The anterior chambers in 16 dogs with normotensive eyes and 3 Beagles with glaucomatous eyes were treated with 0, 25, 50, or 100 IU of bovine testicular hyaluronidase. Aqueous outflow resistance was then determined by constant-pressure perfusion of 0.9% NaCl solution for 30 or 60 minutes. In normotensive eyes, 25, 50, or 100 IU of hyaluronidase significantly (P < 0.02) increased the rate of constant-pressure perfusion compared with that of untreated eyes during 30- or 60-minute perfusions. Treatment of glaucomatous eyes with 25, 50, or 100 IU of hyaluronidase did not significantly increase the rate of constant-pressure perfusion over controls during a 30-minute perfusion. Bovine testicular hyaluronidase at all doses removed the staining of colloidal iron from the trabecular meshwork in normotensive eyes. In Beagles with glaucoma, the trabecular meshworks remained stained with colloidal iron when treated with the hyaluronidase, which suggested that some glycosaminoglycans were resistant to this enzyme's action.

A panel of monoclonal antibodies (MAb) developed against Mycoplasma gallisepticum strain PG31 was used to probe the antigenic profiles of 5 recognized strains (PG31, R, S6, F, A5969) and 6 field isolates of M gallisepticum. Monoclonal antibody G9 predominantly recognized antigens at apparent molecular mass positions of 90 to 98 kDA. The MAb reacted with all strains and isolates, but the molecular mass position of the antigens varied among some mycoplasmas. Monoclonal antibody G12 reacted with all strains and isolates of M gallisepticum and had an identical banding pattern. However, MAb G10 and G11 reacted selectively only with a limited number of strains and/or isolates. Surface distribution of the MAb-recognized antigens was revealed by immunoelectron microscopy. Partial physicochemical characterization of MAb G9-recognized antigens identified glycopeptide characteristics. Monoclonal antibody G9 reacted with surface antigens and, hence, participated in agglutination of M gallisepticum. However, the degree of agglutination varied among the various strains and isolates, indicating a quantitative or conformational limitation or an alteration in the anomeric expression of the epitopes. Antigenic variation in M gallisepticum may be mediated by immunologic selective pressures, or a proclivity for habit niche in the host.

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.

Histomorphometric and scanning electron microscopic analyses were carried out on 74 embryos and fetuses and 20 sheep (early postnatal to adult age). Histodifferentiation of the rumen took place at 33 days of fetal fife. Ruminal pillars were observed at 42 days, and at 61 days, ruminal papillae appeared as evaginations of the epithelial stratum basale. Neutral mucopolysaccharides first appeared in epithelial cells at 46 days of fetal life; thereafter, numbers decreased gradually and subsequently stabilized in postnatal life. Acid mucopolysaccharides, mucins, and mucoid compounds were not detected. Age and diet were recognized as factors that determine the structure of the ruminal mucosa. Growth curves and formulas were set out for each tissue layer.

When Salmonella typhimurium and Clostridium perfringens were tested in conventional chickens, larger numbers of S typhimurium and C perfringens adhered to Eimeria tenella-infected ceca than to uninfected ceca. In germ-free chickens, S typhimurium and C perfringens adhered to the E tenella-infected cecal mucosa more than to the uninfected cecal mucosa, but fewer Bacteroides vulgatus and Bifidobacterium thermophilum adhered to the E tenella-infected ceca than to the uninfected ceca. Many bacteria adhered to the lesions caused by E tenella as observed by scanning electron microscopy. On the basis of our findings, we suggest that infection with E tenella upsets the balance of competitive adherence of bacteria, allowing more colonization of S typhimurium and C perfringens.

Chorioallantoic membranae (CAM) explants were used to determine the in vitro growth and cytotoxic potential of 3 strains of Brucella abortus. Bovine CAM explants were inoculated with 2 X 10(7) colony-forming units of the pathonic strain 2308, attenuated strain 19, or the rough strain RB51 of B abortus. After inoculation, the explants were harvested and examined at 2 or 4 hours, 12 or 14 hours, and 24 or 26 hours of incubation. Bacterial growth associated with each explant was determined by counting colony-forming units. The degree of cellular damage in each explant associated with bacterial growth or bacterial toxins were evaluated by morphometric analysis after trypan blue staining. Significant differences were not detected in the numbers of bacteria of any strain of B abortus in the CAM explants at comparable time intervals. The rate of growth of the bacteria in CAM explants was higher between 2 and 12 hours after inoculation than between 12 and 24 hours after inoculation. Cytotoxic effects associated with strain 2308 were significantly (P < 0.05) greater than that caused by other strains. Cytotoxic effects associated with strain 19 and rough strain RB51 were similar, and both were significantly (P < 0.05) greater than the phosphate buffer solution control. Chorioallantoic membrane explants inoculated with a filtrate of heat-killed strain 2308 induced minimal cellular damage, compared with that caused by the viable bacteria. These results indicated that the number of B abortus in trophoblasts was independent of the degree of cellular damage.

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.

Mast cells isolated from feline splenic mastocytomas were cultured to study their structural and functional properties. isolated cells from various cats were grown as monolayer cultures for a mean of 56 days (range, 30 to 76 days). Cat mast cells released allergic mediators in response to compound 48/80, anti-cat serum antibodies, and concanavalin A. On the basis of the finding that secretion from cat mast cells was stimulated by anti-cat serum antibodies and concanavalin A, these cells contain surface-bound immunoglobulins. The presence of mast cell-sensitizing antibodies has been suspected in cats, but never before directly demonstrated. Cultured cat mast cells have cytochemical and functional characteristics common to connective tissue-type mast cells and provide one of the few non-rodent models of cultured cells for the study of this type of mast cell.

The microvascular anatomic features of the small intestine was described by correlating results of microangiography, light microscopy, gross studies, and scanning electron microscopy of vascular replicas in 14 horses. After heparinization, the horses were euthanatized, a length of jejunum was transected, and blood was flushed free of the circulation, using isotonic NaCl solution. In six horses, the circulatory system was perfused with a modified radiopaque medium and evaluated radiographically. These sections were then evaluated by standard histologic methods. Sections from 8 horses were perfused with 1 of 2 types of plastics and studied grossly or by scanning electron microscopy. The marginal arterial arcade gives rise to vessels that enter the jejunum at the mesenteric angle. These vessels penetrated either directly, by branching and entering on both sides of the mesenteric angle, or supplying only 1 side of the mesenteric angle. All these vessels continued in the submucosa branching extensively, forming a submucosal plexus. This submucosal plexus supplied the tunica muscularis, tunica serosa, and the mucosa. Vessels within the 2 muscle layers ran parallel to the muscle fibers and, consequently, perpendicular to each other. The arterial supply to the mucosa penetrated the muscularis mucosae and branched to supply 2 mucosal capillary networks. An eccentrically placed arteriole penetrated the base of the villus and spiralled to the tip where it "fountained" into a mesh-like capillary network, which descended peripherally in the villus to drain via 1 to 3, but most commonly 2 venules. Venules from adjacent villi united and drained via the submucosal veins. The second capillary network supplied the glands of the intestinal crypts. The capillary network around adjacent glands anastomosed just below the luminal surface. There were connections between this network and the base of the villus capillary network. Drainage of the glandular capillary network was through these connections and through the villus venules. There was no evidence of arterovenous anastomoses.

Changes in the common bile duct that contained adult Fasciola hepatica of sheep were evaluated by light (LM) and scanning electron microscopy (SEM). Nine ewes were inoculated with F hepatica metacercariae and necropsied 18 weeks after inoculation. The proximal portion of the common bile duct (CBD) that contained adult flukes was recovered and examined by Lm and SEM. The CBD from 2 noninoculated ewes were used for control. On gross examination, CBD were markedly large because of the adult flukes, which were free in the lumen of the ducts. Extensive hemorrhage was not found either in intrahepatic or in extrahepatic bile ducts of any sheep. Histologic examination revealed changes, such as villous hyperplasia and hypertrophy of the epithelium; cell infiltration, predominately with eosinophils or macrophages; and arterial intimal proliferation. By SEM, the epithelial surface of the CBD appeared intact. Villous hyperplasia and hypertrophy of the epithelium observed by LM was clearly seen by SEM. Epithelial damage, seen as small areas of denuded surface by LM and SEM, was confined to a few areas of the mucosa. Lack of extensive hemorrhage and confined epithelial damage were evaluated relative to the mode of feeding of adult flukes.