The effects of butorphanol tartrate on arterial pressure, jejunal blood flow, vascular resistance, oxygen extraction, and oxygen uptake were determined in 10 anesthetized ponies ventilated with a mixture of halothane and 100% oxygen, using isolated autoperfused jejunal segments. Physiologic saline solution or butorphanol tartrate (0.2 mg/kg of body weight) was administered as a single bolus into the left jugular vein. By 2 minutes, butorphanol decreased arterial blood pressure and intestinal blood flow, and increased intestinal oxygen extraction. However, intestinal vascular resistance and oxygen uptake were unaffected. Results of this study indicate that butorphanol tartrate induces a hypotension that secondarily decreases intestinal blood flow, but intestinal vascular resistance and metabolism are not adversely affected. We conclude that butorphanol tartrate does not compromise intestinal viability in halothane-anesthetized ponies and, therefore, may be a good analgesic choice for the equid destined for abdominal surgery.

The influence of distention (high baseline intraluminal pressure) and neostigmine methylsulfate on intestinal vascular resistance, oxygen uptake, and intraluminal pressure changes (rhythmic contractions) was studied in terminal jejunal segments which were perfused at a constant rate, in 16 anesthetized ponies. When baseline intraluminal pressure was increased to 10 mm of Hg, the intestinal vascular resistance and amplitude of rhythmic contractions were increased. Neostigmine induced cyclic increases in amplitude of rhythmic contractions whether intraluminal pressure was 0 or 10 mm of Hg. Neostigmine also increased intestinal oxygen uptake at intraluminal pressures of 0 mm of Hg, but not at 10 mm of Hg, and vascular resistance was not altered at either intraluminal pressure. The results indicate that intestinal hemodynamics are adversely affected by distention. Further, neostigmine did not adversely affect intestinal hemodynamics while increasing rhythmic contractions, suggesting that neostigmine may be useful in the treatment of ileus in equids.

The 51Cr-labeled EDTA was validated as a suitable permeability probe in dogs for measurement of passive, unmediated diffusion across intestinal mucosa via intercellular pathways. The 51Cr-labeled EDTA was stable in aqueous solution and did not bind to biologic tissue and fluids. After incubation of 51Cr-labeled EDTA in isolated jejunal loops, analytic subcellular fractionation of jejunal mucosa on reorientating sucrose-density gradients was performed, and no association of 51Cr-labeled EDTA with particulate intracellular organelles was detected. Intravenously administered 51Cr-labeled EDTA was rapidly and completely excreted in urine. Intestinal permeability to 51Cr-labeled EDTA after oral administration was assessed in healthy dogs. The percentage of the administered dose of 51Cr-labeled EDTA excreted in the urine in 24 hours ranged from 2.3 to 17.6% (median, 13%).

Intestinal lesions of transmissible gastroenteritis (TGE) virus infection in conventionally reared pigs suckling either nonvaccinated, vaccinated, or previously infected sows were studied by scanning electron microscopy, light microscopy, and immunofluorescent microscopy for TGE viral antigen. Pigs were inoculated with virulent TGE virus when they were 5 or 21 days old and were euthanatized shortly after the onset of diarrhea or 96 hours after inoculation if no diarrhea developed. Pigs inoculated when they were either 5 or 21 days old and suckling nonvaccinated sows developed severe lesions, including swelling and necrosis of enterocytes and severe villus atrophy. Pigs inoculated when they were 5 days old and suckling sows vaccinated with attenuated vaccines developed less-severe villus atrophy, and those suckling sows immunized by exposure to nonattenuated TGE virus developed moderate or no villus atrophy. Pigs inoculated when they were 21 days old and suckling sows vaccinated with attenuated vaccines had severe villus atrophy, whereas those suckling sows immunized by exposure to nonattenuated virus had more-moderate villus lesions. Villus atrophy was inhibited to various degrees in pigs suckling immunized sows, depending in part on the antibody titer in the colostrum and milk.

Five 5 to 6 month old horses were surgically prepared with silver electrodes sutured to the serosa of gastric antrum, duodenum and proximal portions of the jejunum. Normal migrating motility complex (MMC) periodicity was determined during daytime hours in horses that were fed and horses from which food was withheld for 24 hours. Periodicity was defined as time span from the end of one period of regular spike activity (RSA) to the end of the next RSA in the MMC. The periodicity was 120.5 +/- 9.5 (SEM) minutes in horses from which food was withheld, and was 125.7 +/- 20.3 minutes in horses fed hay free choice. Coincident with each duodenal RSA, antral spike activity ceased. Xylazine (0.25 and 0.5 mg/kg), given IV during the period of intermittent spike activity of the MMC to either fed or unfed horses induced, within 2 minutes, a RSA complex in the duodenum that migrated to the proximal portion of the jejunum. This was followed by a period of no spike activity of normal duration, which proceeded on to a period of intermittent spike activity of varying duration to complete the MMC cycle. Pretreatment IV administration of an alpha 2-adrenergic antagonist, tolazoline (1 mg/kg) also provoked a RSA complex, but blocked the xylazine effect. The results indicated that xylazine resets the duodenal MMC in the horse, but does not seriously disrupt proximal gastrointestinal tract motility, and that control of MMC periodicity in this region probably involves more than alpha 2-adrenergic receptors.

The virulence of 2 porcine group-A rotavirus isolates was compared. Forty hysterotomy-derived 3-day-old gnotobiotic pigs were inoculated orally with 2 ml of intestinal homogenate containing either the Ohio State University (OSU) or the South Dakota State University (SDSU) strain of porcine rotavirus or were inoculated with medium only. Clinical signs of disease, body weight, distribution of viral antigen, fecal excretion of virus, and histologic lesions (observed by light and scanning electron microscopy) were determined. Morphometric measurements of villi and crypts were made. In pigs inoculated with OSU or SDSU strains, diarrhea began at postinoculation hours (PIH) 19 to 48 and PIH 24 to 54, respectively. None of the virus-infected pigs died as a consequence of infection and all had similar clinical signs of disease, body weight changes and virus-shedding patterns, regardless of the strain of rotavirus with which they were infected. Microscopic findings in the small intestine of virus-infected pigs were similar, except that the SDSU strain caused more severe villus atrophy and villus fusion in the duodenum at PIH 72 and 168 than was associated with the OSU strain. Viral antigen in the small intestine of pigs infected with either virus was observed by use of immunofluorescence at PIH 24 and 72, but was seldom seen at PIH 168.