Background: Sepsis is an important cause for neonatal foal mortality. The hypothalamic-pituitary-adrenal axis (HPAA) responses to sepsis are well documented in critically ill humans, but limited data exist in foals. The purpose of this study was to evaluate the HPAA response to sepsis in foals, and to associate these endocrine changes with survival.Hypothesis: Blood concentrations of arginine vasopressin (AVP), adrenocorticotropin hormone (ACTH), and cortisol will be higher in septic foals as compared with sick nonseptic and healthy foals. The magnitude of increase in hormone concentration will be negatively associated with survival.Animals: Fifty-one septic, 29 sick nonseptic, and 31 healthy foals of 7 days of age were included. Methods: Blood was collected at admission for analysis. Foals with positive blood culture or sepsis score !14 were considered septic. Foals admitted with disease other than sepsis and healthy foals were used as controls. AVP, ACTH, and cortisol concentrations were measured using validated immunoassays.Results: AVP, ACTH, and cortisol concentrations were increased in septic foals. Septic nonsurvivor foals (n 5 26/51) had higher plasma ACTH and AVP concentrations than did survivors (n 5 25/51). Some septic foals had normal or low cortisol concentrations despite increased ACTH, suggesting relative adrenal insufficiency. AVP, ACTH, and cortisol concentrations were higher in sick nonseptic foals compared with healthy foals.Conclusions and Clinical Importance: Increased plasma AVP and ACTH concentrations in septic foals were associated with mortality. Several septic foals had increased AVP : ACTH and ACTH : cortisol ratios, which indicates relative adenohypophyseal and adrenal insufficiency.

Background: Insulin resistance has been associated with risk of laminitis in horses. Genes coding for proinflammatory cytokines and chemokines are expressed more in visceral adipose tissue than in subcutaneous adipose tissue of insulin-resistant (IR) humans and rodents.Hypothesis/Objectives: To investigate adipose depot-specific cytokine and chemokine gene expression in horses and its relationship to insulin sensitivity (SI).Animals: Eleven light breed mares. Methods: Animals were classified as IR (SI 5 0.58 AE 0.31 Â 10 À4 L/min/mU; n 5 5) or insulin sensitive (IS; SI 5 2.59 AE 1.21 Â 10 À4 L/min/mU; n 5 6) based on results of a frequently sampled intravenous glucose tolerance test. Omental, retroperitoneal, and mesocolonic fat was collected by ventral midline celiotomy; incisional nuchal ligament and tail head adipose tissue biopsy specimens were collected concurrently. The expression of tumor necrosis factor-a (TNF-a), interleukin (IL)-1b, IL-6, plasminogen activator inhibitor-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) in each depot was measured by real-time quantitative polymerase chain reaction. Data were analyzed by 2-way analysis of variance for repeated measures (P o .05).Results: No differences in TNF-a, IL-1b, IL-6, PAI-1, or MCP-1 mRNA concentrations were noted between IR and IS groups for each depot. Concentrations of mRNA coding for IL-1b (P 5 .0005) and IL-6 (P 5 .004) were significantly higher in nuchal ligament adipose tissue than in other depots.Conclusions and Clinical Importance: These data suggest that the nuchal ligament depot has unique biological behavior in the horse and is more likely to adopt an inflammatory phenotype than other depots examined. Visceral fat may not contribute to the pathogenesis of obesity-related disorders in the horse as in other species.

Abnormalities in clinical and clinicopathologic variables differed depending on the type of anemia. Colic, cold extremities, signs of depression, lethargy, tachycardia, tachypnea, low PCV, low hemoglobin concentration, and hyperlactatemia were commonly detected before transfusion and resolved after transfusion.

Background: Insulin resistance (IR) has been widely recognized in humans, and more recently in horses, but its underlying mechanisms are still not well understood. The translocation of glucose transporter 4 (GLUT4) to the cell surface is the limiting step for glucose uptake in insulin-sensitive tissues. Although the downstream signaling pathways regulating GLUT translocation are not well defined, AS160 recently has emerged as a potential key component. In addition, the role of GLUT12, one of the most recently identified insulin-sensitive GLUTs, during IR is unknown.Hypothesis/Objectives: We hypothesized that cell-surface GLUT will be decreased in muscle by an AS160-dependent pathway in horses with IR.Animals: Insulin-sensitive (IS) or IR mares (n 5 5/group). Methods: Muscle biopsies were performed in mares classified as IS or IR based on results of an insulin-modified frequently sampled IV glucose tolerance test. By an exofacial bis-mannose photolabeled method, we specifically quantified active cellsurface GLUT4 and GLUT12 transporters. Total GLUT4 and GLUT12 and AS160 protein expression were measured by Western blots.Results: IR decreased basal cell-surface GLUT4 expression (P 5 .027), but not GLUT12, by an AS160-independent pathway, without affecting total GLUT4 and GLUT12 content. Cell-surface GLUT4 was not further enhanced by insulin stimulation in either group.Conclusions and Clinical Importance: IR induced defects in the skeletal muscle glucose transport pathway by decreasing active cell-surface GLUT4.

Commercial CPDA-1 bags appear to be the optimal storage method for equine whole blood.