Systemic and colonic venous hemostatic alterations in horses during low-flow ischemia and reperfusion of the large colon

Rustin M. Moore From the Departments of Veterinary Clinical Sciences (RM Moore, Couto, Muir, BR Moore) and Veterinary Biosciences (Kociba), College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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C. Guillermo Couto From the Departments of Veterinary Clinical Sciences (RM Moore, Couto, Muir, BR Moore) and Veterinary Biosciences (Kociba), College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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William W. Muir From the Departments of Veterinary Clinical Sciences (RM Moore, Couto, Muir, BR Moore) and Veterinary Biosciences (Kociba), College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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Bonnie Rush Moore From the Departments of Veterinary Clinical Sciences (RM Moore, Couto, Muir, BR Moore) and Veterinary Biosciences (Kociba), College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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Gary J. Kociba From the Departments of Veterinary Clinical Sciences (RM Moore, Couto, Muir, BR Moore) and Veterinary Biosciences (Kociba), College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210-1089.

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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.

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.

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