Telemetric techniques for the monitoring of physiological parameters during housing, handling and transport may help producers to reduce mortality and improve meat quality. In order to know the reliability of electrocardiogram parameters as stress indicators, piglets (12 to 23 kg) being different with respect to the halothane gene (homozygous halothane sensitive (nn) and non-sensitive (NN), heterozygotes (nN)), and thus different with respect to stress susceptibility, were monitored with an ambulatory ECG device during housing, handling and transport. Skeletal muscularity of all animals was measured with an ultrasound device.Heterozygotes and homozygote halothane sensitive piglets had a higher muscularity, but only the homozygotes had a higher ST-elevation from the isoelectric line of the QRST-complex of the electrocardiogram when measured within housing conditions. This means a different propagation of the electric current related to the activation of the ventricle. Halothane gene carriers (Nn and nn piglets) had a statistically significant higher mean maximal heart rate during housing conditions. During handling heart rate rose by 14·8%, 0·61% and 42·9% respectively for NN, nN and nn piglets, with nn piglets having the highest values. During transport these measurements were respectively 6·88%, 3·66% and 9·7% higher for lines NN, nN and nn as compared with those in housing conditions. Heart arrhythmicity parameters were not different between housing and transport, but during handling up to a 23-fold increase could be observed.Heart rate and arrhythmicity parameters may generate reliable information to monitor stress during housing, handling and transport of piglets through genotypes and skeletal muscularity.

A fundamental part of the immune response to infection or injury is leukocyte migration. Matrix metalloproteinases (MMPs) are a class of secreted or cell-bound endopeptidases, implicated in every step of the process of inflammatory cell migration. Hence, specific inhibition of MMPs is an interesting approach to control inflammation. We evaluated the potential of a bivalent carboxylate inhibitor to selectively inhibit the trimeric proteoform of MMP-9 and compared this with a corresponding monovalent inhibitor. The bivalent inhibitor efficiently inhibited trimeric MMP-9 (IC50 = 0.1 nM), with at least 500-fold selectivity for MMP-9 trimers over monomers. Surprisingly, in a mouse model for chemotaxis, the bivalent inhibitor amplified leukocyte influxes towards lipopolysaccharide-induced inflammation. We verified by microscopic and flow cytometry analysis increased amounts of neutrophils. In a mouse model for endotoxin shock, mice treated with the bivalent inhibitor had significantly increased levels of MMP-9 in plasma and lungs, indicative for increased inflammation. In conclusion, we propose a new role for MMP-9 trimers in tempering excessive neutrophil migration. In addition, we have identified a small molecule inhibitor with a high selectivity for the trimeric proteoform of MMP-9, which will allow further research on the functions of MMP-9 proteoforms.

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