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  • Author or Editor: Yasushi Ogawa x
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Abstract

Objective—To determine whether small intestinal ischemia and reperfusion induces bacterial translocation and proinflammatory cytokine response in either the systemic or portal circulation in dogs.

Animals—17 healthy adult Beagles.

Procedure—The superior mesenteric artery (SMA) was occluded for 0 (group-3 dogs), 30 (group-1 dogs), or 60 (group-2 dogs) minutes, followed by reperfusion for 180 minutes; serum lactate and endotoxin concentrations and tumor necrosis factor-α (TNF-α), interleukin- 1β (IL-1β), and IL-6 activities in the systemic and portal circulation and intramucosal pH were measured at various time points.

Results—In group-2 dogs, TNF-α activity was found to be significantly increased in the portal circulation, peaking at 60 minutes of reperfusion; TNF-α activity, in the systemic circulation, gradually increased from 60 minutes of reperfusion to the end of the experiment; however, the increase was not significant. In group-1 and -2 dogs, IL-6 activities significantly and gradually increased in the systemic and portal circulation during the reperfusion phase, and the magnitude of these increases was dependent on the duration of the ischemic phase. There were no significant changes in IL-1β activity or endotoxin concentration in any dog group.

Conclusions and Clinical Relevance—Results of the our study indicate that intestinal ischemia and reperfusion leads to significant increases of the circulating TNF-α and IL-6 activities, depending on the duration of the ischemia phase, in the absence of detectable endotoxin in the circulation. This finding suggests that intestinal ischemia and reperfusion induces a systemic proinflammatory cytokine response in dogs. (Am J Vet Res 2002;63:1680–1686)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether continuous infusion of a low dose of lipopolysaccharide (LPS) to induce a condition mimicking septic shock in dogs would affect systemic and hepatosplanchnic circulation and oxygenation.

Animals—12 healthy adult Beagles.

Procedure—Dogs received a low dose of LPS (Escherichia coli O55:B5) by continuous IV infusion at a rate of 1 µg/kg/h for 8 hours. Systemic hemodynamics; systemic oxygenation; blood flow in the cranial mesenteric artery, common hepatic artery, and portal vein; intestinal and hepatic tissue blood flow; mesenteric oxygenation; and intramucosal PCO2 were examined before and at selected time points after onset of the LPS infusion.

Results—After onset of the LPS infusion, cardiac index increased and mean arterial pressure (MAP) and systemic vascular resistance decreased, which is characteristic of the hyperdynamic state in septic patients. Hepatosplanchnic blood flow increased during the hyperdynamic state. Intestinal PCO2 was increased even when blood flows increased. During the latter half of the experimental period, MAP was maintained but hepatosplanchnic blood flows decreased and intestinal PCO2 increased further.

Conclusions and Clinical Relevance—Analysis of the results suggested that hepatosplanchnic blood flow enters the hyperdynamic state during the early stages of sepsis and that intestinal tissue oxygenation is threatened even when hepatosplanchnic blood flow is increased or maintained. Hence, improvement of hepatosplanchnic circulation and intestinal tissue oxygenation is important in dogs with clinical evidence of a septic condition. (Am J Vet Res 2004;65:1347–1354)

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in American Journal of Veterinary Research

Abstract

Objective—To determine the effects of continuous low-dose infusion of lipopolysaccharide (LPS) on the expression of E-selectin and intercellular adhesion molecule-1 (ICAM-1) mRNA and neutrophil accumulation in the lungs, liver, spleen, small intestine, and pancreas in dogs.

Animals—11 healthy adult Beagles.

Procedure—Dogs received a continuous infusion of a low dose (10 µg/kg/h, IV) of LPS ( Escherichia coli055:B5) or saline (0.9% NaCl) solution (20 mL/kg/h, IV) for 8 hours. Activity levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) and the number of WBCs in circulation were examined before and 1, 2, 4, and 8 hours after the onset of LPS infusion. Expression of E-selectin and ICAM-1 mRNA and the number of neutrophils in each tissue were examined.

Results—After the onset of LPS infusion, serum TNF-α and IL-1β activities transiently increased. Thereafter, IL-6 activity increased, and high IL-6 activity was maintained throughout the experiment. In dogs in the LPS group, expression of E-selectin mRNA increased only in the lungs, and expression of ICAM-1 mRNA increased in the lungs and liver; the number of neutrophils in the tissue increased in the lungs and liver.

Conclusions and Clinical Relevance—Results suggested that expression of E-selectin and ICAM-1 mRNA increased during sepsis, particularly in the lungs and liver, and that this increase was associated with neutrophil accumulation. Hence, inhibiting the activation of endothelial cells in the lung and liver may decrease organ damage caused by accumulated neutrophils and help regulate multiple-organ dysfunction. (Am J Vet Res 2005;66:1259–1266)

Full access
in American Journal of Veterinary Research

Abstract

Objective

To evaluate the ability of hyaluronic acid (HA), with and without transforming growth factor β (TGF-β), to stabilize the catabolic processes associated with atrophy of articular cartilage.

Animals

20 adult, skeletally normal, hound-type dogs.

Procedure

Dogs (20 to 30 kg) were randomly assigned to 1 of 5 groups. One group served as untreated controls. Bivalve casts were placed on the left hind limbs of the remaining 16 dogs to limit weightbearing and motion of the limb for 92 days. One group served as the cast control. Beginning on day 56, 3 groups received aseptic intra-articular injections in the left stifles of either 5 mg of HA or 5 mg of HA containing either 20 or 50 μg of TGF-β. Intra-articular injections were repeated at 4-day intervals until the end of the study. On day 92, stifles were harvested at necropsy. Medial femoral condyles were histologically processed, and the articular cartilage was stained for the presence of proteoglycans, stromelysin, tumor necrosis factor (TNF) α, and TNF receptors (p55 and p75).

Results

Decreased metachromasia was evident in the cartilage matrix of all cast groups, with the smallest decrease in the HA-treated group. Stromelysin was immunolocalized in articular cartilage of the cast (left) limbs of cast control and both HA/TGF-β-treated groups. TNF-α was localized in articular cartilage of all cast (left) and right limbs, except those of the HA-treated group. Receptors for TNF were observed in both limbs of untreated control and cast control groups and cast limbs of HA/TGF-β-treated groups. The receptors were not localized in the right limbs of the HA with or without TGF-β-treated groups. TGF-β did not decrease stromelysin or TNF-α or receptors at the doses used.

Conclusions

HA may mediate a chondrostabilizing influence on articular cartilage by down-regulating TNF-α. Importantly, HA appeared to exert its inhibitory influence on TNF-α, as well as stromelysin and TNF receptors, on a systemic basis.

Clinical Relevance

Results provide insight into the mode of action of HA as a therapeutic agent for arthritis and its stabilizing influence on cartilage metabolism. (Am J Vet Res 1996;57:1488-1496)

Free access
in American Journal of Veterinary Research