Effects of particle size reduction of meadow hay on feed intake, performance, and apparent total tract nutrient digestibility in dairy cows.

Forage-based diets are encouraged in organic dairy cattle production as this can increase the net human food supply, but their voluminous nature can limit dry matter intake (DMI) and performance. This study investigates the effects of a substantial particle size reduction of hay on dairy cows' feed intake, performance, and body characteristics, as well as on apparent total tract digestibility (ATTD). Eighteen lactating Holstein cows were allocated to two balanced feeding groups. The control group received long stem hay with a conventional particle size (CON), the experimental group received chopped hay (RED). Both groups were supplemented with concentrates (3.6 kg/d, DM basis). After 14 adaptation days, data were collected for 20 consecutive days. A covariate period of 21 days preceded the experimental feeding period. Particles retained on the 19-, 8- and 4-mm screens and on the pan of the Penn State Particle Separator accounted for 21%, 20%, 20% and 39% of the RED hay. CON hay consisted of 72% large particles, followed by 8%, 7% and 13% retained on the other screens. Average DMI levels of cows in the CON group reached 20.8 kg/d, with a nonsignificant increase (+1.05 kg/d) in the RED group (p = 0.28). Intakes of both NFC (+0.65 kg/d, p = 0.01) and CP (+0.28 kg/d, p = 0.05) were significantly greater in the RED group, resulting in a slightly increased milk yield (+0.8 kg energy corrected milk/d) (p = 0.45), likely because the ATTD decreased significantly when feeding RED hay. No impact was observed on energy balance (103.7 vs 103.9%, p = 0.95), feed conversion efficiency (kg ECM/kg DMI), or N use efficiency. Overall, the results indicate increases in intake of NFC and CP in the RED group when feeding a hay-based (>83%, DM basis) diet, but also a decrease in nutrient digestibility, likely due to increased passage rate, potentially because of the high fraction of hay particles < 4 mm. In conclusion, hay-based rations with a lower proportion of fine particles should be tested to exploit the potential of particle size reduction in terms of improving hay use efficiency.

Reverse right ventricular structural and extracellular matrix remodeling by estrogen in severe pulmonary hypertension.

Chronic pulmonary hypertension (PH) leads to right-ventricular failure (RVF) characterized by RV remodeling. Ventricular remodeling is emerging as an important process during heart failure and recovery. Remodeling in RVF induced by PH is not fully understood. Recently we discovered that estrogen (E2) therapy can rescue severe preexisting PH. Here, we focused on whether E2 (42.5 µg·kg(-1)·day(-1), 10 days) can reverse adverse RV structural and extracellular matrix (ECM) remodeling induced by PH using monocrotaline (MCT, 60 mg/kg). RV fibrosis was evident in RVF males. Intact females developed less severe RV remodeling compared with males and ovariectomized (OVX) females. Novel ECM-degrading disintegrin-metalloproteinases ADAM15 and ADAM17 transcripts were elevated ∼2-fold in all RVF animals. E2 therapy reversed RV remodeling in all groups. In vitro, E2 directly inhibited ANG II-induced expression of fibrosis markers as well as the metalloproteinases in cultured cardiac fibroblasts. Estrogen receptor-ß agonist diarylpropionitrile (DPN) but not estrogen receptor-α agonist 4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) was as effective as E2 in inhibiting expression of these genes. Expression of ECM-interacting cardiac fetal-gene osteopontin (OPN) also increased ∼9-fold in RVF males. Intact females were partially protected from OPN upregulation (∼2-fold) but OVX females were not. E2 reversed OPN upregulation in all groups. Upregulation of OPN was also reversed in vitro by E2. Plasma OPN was elevated in RVF (∼1.5-fold) and decreased to control levels in the E2 group. RVF resulted in elevated Akt phosphorylation, but not ERK, in the RV, and E2 therapy restored Akt phosphorylation. In conclusion, E2 therapy reverses adverse RV remodeling associated with PH by reversing fibrosis and upregulation of novel ECM enzymes ADAM15, ADAM17, and OPN. These effects are likely mediated through estrogen receptor-ß.