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To measure colonic arterial (CA) and colonic venous (CV) plasma neuropeptide concentrations during low-flow ischemia and reperfusion of the large colon in horses.


10 adult horses.


CA and CV plasma samples collected from anesthetized horses during experimentally induced low-flow colonic ischemia and reperfusion were assayed for vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), using radioimmunoassays. In 6 anesthetized horses, colonic ischemia (20% of baseline [BL]) was maintained for 3 hours, then blood flow was restored and monitored for 3 hours. Hemodynamic variables were monitored continuously and recorded at 30-minute intervals. CA resistance was calculated from colonic blood flow (Qcolon) and mean CA pressure values at each time. Blood was obtained from CA and CV catheters at 0, 1, 2, 3, 3.25, 3.5, 4, 5, and 6 hours; plasma VIP, CGRP, and SP concentrations were quantified, using radioimmunoassays. In 4 additional horses, VIP and CGRP were measured in CA and CV blood at 0, 0.25, 0.5, 0.75, and 1 hour.


Heart rate was significantly increased at 5.5 and 6 hours; other alterations in systemic hemodynamic variables were not significant. Decrease in Qcolon during ischemia was significant; Qcolon rebounded to a value significantly greater than BL value within 5 minutes of reperfusion and was maintained above the BL value during 3 hours of reperfusion. Mean CA pressure was significantly decreased during ischemia, but returned to a value not different from the BL value by 3.25 hours. Mean CV pressure remained unchanged from the BL value during ischemia, but increased to a value significantly greater than the BL value by 3.25 hours and remained increased through 6 hours. CA resistance began to decrease during early ischemia and was significantly less than the BL value by 3.25 hours; it remained less than the BL value through 4 hours. Increase in CV VIP concentration was significant by 0.25 hour of ischemia, but decreased to a value not different from BL value by 3.25 hours. Increase in CV CGRP was significant at 3.25 hours, but this variable returned to a value not different from BL value by 3.5 hours.


CV VIP concentration increases during low-flow colonic ischemia, and CV and CA CGRP and CA SP concentrations increase during early reperfusion. (Am J Vet Res 1996;57:1200-1205)

Free access
in American Journal of Veterinary Research



To describe the acute cellular response, inflammatory mediator release, and effect on chondrocyte metabolism of interleukin 1β (IL-1β) in isolated innervated or denervated equine metacarpophalangeal joints.


One metacarpophalangeal joint of 24 adult horses.


The metacarpophalangeal joint was isolated for 6 hours in a pump-perfused, auto-oxygenated, innervated or denervated metacarpophalangeal joint preparation. Isolated joints were assigned to 4 groups: control, control-denervated, inflamed, and inflamed-denervated, and inflammation was induced by intra-articular injection of IL-1β. Synovial fluid was collected for cytologic examination and determination of IL (IL)-1β, (IL-6), prostaglandin E2 (PGE2), and substance P (SP) values. Synovial membrane was immunostained with SP and nerve-specific enolase (NSE) antibodies. Cartilage was collected for determination of proteoglycan (PG) synthesis and degradation.


IL-1β induced significant neutrophilic leukocytosis in synovial fluid and synovial membrane. IL-1β concentration had returned to baseline by 5.5 hours, but IL-6 concentration significantly increased throughout the study. Total SP content was significantly higher in inflamed joints. There was a significant increase in 24- and 48-hour PG degradation in inflamed innervated joints.


Cellular response to IL-1β was rapid and sustained; joint clearance of IL-1β was rapid, and endogenous production of IL-1β did not follow. The IL-6 and PGE2 concentrations significantly increased, and SP content was increased in association with inflammation but not denervation. A degradative response of cartilage to IL-1β was observed, and was enhanced by innervation. This model was useful for investigation of the articular response to acute inflammation and the influence of denervation in modulating this response. (Am J Vet Res 1998;59:88–100)

Free access
in American Journal of Veterinary Research