Evaluating the effects of zinc hydroxychloride on intestinal barrier permeability and biomarkers of inflammation and metabolism during and following heat stress.

Abstract

Heat stress (HS) jeopardizes dairy cow productivity and health. Gastrointestinal tract (GIT) barrier dysfunction appears to be the etiological epicenter of HS-induced pathology. However, the physiology of recovery from HS has scarcely been studied in dairy cows. Thus, objectives were to evaluate the effects of supplemental zinc (Zn) hydroxychloride (HYD) on intestinal barrier permeability, metabolism, and inflammation during and following HS. Holstein cows (n = 24; 130 ± 34 DIM; parity 2 ± 0.5) were balanced by DIM and milk yield and assigned to 1 of 2 ad libitum-fed treatments: (1) control diet (CON; 75 mg/kg Zn from Zn sulfate; n = 12), or (2) HYD (75 mg/kg Zn from HYD; n = 12). Before study initiation, cows were fed their respective diets for 16 d. The trial consisted of 3 experimental periods (P), during which cows continued to receive their respective dietary treatment. Period 1 (5 d) served as the baseline for P2 (5 d), during which HS was artificially induced using electric heat blankets (EHB). During P3 (3 d), the EHB were removed, and cows were allowed to recover in thermoneutral conditions. In vivo total GIT permeability was evaluated on d 4 of P1, d 2 and 4 of P2, and d 2 of P3, using chromium (Cr)-EDTA. As expected, HS increased rectal and skin temperatures (+1.8 and +7.2°C, respectively) and respiration rate (+62 breaths per min) relative to baseline. Heat stress increased Cr appearance (indicative of increased permeability) on both d 2 and 4, and feeding HYD decreased blood Cr appearance on d 2 of P2, with the most pronounced decrease observed during h 1 (29%) relative to controls. Whereas haptoglobin (Hp) concentrations remained constant in CON cows relative to P1, they increased (77%) in HYD-fed cows from d 3 to 5 of HS. During HS recovery, plasma Hp levels remained elevated in HYD and markedly increased in CON (>6-fold) compared with d 5 of P2. Heat stress decreased DMI and milk yield (60% and 42%, respectively) relative to P1. During P3, overall Cr appearance was reduced (reflecting improved barrier function) compared with both P2 and 1. Dry matter intake gradually recovered in both treatments during HS recovery but was increased in HYD-fed cows (10%) relative to CON. Circulating nonesterified fatty acids and BHB progressively increased during HS in both treatments but tended to be lower in HYD from d 3 to 5 (28% and 14%, respectively) relative to CON, and the reducing effects of HYD on BHB continued during the early stage of HS recovery. In summary, HS-induced GIT hyperpermeability, caused inflammation, and altered metabolism; however, whereas inflammation persisted during HS recovery, Cr appearance decreased in P3 compared with P1 and 2. During the early stages of HS, supplementing HYD improved gut barrier function and modified both metabolism and inflammation, and increasing DMI during HS recovery.