Microvascular circulation of the ascending colon in healthy horses was studied using microangiography, light microscopy, and scanning electron microscopy. The pelvic flexure with 30 cm of ventral and dorsal colon attached was removed from 14 adult horses immediately after horses were euthanatized. The lumen was flushed with warm water, and this section of the ascending colon was placed in a 37-C bath of isotonic NaCl. In sections from 8 horses, colic vessels were perfused with a radio-opaque medium for microangiography. After angiographic evaluation, tissue sections were prepared for light microscopic observation, using standard histologic methods. In sections from 6 horses, injection replicas were made by perfusing the vessels with 2 types of plastics. The results of microangiography, light microscopy, and scanning electron microscopy of vascular replicas were correlated, providing acomprehensive documentation of the microvasculature of the ascending colon at the pelvic flexure. Arteries branched from mesenteric colic vessels approximately every 2 cm toward the colonic tissue. Immediately after branching, arterial vessels formed an anastomotic plexus, the colonic rete. However, each branch from the colic vessel eventually continued into the colonic tissue. A second set of vessels originated from the colonic rete and supplied the mesenteric lymph nodes. Arterial vessels penetrated the tunica muscularis into the sub-mucosa 3 to 4 cm toward the antimesenteric border forming a submucosal vascular network. From the submucosal arterioles, branching took place at right angles to supply the mucosal capillaries. Capillaries surrounded the colonic glands and anastomosed at the luminal surface, forming a superficial luminal honeycomb-appearing vascular plexus. Venules, sparsely distributed, drained the superficial plexus. Arterial venous anastomoses were not observed within the mucosa.

Eighteen strains of Escherichia coli serogroup O115:K"V165" isolated from 1- to 8-week-old pigs with diarrhea were tested for toxigenicity, pathogenicity in pigs and mice, serum resistance, mannose-resistant hemagglutination (MRHA), F165 and other surface antigens, colicin V (Col V), aerobactin, and biotype. Twelve strains were positive for heat-stable enterotoxin (STb), MRHA-negative, and F165-negative; 5 strains were enterotoxin-negative, MRHA-positive, and F165-positive; and 1 strain was MRHA-positive, but F165- and enterotoxin-negative. Six of the 12 STb-positive strains moderately colonized the ileum of newborn colostrum-deprived pigs within 24 hours after inoculation. Two of the colonizing strains were able to induce watery diarrhea. All 12 STb-positive strains were nonpathogenic for adult mice and were serum-sensitive; 11 of 12 were Col V-negative, 9 of 12 did not produce aerobactin, and 10 of 12 belonged to biotypes other than 1 or 2. All 6 enterotoxin-negative strains colonized the small and large intestines, associated with peritoneal serosal surfaces, and induced septicemia and polyserositis in newborn colostrum-deprived pigs 1 to 2 days after inoculation. In contrast, 3 STb-positive strains poorly colonized the intestines and did not induce septicemia in pigs at 3 days after inoculation. All 6 enterotoxin-negative strains were Col V-positive, produced aerobactin, and belonged to biotype 1 or 2. Of the 5 enterotoxin-negative, F165-positive strains, only 4 were pathogenic for intraperitoneally inoculated adult mice and were serum-resistant. The enterotoxin-negative, F165-negative strain was neither serum-resistant nor mouse-pathogenic. O-agglutinable mutants of the mouse-pathogenic strains were, for the most part, no longer pathogenic for adult mice, although these strains remained unchanged for biotype and production of MRHA, F165, and Col V, and 3 of 4 mutant strains were serum-resistant. Thus, E coli strains of the same serogroup isolated from diarrheic pigs may cause either intestinal or extraintestinal disease upon reinoculation of pigs, depending on the virulence attributes produced by the strains.

The myoelectric activity of the cecum and right ventral colon (RVC) was studied in 4 female ponies. Eight, bipolar Ag-AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and RVC (2 electrodes), and recordings were begun 14 days after surgery. The myoelectric activity for each pony was recorded during 12, 60-minute recording sessions done during the interdigestive period (3 to 7 hours after the morning feeding). Coordinated series of spike bursts were recognized as independent motility patterns in the cecum and in the RVC. Local haustra-haustra myoelectric activity involving approximately 40 cm of the cecal body (0.45 +/- 0.03 spike bursts/min) were detected. A series of spike bursts started at the cecal apex and progressed to, but stopped at, the caudal cecal base (0.04 +/- 0.03 spike bursts/min). Infrequently, a series of spike bursts started at the apex and progressed to the cranial cecal base (0.09 +/- 0.01 spike bursts/min). More commonly, a series of spike bursts with a conduction velocity of 3.8 +/- 0.07 cm/s, began in the cranial base and progressed orally to the cecal apex (0.46 +/- 0.03 spike bursts/min). Spike bursts conducted aborally (propulsion) beginning at the origin of the RVC (0.05 +/- 0.07 spike bursts/min) and spike bursts conducted orally (retropulsion; 0.15 +/- 0.02 spike bursts/min) were seen independent of cecal myoelectric activity. A progessive series of coordinated spike bursts, which began at the cecal apex, were conducted through the cecolic orifice and continued into the RVC (0.42 +/- 0.02 spike bursts/min), representing the only pattern common to the cecum and RVC. This pattern, associated with a loud rush of ingesta heard on auscultation, had a conduction velocity of 5.65 +/- 0.12 cm/s and was always generated in the cecal body, near the apex. An apparent electrical pace-maker area was proposed in this area. Duration of spiking activity during the progressive pattern was significantly (P = 0.0001) greater at electrodes 7 and 8 in the RVC than at any electrode locus in the cecum. Coordinated orally directed spike bursts were detected frequently in the cecum before and after the progressive pattern, indicating a complex sequence of motility patterns may exist.

Isolated segments of left dorsal colon and a side-to-side colocolostomy (between the left ventral colon and left dorsal colon) were surgically created in 6 adult ponies. Four segments, each separated by an empty segment, were inoculated (20 ml) with 1 of the following 4 solutions: phosphate buffered saline solution (PBSS)/1% polyethylene glycol (PEG); purified cholera toxin in PBSS/1% PEG (5 micrograms cholera toxin/ml of PBSS/1% PEG); lyophilized Salmonella typhimurium UCD 1755 culture lysate, reconstituted in PBSS/1% PEG; and viable S typhimurium UCD 1755 (10(8) organisms/ml of PBSS/1% PEG). Twenty hours following inoculation of the treatment solutions into the isolated colon segments, the ponies were reanesthetized. Fluid accumulation in the isolated segments was measured, and tissue samples from isolated segments were taken for examination by light microscopy and electron microscopy, and for measurement of mucosal cyclic adenosine monophosphate levels. There was fluid accumulation in segments inoculated with cholera toxin in 4 ponies (29.5 +/- 12.7 ml), and in segments inoculated with S typhimurium UCD 1755 culture lysate in 3 ponies. (14.0 +/- 8.7 ml). There was no fluid accumulation in segments inoculated with either the control solution (PBSS/1% PEG) or viable S typhimurium UCD 1755. There was significantly (P less than 0.05) less cyclic adenosine monophosphate in segments inoculated with cholera toxin, Salmonella lysate, and viable Salmonella, compared with control segments. Histologically, there were minimal changes in control segments, consisting of mild to moderate submucosal edema and capillary congestion. Changes in the other segments were more pronounced and included neutrophilic infiltration and exocytosis, with the changes increasing in severity in the segments inoculated with cholera toxin, S typhimurium culture lysate UCD 1755, and viable S typhimurium UCD 1755, respectively. Ultrastructurally, mucosa from control segments was normal. Mucosa from segments inoculated with cholera toxin had swollen endoplasmic reticula and basolateral separation of surface epithelial cells. Mucosa from segments inoculated with S typhimurium UCD 1755 culture lysate and viable S typhimurium UCD 1755 had swollen smooth and rough endoplasmic reticula, separation of epithelial cells, degeneration of microvilli, and goblet cell degeneration.

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity in the duodenum, right ventral colon, cecal body, and cecal apex were measured in 6 conscious healthy horses for 60 minutes during and for 120 minutes after IV infusion of 0.9% NaCl solution (control) or fenoldopam. There were no significant changes in these measurements during or after infusion of 0.9% NaCl (saline) solution. Fenoldopam, a selective dopamine- 1 receptor agonist, was administered in saline solution at dosages of 0.01, 0.05, and 0.1 ug/kg/min. Intravenous infusion of fenoldopam at 0.01 ug/kg/min significantly increased heart rate, but did not change average carotid arterial pressure or lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at both 0.05 and 0.1 ug/kg/min significantly increased heart rate, significantly decreased average carotid arterial pressure, and significantly increased lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at 0.01, 0.05 and 0.1 ug/kg/min did not significantly change the mechanical activity measured by the area under the strain gauge defection curve for the duodenum, right ventral colon, cecal body, or cecal apex. These results suggest that dopaminergic-1 receptors are present on the colonic vascudopaminergic-1 receptors exist on the visceral smooth muscle of the duodenum, right ventral colon, cecal body, or cecal apex of horses.

Fecal excretion of a particulate marker, ytterbium (Yb), was evaluated in 9 horses before surgery and 3 weeks, 3 months, and 6 months (4 trials) after sham-operation (group 1; n = 3) or extensive large colon resection (group 2; n = 6). Fecal excretion curves of total Yb excretion, log(e) Yb excretion, % Yb excretion, log(e) % Yb excretion, and cumulative % Yb excretion were evaluated, and kinectic analysis was performed on the log(e) Yb excretion curves to detect mixing pools and to calculate the fractional rate of particulate passage, turnover rate, and pool size. Calculations were performed to determined transit time, mean overall retention time, adjusted mean retention time, peak time, and disappearance time. Values were statistically analyzed to determine differences between groups and among trials (P less than 0.05). Group-2 horses had significantly shorter transit, peak, and mean overall retention times, compared with preoperative values and with values for group-1 horses. Two mixing pools were identified: a slower emptying pool of 5.7% hour-1 (k1) and a faster emptying pool of 12.3% hour-1 (k2). The rate of passage from the first pool (k1) was not altered by colon, resection, and was interpreted as being most influenced by the cecum. In further support of this interpretation, the capacity of the k1 pool approximated the capacity of the cecum (17 L). The capacity of the k1 pool significantly expanded by 6 months in the resected horses. The rate of passage from the second pool (k2) significantly increased initially after colon resection (3 weeks and 3 months), but returned to preoperative values by 6 months. This pool was affected by colon resection, and was therefore interpreted as being influenced by a portion of the colon. Despite these changes in rate of passage and capacity of the mixing pools, on all the trials, colon resection decreased intestinal transit time and overall mean retention time because of a decrease in the total large intestinal length or capacity. This decrease in particulate matter retention and transit time may partially or totally explain the decrease in fiber digestion reported in horses with extensive large colon resection.

Nutritional alterations were evaluated in 9 horses before surgery and 3 weeks, 3 months, and 6 months (4 total trials) after sham operation (group 1; n = 3) or extensive large colon resection (group 2; n = 6). Feed and fecal analyses were performed to determine apparent digestion of dry matter, organic matter, crude protein, calcium, phosphorus, magnesium, potassium, manganese, zinc, copper, and iron, and true digestion of dry matter, organic matter, crude protein, total plant cell wall, hemicellulose, cellulose, and lignin. Additional fecal and metabolic variables included the percentage of fecal water (water in the feces), total fecal water, metabolic organic matter, metabolic crude protein, and metabolic nitrogen. A CBC and standard series of biochemical tests were performed. Large colon resection decreased (P less than 0.05) the true digestion of dietary crude protein and cellulose and apparent digestion of phosphorus, and it increased the fecal metabolic matter and water loss. Total fecal output increased 45% and total fecal water increased 55%. Phosphorus digestion was decreased (P less than 0.05) in group-2 horses, but effects of this were not detected on analysis of blood variables or on physical examination. Nevertheless, after extensive large colon resection, horses can regain body weight lost after surgery and have no overt physical changes when fed an alfalfa pellet diet that meets greater-than-maintenance requirements. Ad libitum water access is suggested, because these horses may have to consume 2 gal/day more than would normal horses.

The vasculature of 22 small colons from dead adult ponies was perfused with latex or barium sulphate solution. The vascular anatomy was studied by use of dissection and alkali digestion of the latex specimens and microangiography of the barium sulphate-perfused specimens. The small colon is supplied by the caudal mesentric artery. The left colic artery arises from the caudal mesenteric artery, which then becomes the cranial rectal artery. Branches from the left colic and cranial rectal arteries form anastomosing arcades that become narrower distally along the length of the small colon. From these arcades arise terminal arteries, which enter the small colon wall and give rise to a subserosal, an intermuscular, and a large submucosal plexus, with frequent anastomoses between them. The venous drainage closely parallels the arterial supply, except near to its origin from the portal vein, when the left colic vein and caudal mesentric vein are separate from the corresponding arteries.

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.