BACKGROUND: Ischemia-reperfusion injury (IRI) can induce major changes in the function of different organs, including the liver. Studies have indicated that ischemic post-conditioning (HIPO) can protect the tissues against ischemia-reperfusion injury.OBJECTIVES: To investigate the antioxidant and anti-inflammatory effects of ischemia post-conditioning against the IRI of the rat liver through four 30-second cycles of alternating ischemia and reperfusion, before 24-hour persistent reperfusion.METHODS: Fifteen rats were randomly divided into 3 groups 1) operation control group, 2) ischemia-reperfusion (IR) group whose liver was exposed to 60-miute ischemia of by 24-hour reperfusion and 3) ischemic post-conditioning (IR+IPO) group underwent the same procedure as the second group except that before persistent reperfusion, the rats were subject to post-conditioning by four 30-second cycles of alternating ischemia and reperfusion. The changes induced by IRI and the antioxidant and anti-inflammatory effects of ischemic post-conditioning were assessed by the serum level of IL-6 using the ELISA method, malondialdehyde (MDA), and total antioxidant capacity (TAC). RESULTS: Ischemic post-conditioning potentiated antioxidant effects and reduced the inflammation caused by the IR in the liver. The serum level of IL-6 reduced from 394.4±126.4 to 124.4±29.07 pg/ml (post-conditioning group), and the tissue MDA reduced from 431.4±76.53 to 207.2±25.77 nmol/g) compared to the IR group. The data revealed that the levels of the indices returned almost to the level of the operation control group (P<0.001). Additionally, the total antioxidant capacity of the liver significantly improved (P<0.01) from 11.58±1.87 (in the IR group) to 17.53±2.51 mmol/mg (in the IR+IPO group).CONCLUSIONS: The study demonstrates that the protective effect of ischemic post-conditioning against IR-induced injury may be mediated through decreasing inflammation and improving antioxidant activities.

Cytologic examination of bronchoalveolar lavage fluid (BALF), including phenotypic analysis of lymphocytes, was performed on 32 Standardbreds with poor race performance and endoscopic examination findings characteristic of inflammatory airway disease (IAD). Nucleated cell counts in BALF from IAD-affected horses were higher than those in control horses; the cytologic profile of BALF in affected horses included mixed inflammation, characterized by mild neutrophilia, lymphocytosis, and monocytosis. Eosinophil and mast cell counts were not higher in the IAD-affected group, compared with those in the control group; however, 4 IAD-affected horses had marked eosinophilia (24.7 +/- 4.8% SEM) in BALF. Phenotypic analysis of lymphocytes in BALF obtained from IAD-affected horses revealed a low proportion of CD4-positive cells and B cells, compared with those in the control group; these findings may have been representative of a greater proportion of non-B, non-T cells (null cells) in horses with IAD. The cytologic profile of BALF obtained from horses with IAD differed from that in horses affected with chronic obstructive pulmonary disease, suggesting that the pathogenesis of inflammation in horses with IAD may differ from that of chronic obstructive pulmonary disease.

Because hepatocyte-stimulating factor/interleukin 6 (IL-6) the principal inducer of acute-phase protein synthesis in the liver, quantification of its activity in blood provides an early and sensitive assessment of the acute-phase response. Circulating IL-6 activity was monitored in 4 adult horses for 72 hours after IV administration of endotoxin. In 4 experiments performed at weekly intervals and in randomized order, each horse was given endotoxin-1,000, 30, 1, and 0 ng/kg of body weight. Plasma IL-6 activity was quantified as the ability to promote growth of the IL-6-dependent B-cell hybridoma, B13.29 clone B9. Interleukin-6 activity (171 +/- 10.2 U/ml) was found in all pretreatment plasma samples and was significantly (P < 0.05) increased above baseline from 2 to 12 hours after 1,000 ng of endotoxin/kg was given and at 3 hours after 30 ng of endotoxin/kg was given. After 1,000- or 30-ng/kg dosage of endotoxin, peak plasma IL-6 activity (10,128 +/- 4,096 and 1,555 +/- 1,326 U/ml, respectively) was observed for 3 hours. The IL-6 response of endotoxin-treated horses began about 1 hour after tumor necrosis factor appeared in the circulation, and its course closely approximated the endotoxin-induced febrile reaction. Significant increase in plasma IL-6 activity was not detected in horses given 1 ng of endotoxin/kg or control buffer.

An experimental model of keratoconjunctivitis sicca (KCS) was produced by removing the lacrimal gland and the gland of the third eyelid from the left eye of 6 cats. The right eye of each cat was left intact and used as a control. After 2 weeks, cats were euthanatized and the central portion of the upper eyelid from both eyes of each cat was excised. Histologic sections were stained with either hematoxylin and eosin or with a battery of biotinylated lectins including concanavalin A (conA), soybean agglutinin (SBA), wheat germ agglutinin (WGA), succinylated wheat germ agglutinin (S-WGA), Ulex europaeus agglutinin I (UEA), Dolichos biflorus agglutinin (DBA), Ricinus communis agglutinin (RCA), peanut agglutinin (PNA), and PNA pretreated with neuraminidase. Consistent differences in histologic features were not observed between conjunctivas with KCS and control conjunctivas. A variable degree of mononuclear cell infiltration of the substantia propria was observed in control conjunctivas and those with KCS. In both groups, conjunctival goblet cell density decreased and epithelial stratification increased as the degree of submucosal inflammatory cell infiltration increased. Lectin binding sites for DBA, WGA, S-WGA, UEA, PNA, and PNA pretreated with neuraminidase were detected on conjunctival goblet cells of conjunctivas with KCS and control conjunctivas. The mucus/glycocalyx layer of conjunctival epithelial cells in both groups of conjunctivas bound lectins RCA, WGA, UEA, and conA, but inconsistently bound S-WGA. In both groups, DBA principally bound to the mucus layer overlying normal epithelium, whereas PNA pretreated with neuraminidase consistently bound to the mucus layer of stratified epithelial surfaces free of goblet cells. Binding of SBA to goblet cells and the mucus/glycocalyx layer was variable.

Serum C-reactive protein (CRP) concentration was measured, using an automated immunoturbidimetric assay, in 44 clinically normal dogs and 67 dogs with band neutrophil count greater than or equal to 10(9) cells/L, and values were found to be significantly (P less than or equal to 0.05) different. Correlation of serum CRP concentration and band neutrophil count in the 67 dogs with greater than or equal to 10(9) band neutrophils/L resulted in a statistically significant P less than or equal to 0.05), but low correlation coefficient of 0.34. Serum CRP concentration and CBC values were determined for 6 clinically normal dogs undergoing anesthesia (controls) and 6 clinically normal dogs undergoing anesthesia and ovariohysterectomy. Significant alterations in CBC results and serum CRP concentration, compared with baseline values, were lacking in dogs of the control group. Serum CRP concentration was significantly (P less than or equal to 0.05) increased above baseline values in dogs undergoing surgery and was significantly (P less than or equal to 0.05) increased, compared with values in control dogs by 12 hours after surgery. In dogs undergoing surgery, serum CRP concentration was also significantly (P less than or equal to 0.05) different from values in control dogs at 28 and 36 hours, but not at the 76- and 124-hour sample collection times. Alterations in CBC values compatible with possible or convincing inflammation were detected in 83% of the dogs undergoing surgery at the 8- and 12-hour postsurgery sample collection times, 100% of dogs at 16, 22, 28, and 36 hours after surgery, 83% of dogs at 52 and 76 hours after surgery, 67% of dogs at 100 hours after surgery, and 0% of dogs at 124 hours after surgery It was concluded that significant increases in CRP, concentration in dogs with surgical trauma were not detected earlier than CBC alterations compatible with possible or convincing inflammation.

Systemic and pulmonary antibody responses of calves to Pasteurella haemolytica were evaluated by measuring immunoglobulin production in blood for 9 days and in pulmonary lavage fluid for 7 days after intrapulmonary inoculation. Clinical signs, pulmonary lesions, pulmonary and systemic inflammatory response, and amount of antigen in lavage fluid were used to evaluate the response of calves to challenge with P haemolytica. The pulmonary response consisted of production of IgG, IgE, and IgM antibodies to P haemolytica antigens and a 17- to 68-fold increase of cells in lavage fluid 8 hours after inoculation, with a gradual decrease toward normal. Antibodies of the IgM isotype to P haemolytica were demonstrated as early as 8 hours through 7 days after inoculation in 3 of 3 calves. Of the anti-P haemolytica isotypes, IgM was found in the highest concentration. In all of the inoculated calves, IgE was found 1 to 2 days after inoculation, and IgG was found in 2 of 3 inoculated calves from day 1 through 7 after inoculation. Detection of IgG correlated with smaller pulmonary lesions. Immunoglobulin A was not detected in lavage fluid. Serum was evaluated for IgG and IgM antibody response to P haemolytica. Specific IgM was detectable 5 days after inoculation, and IgG was detectable 7 days after inoculation. Pasteurella haemolytica antigens were not detected in serum or plasma. A transient increase in neutrophil count was found 8 hours after inoculation, with return to baseline values by 24 hours after inoculation. Antigen was detected in lavage fluid by use of monoclonal antibodies against selected P haemolytica capsular antigen, outer membrane antigens, and leukotoxin in all inoculated calves 8 hours after inoculation. The monoclonal antibody specific for P haemolytica capsule provided the best detection of antigen. The other monoclonal antibodies detected antigen, but were less consistent.

Uveitis was induced in dogs by intracameral injection of canine lens protein. The lipoxygenase inhibitors phenidone and norhydroguaiaretic acid, and dimethyl sulfoxide decreased fibrin production at 0.5 and 1 hour after induction uveitis. Phenidone and norhydroguaiaretic acid also inhibited the initial increase intraocular pressure early in the course of inflammation. Leukotriene B4 in the aqueous was measured by use of radioimmunoassay at 1 hour after inflammation. In control dogs, 230 to 1,700 pg of leukotriene B4/ml was measured; in dogs treated with phenidone, leukotriene, B4 was not measured.