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SUMMARY

Twenty-four horses were randomly allocated to 3 groups. All horses underwent a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls, group-2 horses underwent 6 hours of colonic ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline blood samples were collected, then low-flow colonic ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. All horses were monitored for 6 hours. Citrated systemic venous ( sv ) blood samples were collected from the main pulmonary artery, and colonic venous (cv) samples were collected from the colonic vein draining the ventral colon. Samples were collected at 0, and 2, 3, 3.25, 4, and 6 hours for determination of one-stage prothrombin time, activated partial thromboplastin time, antithrombin III activity, and fibrinogen concentration. Data were analyzed statistically, using two-way anova for repeated measures, and post-hoc comparisons were made by use of Student Newman Keul's test. Statistical significance was set at P < 0.05. There were significant decreases in all hemostatic variables by 2 hours in sv and cv samples from horses of all 3 groups, but there were no differences among the 3 groups for any of these variables. These hemostatic alterations could have been secondary to a hypercoagulable state or to fluid therapy-induced hemodilution. Colonic ischemia-reperfusion was not the cause of these alterations because these alterations also were observed in the sham-operated control horses. Significant temporal alterations existed even after accounting for the hemodilution. The most plausible explanation for these alterations is that hemostatic activation was incited by the celiotomy and manipulation of the colon during exteriorization and instrumentation. Comparison of paired sv and cv samples for each hemostatic variable revealed significant differences for the absolute values of one-stage prothrombin time and fibrinogen concentration, but not for activated partial thromboplastin time or antithrombin III activity. This indicates that monitoring sv hemostatic variables does not necessarily provide an accurate assessment of hemostatic function in regional vascular beds. Largecolon ischemia with or without reperfusion did not alter hemostatic function.

Free access
in American Journal of Veterinary Research

SUMMARY

Six horses were subjected to 3 hours of low-flow ischemia and 3 hours of reperfusion of the large colon. After induction of anesthesia, the large colon was exteriorized through a ventral midline celiotomy. Colonic blood flow was measured continuously, using Doppler ultrasonic flow probes placed on the colonic arteries supplying the dorsal and ventral colons and was allowed to stabilize for 15 to 30 minutes after instrumentation. Low-flow ischemia was induced by reducing colonic arterial blood flow to 20% of baseline (bl) flow. Colonic mucosal, seromuscular, and full-thickness blood flow were determined on a tissue-weight basis by injecting colored microspheres proximally into the colonic artery supplying the ventral colon. Reference blood samples were obtained at a known flow rate from the colonic artery and vein at a site more distal to the site of injection. Left ventral colon biopsy specimens were harvested at bl, 3 hours of ischemia, and 15 minutes of reperfusion. Blood and tissue samples were digested and filtered to collect the microspheres, and dimethylformamide was added to release the colored dyes. Dye concentration in blood and tissue samples was measured by use of spectrophotometry, and tissue-blood flow was calculated. Data were analyzed, using two-way anova for repeated measures; statistical significance was set at P < 0.05. Doppler blood flow decreased to approximately 20% of BL, whereas microsphere blood flow ranged between 13.7 and 15.5% of bl at 3 hours of ischemia. Doppler-determined blood flow increased immediately on restoration of blood flow, reached 183% of bl at 15 minutes of reperfusion, and remained at or above bl throughout 3 hours of reperfusion. This reactive hyperemia was also detected, using the colored microspheres; blood flow increased to 242 and 327% of bl at 15 minutes of reperfusion in the mucosal and seromuscular layers, respectively. Mucosal blood flow was not different from seromuscular blood flow at any time, indicating relatively equal distribution of blood flow between these 2 layers. As determined from the venous reference samples, there was no evidence of arteriovenous anastomoses.

Free access
in American Journal of Veterinary Research

SUMMARY

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (bl) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of bl. All horses were monitored for 6 hours after bl data were collected. blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [sv]) for measurement of plasma endotoxin, 6-keto prostaglandin F (6-kPG), thromboxane B2 (txb 2), and prostaglandin E2 (pge 2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (cv) serum samples. Data were analyzed, using two-way anova, and post-hoc comparisons were made, using Dunnett's and Tu- key's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or sv plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at bl among groups for CV or sv 6-kPG, pge 2, or txb 2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group- 2 horses. Colonic venous pge 2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 horses. There were no temporal alterations in sv pge 2 concentration. There was no difference in CV or sv ixb2 concentration among or within groups across time; however, there was a trend (P = 0.075) toward greater CV txb 2 concentration at 3.25 hours, compared with bl, in group-3 horses. Eicosanoid concentrations were significantly lower in sv, compared with CV plasma. Prostaglandin E2 and 6-kPG concentrations were approximately 3 to 8 and 5 to 10 times greater, respectively, in CV than in sv plasma. The increased concentrations of 6-kPG and pge 2 in CV plasma were likely attributable to their accumulation secondary to colonic ischemia. The increased values of these vasodilator eicosanoids may have a role in the reactive hyperemia observed during reperfusion. The increased 6-kPG concentration in sv plasma may represent spillover from the colonic vasculature, but more likely reflects systemic production.

Free access
in American Journal of Veterinary Research

SUMMARY

Thirty horses were randomly assigned to 1 of 5 groups. All horses were anesthetized and subjected to ventral midline celiotomy, then the large colon was exteriorized and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (bl) and was maintained for 3 hours. Colonic blood flow was then restored, and the colon was reperfused for an additional 3 hours. One of 5 drug solutions was administered via the jugular vein 30 minutes prior to colonic reperfusion: group 1, 0.9% NaCl; group 2, dimethyl sulfoxide: 1 g/kg of body weight; group 3, allopurinol: 25 mg/kg; group 4, 21-aminosteroid U-74389G: 10 mg/kg; and group 5, manganese chloride (MnCl2): 10 mg/kg. Hemodynamic variables were monitored and recorded at 30-minutes intervals. Systemic arterial, systemic venous (sv), and colonic venous (cv) blood samples were collected for measurement of blood gas tensions, oximetry, lactate concentration, Pcv, and plasma total protein concentration. The eicosanoids, 6-keto prostaglandin F, prostaglandin E2 and thromboxane B2, were measured in cv blood, and endotoxin was measured in cv and sv blood. Full-thickness biopsy specimens were harvested from the left ventral colon for histologic evaluation and determination of wet weight-to-dry weight ratios (WW:DW). Data were analyzed, using two-way ANOVA for repeated measures, and statistical significance was set at P < 0.05. Heart rate, mean arterial pressure, and cardiac output increased with MnCl2 infusion; heart rate and cardiac output remained increased throughout the study, but mean arterial pressure returned to bl values within 30 minutes after completion of MnCI2 infusion. Other drug-induced changes were not significant. There were significant increases in mean pulmonary artery and mean right atrial pressures at 2 and 2.5 hours in horses of all groups, but other changes across time or differences among groups were not observed. Mean pulmonary artery pressure remained increased through 6 hours in all groups, but mean right atrial pressure had returned to bl values at 3 hours. Mean colonic arterial pressure was significantly decreased at 30 minutes of ischemia and remained decreased through 6 hours; however, by 3.25 hours it was significantly higher than the value at 3 hours of ischemia. Colonic arterial resistance decreased during ischemia and remained decreased throughout reperfusion in all groups; there were no differences among groups for colonic arterial resistance. Colonic venous Po2, oxygen content, and pH decreased, and Pco2 and lactate concentration increased during ischemia but returned to bl values during reperfusion. Compared with bl values, colonic oxygen extraction ratio was increased from 0.5 to 3 hours. By 15 minutes of reperfusion, colonic oxygen extraction ratio had decreased from the bl value in all groups and either remained decreased or returned to values not different from bl through 6 hours. Colonic venous 6-keto prostaglandin F and prostaglandin E2 concentrations increased during ischemia, but returned to bl on reperfusion; there were no changes in thrombox- ane2 concentration among or within groups. Endotoxin was not detected in cv or sv blood after ischemia or reperfusion. There were no differences among or within groups for these variables. Low-flow ischemia and reperfusion (i-r) of the large colon caused mucosal injury, as evidenced by increases in percentage of surface mucosal disruption, percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, mucosal interstitial-to-crypt ratio, mucosal neutrophil index, submucosal venular neutrophil numbers, and mucosal cellular debris index. There was a trend (P = 0.06) toward greater percentage depth of mucosal loss at 6 hours in horses treated with dimethyl sulfoxide, compared with the vehicle control solution. There were no differences in the remainder of the histologic variables among groups. Full-thickness and mucosal WW:DW increased with colonic I-R, but there were no differences among groups. There was a trend (P = 0.09) toward neutrophil accumulation, as measured by myeloperoxidase activity, in the lungs after colonic I-R, but there were no differences among groups. There was no change in lung WW:DW after colonic I-R. There were no beneficial effects of drugs directed against oxygen-derived free radical-mediated damage on colonic mucosal injury associated with low-flow I-R. Deleterious drug-induced hemodynamic effects were not observed in this study.

Free access
in American Journal of Veterinary Research

an exploratory celiotomy within a mean of 4.6 hours (range, 2 to 16 hours) of admission. A closed-suction abdominal drain was placed in all dogs for postoperative management. Blood samples were collected each morning until abdominal drain removal

Full access
in American Journal of Veterinary Research

monitored through a 20-gauge, 5.1-cm catheter placed in the facial artery. Mean arterial blood pressure was maintained at ≥ 70 mm Hg. Horses were positioned in dorsal recumbency and prepared for an aseptic ventral midline celiotomy, through which the large

Full access
in American Journal of Veterinary Research

performed through a ventral celiotomy incision to limit the variable hemodynamic effects of splenic contraction, which can occur during hemorrhagic shock. 18 The abdomen was partially closed to prevent dehydration and loss of heat; however, a loop of

Full access
in American Journal of Veterinary Research

. Surgical techniques For each cat, a ventral midline celiotomy was performed, and the kidneys, ureters, urinary bladder, and other internal organs were examined. The left kidney was harvested for autotransplantation. In preparation for harvest, the left

Full access
in American Journal of Veterinary Research

. The ventral abdomen of each horse was prepared and draped for aseptic surgery, and ventral midline celiotomy was performed. The large colon was exteriorized and positioned on a sterile drape on the ventral abdomen. To induce ischemia, a 40-cm segment

Full access
in American Journal of Veterinary Research