[Tibial nerve paresis in eight dairy cows: symptomatic therapy with a synthetic resin cast]. / Nervus-tibialis-Parese bei acht Milchkühen - symptomatische Therapie mithilfe eines Kunstharzverbands.

OBJECTIVE: Tibial paresis is commonly seen in bovine practice as a sequel to dystocia. The tibial nerve supplies the extensor muscles of the hock joint and the flexor muscles of the digits; affected cows are lame and have a dropped hock and knuckling of the fetlock. Complete functional recovery occurs not consistently after a conservative "wait and see" approach. The aim of this study was to investigate the usefulness of a cast applied to the lower portion of the affected limb as a supportive treatment of tibial nerve paresis in cows. MATERIALS AND METHODS: Eight dairy cows with tibial nerve paresis from different farms were presented for treatment. Seven cows had unilateral tibial nerve paresis and one cow, which was barely able to stand, had bilateral tibial paresis. The affected legs of the seven cows with unilateral paresis and the more severely affected leg of the remaining cow were stabilized using a cast made of synthetic resin. The claws and the skin of the affected limbs were cleaned and a thick layer of cotton was applied to pad the leg from the foot to the hock. A cast was then applied with the foot and metatarsus aligned in a straight line. The cast included the entire foot and extended to the hock. The cast was removed after 4 weeks. RESULTS: All of the eight cows could be kept in their normal environment. They were able to walk well with the cast and were only mildly lame. Feed intake and milk yield increased. After removal of the cast, seven of the eight cows walked normally, including the cow of which both legs had been affected. One cow was slightly lame with a dropped hock after cast removal but showed a normal gait 3 weeks later. CONCLUSIONS AND CLINICAL RELEVANCE: In cows with tibial paresis, casting of the lower portion of the leg was a useful supportive treatment that resulted in restoration of normal gait. In seven of eight treated cows limb function was normal after 4 weeks, and in one cow after 7 weeks. This supportive therapeutic procedure is straightforward, minimizes aftercare and allows the cow to be kept in her normal environment.

Histamine-induced chloride secretion is mediated via H2-receptors in the pig proximal colon.

OBJECTIVE: The aim of this study was to investigate the action of histamine on function of epithelia in the pig proximal colon. MATERIAL AND METHODS: Isolated epithelia of the pig proximal colon were prepared by slide-stripping and mounted in Ussing chambers. Short-circuit current (Isc) was measured after serosal addition of histamine (20 micromol/l) with or without pretreatment with histamine receptor antagonists (H1: chlorpyramine, 10 micromol/l; H2: famotidine, 100 micromol/l; H3: thioperamide, 10 micromol/l), a cyclooxygenase inhibitor (indomethacin, 10 micromol/l), or a neuronal conduction blocker (tetrodotoxin, 1 micromol/l). Alternatively, histamine receptor agonists (H1: 2-pyridylethylamine; H2: dimaprit; H3: R-alpha-methylhistamine, each 100 micromol/l) were added to the serosal side. Flux studies using 14C-mannitol, 22Na+ and 36Cl- were performed in the presence of 100 micromol/l histamine on the serosal side. RESULTS: Serosal application of histamine induced a rapid rise in Isc with a maximum 3 min after addition, followed by a slow decrease. Only pretreatment with famotidine decreased the epithelial response to histamine. Pretreatments with chlorpyramine, thioperamide, indomethacin or tetrodotoxin did not change histamine-induced increases in Isc. Action of histamine could be simulated by dimaprit, but not by 2-pyridylethylamine or R-alpha-methylhistamine. Histamine induced an increase in serosal-to-mucosal chloride flux leading to a decrease of chloride net absorption. Fluxes of sodium and mannitol were not affected by histamine. CONCLUSIONS: In contrast to the importance of H1-receptors in other gut epithelia, histamine acts directly via H2-receptors in the porcine proximal colon. Changes in Isc after histamine addition are primarily due to chloride secretion. The paracellular permeability is not influenced by histamine.

Effect of nitric oxide on electrolyte transport across the porcine proximal colon.

The effect of nitric oxide (NO) on ion transport in the porcine proximal colon was investigated in slide-stripped epithelia mounted in Ussing chambers. The serosal addition of the NO-donors sodium nitroprusside (SNP, 0.5 mM) or S-nitroso-N-acetylpenicillamine (SNAP, 0.5 mM) induced a steep increase of short-circuit current ( I(sc)). The stimulatory effect of SNP on I(sc) could not be blocked by piroxicam or tetrodotoxin. Potassium channel inhibitors (quinidine, tetraethylammonium or barium) added serosally reduced the SNP- or SNAP-induced increases of I(sc). In chloride-free solutions, the SNP-induced increase of I(sc) was smaller than in chloride-containing solutions. Cl(- )and Na(+) flux measurements demonstrated that SNP diminished Cl(-) and Na(+) net absorption. Pre-treatment with barium was able to block the inhibitory effect of SNP on NaCl net absorption totally. NO effects on paracellular pathways were assessed by measuring flux rates of [(14)C]-D-mannitol. SNP did not change unidirectional D-mannitol flux rates. In conclusion, NO inhibits NaCl net absorption in the proximal colon of pigs by acting directly on the enterocyte. The antiabsorptive (and/or prosecretory) effect of NO depends on a functional basolateral potassium conductance.

Luminal salmonella endotoxin affects epithelial and mast cell function in the proximal colon of pigs.

BACKGROUND: Salmonellosis and systemic endotoxaemia affect intestinal function. However, little is known about the functional importance of luminal Salmonella (S.) endotoxin during intestinal infection. METHODS: Pigs were either given or not given lipopolysaccharide (LPS, 30 mg day(-1)) of S. Typhimurium DT-104 orally for 14 days. Blood samples were taken weekly. After slaughter (day 14), epithelia of the proximal colon were investigated in Ussing chambers. Bacterial translocations to lung, liver, spleen and several lymph nodes were determined by culture. RESULTS: Endotoxin feeding increased plasma C-reactive protein (CRP) and histamine levels without evoking clinical signs. Postmortem, proximal colonic epithelia of LPS-treated animals showed both a decreased histamine release after mast cell stimulation with A23187 and a smaller increase in short-circuit current after A23187 application. Addition of the nitric oxide donor, sodium nitroprusside (SNP), also elicited lower increases in short-circuit current in the proximal colon of endotoxin-treated pigs. Endotoxin pre-feeding decreased colonic ion conductance, although mannitol and histamine fluxes were high in some epithelia of this group. Luminal Salmonella endotoxin increased bacterial translocation to proximal jejunal lymph nodes. LPS applied to colonic epithelia in vitro had no electrophysiological effects. CONCLUSIONS: Luminal endotoxin elicits an acute phase response and affects intestinal electrolyte transport and mast cell function. Furthermore, LPS induces epithelial spots of increased mannitol permeability that could be identical to spots of enhanced bacterial translocation.