Animal inflammation

Incompatible chemical substances Chemical substances that may cause dangerous reactions from direct contact with one another Induction period The length of time (at least 1 week) following a sensitization during which a hypersensitive state is developed by the animal Inflammation Response of the body tissues to injury typical signs are swelling, redness, and pain... 

Triamcinolone acetonide is approximately 8 times more potent than prednisone in animal inflammation models. Topically applied triamcinolone acetonide is a potent anti-inflammatory agent (sec Table 23-8). about 10 times more so... 

Since Rocha e Silva et al. [76] have reported that a number of sulphated polymers show antiinflammatory potential, counter irritation has been discussed as one possible mechanism. Beside turpentine [71] and sulphated polysaccharides, a neutral glucan was also found to possess irritating and inflammation-inducing activity [77]. Most likely this class of polysaccharides also exhibits antiinflammatory effects in the carrageenan rat paw edema through counter irritation. This could be of great importance in acute animal inflammation models, since Ferreira et al. [78] demonstrated that counter irritant effects were able to reduce edema formation as early as 2 h after administration of the irritating substance. 

Repeated exposures of animals to high (near-lethal) concentrations of vapors result in inflammation of the respiratory tract, as weU as degenerative changes in the Hver, kidneys, and heart muscle. These effects arise at concentrations far above those causing irritation. Such effects have not been reported in humans. The low odor threshold and irritating properties of acrylates cause humans to leave a contaminated area rather than tolerate the irritation. 

Toxicity. Many /V-nitrosamines are toxic to animals and cells in culture (4,6—8,88). /V-Nitrosodimethy1amine [62-75-9] (NDMA) is known to be acutely toxic to the Hver in humans, and exposure can result in death (89). Liver damage, diffuse bleeding, edema, and inflammation are toxic effects observed in humans as a result of acute and subacute exposure to NDMA. These effects closely resemble those observed in animals dosed with NDMA (89,90). 

In 1956 selenium was identified (123) as an essential micronutrient iu nutrition. In conjunction with vitamin E, selenium is effective iu the prevention of muscular dystrophy iu animals. Sodium selenite is adrninistered to prevent exudative diathesis iu chicks, a condition iu which fluid leaks out of the tissues white muscle disease iu sheep and infertility iu ewes (see Eeed ADDITIVES). Selenium lessens the iacidence of pneumonia iu lambs and of premature, weak, and stillborn calves controls hepatosis dietetica iu pigs and decreases muscular inflammation iu horses. White muscle disease, widespread iu sheep and cattle of the selenium-deficient areas of New Zealand and the United States, is insignificant iu high selenium soil areas. The supplementation of animal feeds with selenium was approved by the U.S. EDA iu 1974 (see Eeed additives). Much of selenium s metaboHc activity results from its involvement iu the selenoproteia enzyme, glutathione peroxidase. 

The primary routes of entry for animal exposure to chromium compounds are inhalation, ingestion, and, for hexavalent compounds, skin penetration. This last route is more important in industrial exposures. Most hexavalent chromium compounds are readily absorbed, are more soluble than trivalent chromium in the pH range 5 to 7, and react with cell membranes. Although hexavalent compounds are more toxic than those of Cr(III), an overexposure to compounds of either oxidation state may lead to inflammation and irritation of the eyes, skin, and the mucous membranes associated with the respiratory and gastrointestinal tracts. Skin ulcers and perforations of nasal septa have been observed in some industrial workers after prolonged exposure to certain hexavalent chromium compounds (108—110), ie, to chromic acid mist or sodium and potassium dichromate. 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

There are two isoforms of COX in animals COX-1 (figure a), which carries out normal, physiological production of prostaglandins, and COX-2 (figure b), which is induced by cytokines, mitogens, and endotoxins in inflammatory cells and is responsible for the production of prostaglandins in inflammation. 

Colon inflammation 1. AEA levels are elevated in the colon of DNBS-treated mice and in the colon submucosa of TNBS-treated rats, two animal models of inflammatory bowel diseases, and in the biopsies of patients with ulcerative colitis, to control inflammation 1. Inhibitors of degradation (both FAAH and cellular re-uptake)... 

They act as analgesics by inhibiting release of nociceptive neurotransmitters from primary afferent terminals as well as by depressing post-synaptic potentials on second order neurons. Opioid receptors are also present on some nociceptors and their expression and peripheral transport is increased upon peripheral inflammation. Peripheral opioid analgesia has been established in animal models. Although clinical studies have yielded mixed results so far, this field holds great promise. Despite side effects, such as euphoria, dysphoria, sedation, respiratory depression and obstipation and tolerance and dependence phenomena which arise upon... 

Local inflammation of the lungs and dilated alveoli were observed in rats administered 10 mg/kg/day of endosulfan in peanut oil by gavage for 15 days (Gupta and Chandra 1977). However, there was high mortality in this dose group (3 of 8 animals died prior to study termination), and it is not clear if these effects were observed primarily in the intercurrent deaths or in animals surviving for the full 15 days of exposure. 

In addition to the reports of uptake of intact small liposomes (SUV) by hepatocytes (Scherphof et al., 1983), there is some evidence of uptake of intravenously administered liposomes as intact structures by cells other than mononuclear phagocytes of the MPS. Recently, the integrity of the capillary endothelial barrier in several pathophysiological conditions was discussed (Bodor and Brewster, 1986). Several studies already indicated an increased capillary permeability during inflammation both in animals (Lopez-Berestein et al., 1984a) and in man (Morgan et al., 1985 Williams et al., 1987). 

Behavioural studies are generally unable to find a role for spinal NO in nociceptive reflexes in normal animals, whereas NO inhibitors are highly effective in blocking these same reflexes following the induction of peripheral inflammation or neuropathy. Although a complication is that NO may also play a role in peripheral vascular events during inflammation, these results do suggest that the gas is produced only under certain conditions. 

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