Effects of hindgut acidosis on production, metabolism, and inflammatory biomarkers in previously immune-activated lactating dairy cows.

Previous stressors and systemic inflammation may increase the intestine's susceptibility to hindgut acidosis (HGA). Therefore, our experimental objectives were to evaluate the effects of isolated HGA on metabolism, production, and inflammation in simultaneously immune-activated lactating cows. Twelve rumen-cannulated Holstein cows (118 ± 41 d in milk; 1.7 ± 0.8 parity) were enrolled in a study with 3 experimental periods (P). Baseline data were collected during P1 (5 d). On d 1 of P2 (2 d), all cows received an i.v. lipopolysaccharide (LPS) bolus (0.2 µg/kg of body weight; BW). During P3 (4 d), cows were randomly assigned to 1 of 2 abomasal infusion treatments: (1) control (LPS-CON; 6 L of H2O/d; n = 6) or (2) starch infused (LPS-ST; 4 kg of corn starch + 6 L of H2O/d; n = 6). Treatments were allocated into 4 equal doses (1.5 L of H2O or 1 kg of starch and 1.5 L of H2O, respectively) and administered at 0000, 0600, 1200, and 1800 h daily. Additionally, both treatments received i.v. LPS on d 1 and 3 of P3 (0.8 and 1.6 µg/kg of BW, respectively) to maintain an inflamed state. Effects of treatment, time, and their interaction were assessed. Repeated LPS administration initiated and maintained an immune-activated state, as indicated by increased circulating white blood cells (WBC), serum amyloid A (SAA), and LPS-binding protein (LBP) during P2 and P3 (29%, 3-fold, and 50% relative to P1, respectively) for both abomasal infusion treatments. Regardless of abomasal treatment, milk yield and dry matter intake were decreased throughout P2 and P3 but with lesser severity following each LPS challenge (54, 44, and 37%, and 49, 42, and 40% relative to baseline on d 1 of P2, d 1 and d 3 of P3, respectively). As expected, starch infusions markedly decreased fecal pH (5.56 at nadir vs. 6.57 during P1) and increased P3 fecal starch relative to LPS-CON (23.7 vs. 2.4% of dry matter). Neither LPS nor starch infusions altered circulating glucose, insulin, nonesterified fatty acids, or ß-hydroxybutyrate, although LPS-ST cows had decreased blood urea nitrogen throughout P3 (16% relative to LPS-CON). Despite the striking reduction in fecal pH, HGA had no additional effect on circulating WBC, SAA, or LBP. Thus, in previously immune-activated dairy cows, HGA did not augment the inflammatory state, as indicated by a lack of perturbations in production, metabolism, and inflammatory biomarkers.

Effects of hindgut acidosis on production, metabolism, and inflammatory biomarkers in feed-restricted lactating dairy cows.

Study objectives were to evaluate the effects of hindgut acidosis (HGA) on production, metabolism, and inflammation in feed-restricted (FR) dairy cows. Twelve rumen-cannulated cows were enrolled in a study with 3 experimental periods (P). During P1 (5 d), baseline data were collected. During P2 (2 d), all cows were FR to 40% of their baseline feed intake. During P3 (4 d), cows remained FR and were assigned to 1 of 2 abomasal infusion treatments: (1) control (FR-CON; 6 L of H2O/d; n = 6) or (2) starch (FR-ST; 4 kg of corn starch + 6 L of H2O/d; n = 6). Respective treatments were partitioned into 4 equal doses (1 kg of corn starch/infusion) and were abomasally infused daily at 0000, 0600, 1200, and 1800 h. All 3 P were analyzed independently and the effects of treatment, time, and treatment × time were assessed using PROC MIXED, and P1 and P2 data were analyzed using the treatments cows were destined to be assigned to during P3. Hallmark production and metabolic responses to feed restriction were observed in both treatments, including decreased milk yield (39%) and energy-corrected milk (32%), circulating glucose (12%), insulin (71%), and increased circulating nonesterified fatty acids (3.2-fold) throughout both P2 and P3, relative to P1. However, despite a marked reduction in fecal pH (0.96 units), the aforementioned metrics were unaltered by HGA. During P3, starch infusions increased circulating ß-hydroxybutyrate, with the most pronounced increase occurring on d 2 (81% relative to FR-CON). Further, feed restriction decreased blood urea nitrogen during P2 (17% relative to P1) in both treatments, and this was exacerbated by starch infusions during P3 (31% decrease relative to FR-CON). In contrast to our hypothesis, neither feed restriction nor HGA increased circulating acute-phase proteins (serum amyloid A and lipopolysaccharide binding protein) relative to P1 or FR-CON, respectively. Thus, despite marked reductions in fecal pH, prior feed restriction did not appear to increase the susceptibility to HGA.