reduced phosphorus and K (P < 0.05 < 0.1) in 3mP, indicate a single HS causes rapid and lasting impairments in renal function. Heat stress also increased aspartate aminotransferase (AST; P < 0.05) 24hP but decreased alkaline phosphatase (P < 0.05) and total bilirubin in 24hP (P < 0.1) and AST (P < 0.05) and total bilirubin in 3mP (P < 0.05). In total, these data suggest that HS causes both immediate and long-term cardiac, liver, and renal dysfunction and this appears to be influenced, at least in part, by biological sex.