61 Effects of a calcareous marine algae on blood biochemistry during a heat wave in grain-fed steers
Authors: Sammes Stephanie L , Gaughan John B , O’Connell Shane , Lees Angela 
Published: September 2024

Insult to the gastrointestinal tract (GIT) during heat stress has profound effects on epithelium integrity and subsequent regulation of inflammatory immune responses. The objective of this study was to evaluate the effects of different dietary buffering feeding strategies, on serum amyloid A (SAA), lipopolysaccharide-binding protein (LBP), aspartate aminotransferase (AST), glutamate dehydrogenase (GLDH), gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (ALP), partial pressure of carbon dioxide (pCO2), base excess (BE), blood pH and bicarbonate (HCO3) of grain-fed steers exposed to a simulated heat wave event. Angus steers [n = 12; body weight (BW) = 582 ± 8.92 kg) were housed within climate control rooms for 21 d and randomly allocated into one of three dietary treatments (4 steers/treatment): 1) Treatment 1 (T1), finisher diet; 2) Treatment 2 (T2), transitioned from finisher to heat load diet (HLD) on d 4, fed HLD until d 16; 3) Treatment 3 (T3), fed finisher and supplemented with a calcareous marine algae (CMA; Acid Buffer, Celtic Sea Minerals) on d 4 until d 16. On d 17, T2 and T3 transitioned back to finisher. Days were split into three phases consisting of i) d 0 to 6 [PI, Temperature Humidity Index (THI), 65-78); ii) d 7 to 11 (PII, THI 83-87); iii) d 12 to 20 (PIII, THI 65-78). Individual steer jugular vein blood samples (40 mL) were obtained on d 0, 4 (PI), 7 to 11 (PII), 12 to 17, 18 and 20 (PIII), with plasma extracted. Data were analyzed using a repeated measures model, with a first order auto-regressive error structure, including fixed effects for treatment, phase and day, animal ID as a random effect. During PII, all steers had decreased pCO2 (P &lt; 0.0001), HCO3 (P &lt; 0.04) and BE (P &lt; 0.01), indicating compensated respiratory alkalosis associated with hyperventilation, as blood pH remained unchanged (P = 0.15; Table 1). Both AST (P ≤ 0.009) and GLDH (P ≤ 0.004) were at a maximum during PIII, with T1 having greater AST (P ≤ 0.01) and GLDH (P ≤ 0.04) compared with T2 and T3. Greater AST and GLDH are suggestive of liver damage with reduced detoxifying capabilities becoming overloaded during PII. Interestingly, GGT remained similar (P ≤ 0.94) for TRT × phase, it remains unclear why, warranting further exploration. Alkaline phosphatase was decreased (P &lt; 0.0001) for all treatments during PII and PIII compared with PI, potentially ALP was diverted to the GIT to aide in protection from endotoxemia. During PII, SAA tended to increase (P = 0.08), LBP remained at similar (P = 0.12) levels to PI, before both inflammatory markers decreased (P ≤ 0.05) during PIII. Observationally, steers had gut lining epithelium (mucin casts) within their feces from d 10 to 13. In conclusion, the heat wave initiated a respiratory alkalosis, upregulation of inflammatory marker SAA and mucin casts within feces, suggestive of acute heat stress. Subsequent liver damage, as indicated by greater AST and GLDH post-heat wave, were potentially mediated by inclusion of CMA in the diet.