The microvascular circulation of the descending colon was studied in 5 adult horses, using microangiography and light microscopy combined with gross studies and scanning electron microscopy of vascular replicas. After heparinization, horses were euthanatized, and 3 segments of the descending colon and its mesentery containing 1 vascular arcade were removed from each horse. The fecal bars were gently massaged from the lumen, and the blood was flushed free of the circulation with isotonic NaCl. In 5 segments, the vascular system was injected with a modified radiopaque medium and evaluated radiographically. Specimens examined radiographically also were prepared for histologic examination, using standard methods. Ten segments were injected with 1 of 2 types of plastics and studied grossly or by scanning electron microscopy. Arcuate arteries gave rise to a descending colonic rete that surrounded the vein and supplied numerous descending colonic lymph nodes. The rete also supplied the mesocolon and the descending colonic tissue. Short filamentous vessels arising from the rete directly penetrated the mesenteric tenia to supply an intermuscular plexus between the longitudinal and circular muscle layers of the muscularis externa. Larger vessels arising from either side of the rete divided into the long- and short-terminal arteries that supplied an extensive submucosal plexus, which was continuous around the circumference. The submucosal plexus supplied the mucosa, the tunica muscularis, and the serosa. Vessels running centrifugally from the submucosal plexus formed an intermuscular plexus between the longitudinal and circular muscle layers of the muscularis externa. The intermuscular plexus at the mesenteric angle also was supplied by vessels branching from the short-terminal arteries as they penetrated the muscularis externa. At the antimesenteric tenia, the submucosal plexus gave rise to larger vessels that formed a subserosal loop. From this loop, 5 vessels penetrated the longitudinal muscle layer to contribute to the intermuscular plexus. Vessels within the longitudinal and circular muscles of the muscularis externa ran parallel to the muscle fibers and, consequently, perpendicular to each other. Arteries supplying the mucosa penetrated the muscularis mucosa and branched into a capillary network at the base of the descending colonic glands. These capillary networks anastomosed with the networks around adjacent glands at the luminal surface, forming a honeycomb-like pattern. Drainage was facilitated by more sparsely distributed venules that united with venules from adjacent areas and descended to the submucosal plexus. These veins were characterized by regular, helical, smooth muscle constrictions.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.

Effects of 1 hour of colonic volvulus and 3 hours of reperfusion on concentrations of thromboxane (TXB2) and prostacyclin (6-keto-PGF 1-alpha) in portal, pulmonary arterial, and jugular blood were determined by radioimmunoassay to assess the site of production and clearance of these eicosanoids from the circulation in 5 anesthetized ponies. Colonic volvulus had no significant effect on mean arterial pressure or TXB2 concentrations, but significantly (P < 0.05) increased 6-keto-PGF 1-alpha. concentrations in all blood samples. Immediately after colonic reperfusion, all eicosanoid concentrations were significantly (P < 0.05) increased. Then, TXB2 returned to baseline values, whereas 6-keto-PGF 1-alpha, concentrations remained significantly (P < 0.05) high for the remainder of the study. Eicosanoid concentrations were significantly (P < 0.05) greater in portal blood than in pulmonary arterial and jugular blood samples at all periods. This suggests that the splanchnic circulation is the primary site of eicosanoid production during and after colonic volvulus and the liver appears to provide most of the circulatory clearance of thromboxane and prostacyclin.

Postoperative abdominal fluid changes were compared in 2 groups of horses; those undergoing double small-colon resection and anastomosis (n = 10) and those undergoing exploratory celiotomy alone (n = 5). Peritoneal fluid was collected before surgery and on postoperative days 1, 3, 5, and 7. Total and differential nucleated cell counts, RBC numbers, and total protein and fibrinogen concentrations were evaluated. In both groups, all values were significantly higher than normal on the first postoperative day (after small-colon resection and anastomoses, WBC = 130,350 +/- 23,310 cells/microliter, RBC 7,389,000 +/- 6,234,000 cells/microliter, total protein = 3.63 +/- 0.16 g/dl; after exploratory celiotomy alone, WBC = 166,620 +/- 34,340 cells/microliter, RBC = 295,000 +/- 86,070 cells/microliter, total protein 4.38 +/- 0.54 g/dl). The number of total peritoneal nucleated cells and RBC significantly decreased after the first postoperative day, whereas total protein and fibrinogen concentrations, percent neutrophils, and percent mononuclear cells remained unchanged. None of the values had returned to normal by postoperative day 7 (after small-colon resection and anastomoses, WBC = 45,600 +/- 8,765 cells/microliter, RBC = 95,390 +/- 53,380 cells/microliter, total protein = 4.39 +/- 0.23 g/dl; after exploratory celiotomy alone, WBC = 43,340 +/- 7,746 cells/microliter, RBC = 12,860 +/- 11,790 cells/microliter, total protein = 3.92 +/- 2.20 g/dl.) The resection and anastomosis group had a significantly lower total protein concentration on the first postoperative day and a significantly higher mean total RBC count over the entire 7-day postoperative evaluation than did horses that underwent celiotomy alone. Other values in the 2 groups of horses did not differ significantly. As a result, there was insufficient evidence to conclude that resection and anastomosis of the small colon in healthy horses causes a different inflammatory response than does manipulation of the intestine alone.

The ultrastructural injury that develops sequentially in the ascending colon during experimentally induced ischemia was examined in 6 halothane-anesthetized horses. Colonic ischemia was created by 2 types of vascular occlusion 24 cm proximal and distal to the pelvic flexure. In all horses, transmural vascular compression was created. The colonic venous circulation was obstructed in 3 horses, whereas in the other 3 horses, arterial and venous circulation was obstructed. Two additional horses were anesthetized as controls for determination of any morphologic alterations associated with the experimental protocol. Full-thickness colonic biopsy specimens were obtained from the antimesenteric border of the pelvic flexure at 0, 0.25, 0.5, 1, 1.5, 1.75, 2, 2.25, 2.5, 3, 3.5, 4, 4.5, and 5 hours during occlusion, and were studied by light and transmission electron microscopy. Morphologic alterations did not develop in the colon of control horses. Mucosal congestion was observed by light microscopy in the colon of horses with experimentally induced ischemia, but congestion developed early in those with obstructed colonic venous circulation, compared with those having arterial and venous obstruction. Inter- and intracellular vacuolation and loss of staining initially resulted in groups of 3 to 5 superficial luminal epithelial cells. Alterations in the glandular epithelium lagged behind those in the superficial epithelium, but were observed in both groups by 2 hours of obstruction. These changes progressed to 100% sloughing of all epithelium by 4.5 to 5 hours. The initial cellular alterations, which were observed by transmission electron microscopy, developed at 0.25 hour in horses with colonic venous obstruction and was characterized by inter- and intracellular edema. By 1 hour in horses with colonic venous obstruction, vacuoles were observed within the basal lamina and some vacuoles contained intracellular organelles. These cellular changes were followed by increases in the intercellular gap and breaks between degenerating and more normal-appearing superficial epithelium, which led to sloughing of the epithelium. Endocrine cells by 1 hour also had evidence of ischemic injury. Injury to the vascular circulation, including congestion and platelet accumulations within the mucosal capillaries was apparent by 0.25 hour in horses with venous obstruction. By 1 to 1.5 hours in both groups of horses with experimentally induced ischemia, loss of vascular integrity and leukocyte migration frequently were observed. Platelets, proteinaceous material, and cellular debris continued to accumulate, and by 2.25 hour capillary plugging frequently was observed. These results indicated that the initial ultrastructural injury in the ischemic colon consisted of degenerative changes in epithelial cells, which led to sloughing of degenerating and necrotic cells. Although injury between the 2 types of vascular obstruction differed, end results were similar. Ischemic vascular injury may lead to further vascular thrombosis and necrosis, resulting in an irreversible injury or contribute to difficulty in medically managing horses with natural ischemia during the perioperative period.