Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/-3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease. Supplemental oxygen to dogs with pulmonary hypertension could reduce PPA and right ventricular afterload. This study supports the use of oxygen, but not antihistamine drugs, in the treatment of postadulticide heartworm disease in dogs that are hypoxic, with signs of congestive heart failure or dyspnea.

Twelve biotinylated lectins and an avidin-biotin-peroxidase method were used to detect and localize specific carbohydrate residues on formalin-fixed, paraffin-embedded female canine mammary gland sections. Histologic sections from 3 lactating and 7 nonlactating mixed-breed dogs (age 5.6 +/- 0.35 years) were incubated with Arachis hypogea agglutinin (peanut agglutinin; PNA), Concanavalia ensiformis agglutinin (conA), Dolichos biflorus agglutinin (DBA), Glycine max agglutinin (SBA), Griffonia simplicifolia agglutinin-I (GS-I), Lens culinaris agglutinin (LCA), Lycopersicon esculentum agglutinin (LEA), Phytolacca americana mitogen (pokeweed mitogen; PWM), Ricinus communis agglutinin-I and-II (RCA-I and -II), Triticum vulgaris (WGA), and Ulex europaeus agglutinin-I (UEA-I). Each lectin had a specific binding pattern, except SBA and DBA. In nonlactating glands, PNA, conA, LEA, and UEA-I stained duct cells in a linear-binding pattern, with a mean percentage of positive ducts per section of 28.7 (+/- 0.6), 65.7 (+/- 0.3), 100 (+/- 0), and 8.4 (+/- 0.2), respectively. Strong apical, lateral, basal, and cytoplasmic positivity on duct cells was seen after incubation of the sections with RCA-I, RCA-II, and WGA in all ducts. In acinar cells, the binding pattern and the staining distribution of all the lectins studied were similar to those in duct cells. However, for PNA, conA, and UEA-I, the mean percentage of positive lobules per section was 33.7 (+/- 0.9), 62 (+/- 0.5), and 10.5 (+/- 0.2), respectively. In glands from lactating dogs, conA and UEA-I did not stain. The cytoplasm of all myoepithelial cells was moderately stained with RCA-I, RCA-II, and WGA. Endothelial cells stained with GS-I, PWM, RCA-I, RCA-II, WGA, conA, and LCA. The extracellular matrix, especially the periacinar and periduct regions, and the interstitial fibroblasts were positive for LCA, RCA-I, RCA-II, and WGA. Peripheral unmyelinated nerve fibers of the nipple were strongly positive for GS-I, PWM, RCA-1, RCA-II, and WGA. Some of the lectins used (ie, PNA, conA, UEA-I, GS-I, PWM, and LEA) appear to have selective staining of mammary gland structures that seems to be correlated with various physiologic functions. The contrasting binding pattern of lectins specific for the same sugar indicates a lack of knowledge of interactions between lectins and carbohydrate residues in tissue sections.

The compound nerve action potential (CNAP) of the superficial peroneal nerve of dogs was investigated to determine: (1) the influence of the stimulation technique on the configuration of the CNAP, with particular attention to late components; (2) the fiber diameter (FD) distribution; and (3) the relationship between FD distribution and CNAP configuration, by reconstruction of CNAP made on the basis of FD distributions. The CNAP were evoked in 9 dogs under halothane anesthesia by 2 stimulation methods: percutaneous needle electrode stimulation and direct stimulation of the exposed superficial peroneal nerve. Recordings were made with percutaneous needle electrodes. Full nerve cross sections of 7 superficial peroneal nerves were prepared for FD morphometric analysis. Reconstruction of CNAP were made on the basis of the FD distributions. Late components of the CNAP could be evoked with either stimulation method, but only with a stimulus intensity of 3 to 5 times maximal for the main (early) component of the CNAP. The FD histograms of 7 analyzed nerves had bimodal distribution. In 5 nerves, peaks were at 4.2 to 4.5 micrometer and 9.0 to 10.0 micrometer with 60% of the fibers in the small-diameter group. In 2 nerves with lower maximal conduction velocities, peaks were shifted toward smaller values. The CNAP reconstructions made by use of FD data closely resembled actual recordings when a fifth-order polynomial function was applied to the relationship between nerve conduction velocity and FD. Reconstructions made by use of 1 or 2 linear functions did not accurately resemble actual recordings. The results indicate clinical sensory electroneurographic recordings can provide accurate information regarding both large- and small-diameter fibers, if adequate stimulus intensities are used. To understand the recorded potential more completely, further studies are needed to determine the effects of volume conduction on configuration of the CNAP. It should then be possible to estimate FD distributions even more accurately by analyzing CNAP of normal nerves, or of diseased nerves in which the normal relation between FD and conduction velocity is preserved.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Sonographic and/or anatomic observations were made of the spleen in 27 dogs. Anatomic studies were used to establish precise correlations between the gross anatomic features of the organ and its ultrasonographic image. In 8 anesthetized dogs, ultrasonographic images of the spleen were made in dorsal, transverse, and sagittal planes. When it was incident to the ultrasonic beam, the splenic capsule was represented by a fine echogenic line that defined the boundaries of the organ. The splenic substance had a uniformly mottled echogenicity apart from the anechoic lumen of the splenic venous rami, which were detected at and near the hilus of the spleen. Less regularly, splenic arterial rami were detected at the hilus, but not within the splenic substance. Dorsal and transverse images were made with the ultrasonic transducer perpendicular to the left thoracic and abdominal wall at the 11th intercostal space and caudoventrad to it. Sagittal images were produced with the transducer's face directed craniad, placed parallel to the left lateral abdominal wall, and pushed under the costal arch. The adoption of such an ultrasonographic imaging protocol ensures that all of the spleen is inspected. A definitive opinion can then be given as to whether the spleen is normal or abnormal. Pathologic changes in the spleen must also be differentiated from changes in adjacent organs or structures.

Canine gastric dilatation-volvulus (GDV) is a naturally acquired condition of large-breed dogs primarily and is associated with high mortality. The clinical course suggests that reperfusion injury may be important in the pathogenesis of GDV. To evaluate the role of xanthine oxidase and iron-dependent lipid peroxidation (which are purported mechanisms of reperfusion injury) in the pathogenesis of GDV-related mortality, we created experimental GDV in 21 dogs. These dogs were then treated with either allopurinol (a xanthine oxidase inhibitor), U74006F (an experimental lipid peroxidation inhibitor), or saline solution (NaCl, 0.85%). Three of 8 dogs died in the allopurinol-treated group, none of 5 died in the U74006F-treated group, and 4 of 8 died in the saline solution-treated group. Tissue malondialdehyde concentration, a nonspecific indicator of lipid peroxidation, was significantly (P < 0.05) greater in the duodenum, jejunum, colon, liver, and pancreas of the saline-solution treated and allopurinol-treated dogs than in the same tissues of the U74006F-treated dogs after surgical correction of the GDV (ie, during reperfusion), compared with malondialdehyde concentrations determined before inducing GDV. The results of this study support the concept that lipid peroxidation associated with reperfusion injury is important in the pathogenesis and high mortality of canine GDV. Furthermore, this lipid peroxidation and mortality may be preventable by appropriate and timely treatment.

Two groups of 4 dogs underwent nasal and ethmoidal turbinectomies followed by irradiation (mean minimal doses of 5,390 and 6,550 cGy of radiation, respectively) from implanted intracavitary sources of iridium 192. Two dogs from each group were euthanatized for histologic evaluation at 3 months after irradiation. The remaining 2 dogs from each group were euthanatized for similar evaluation at 6 months after irradiation. During the course of the study, few clinical complications were encountered. Histologic evaluation of the tissues forming the nasal passages revealed loss of epithelial lining and fibrous tissue replacement of surrounding bone. A direct correlation of pathologic changes could not be associated with the amount of radiation received, but there seemed to be a tendency for greater change in those dogs given higher doses and those kept alive for 6 months.

Canine circulating neutrophils, isolated by a blood lysing technique, were incubated with 7-S nerve growth factor (NGF), at final concentrations between 12.5 and 800 ng/ml, for 30 minutes at 37 C. Neutrophil cytosolic H2O2 production, measured by flow cytometry, after 7-S NGF incubation was not significantly different from that produced at 37 C (baseline temperature controls) alone. Phorbol myristate acetate (PMA; 100 ng/ml) stimulation of neutrophils produced cytosolic H2O2 concentrations almost 13 times that of baseline temperature control neutrophils. Preincubation of neutrophils with 7-S NGF (100 to 800 ng/ml, 30 minutes, 37 C) and subsequent stimulation by PMA resulted in augmented H2O2 production in excess of twice that of neutrophils treated with PMA alone, and almost 30 times that of baseline temperature controls.

The feasibility of renal arterial infusion of nonbiodegradable microspheres as a model of chronic renal disease in dogs was evaluated. Resin-coated, styrene-divinyl benzene copolymer microspheres were infused into the kidneys of healthy adult Beagles by direct injections of both renal arteries in a single surgical procedure. Injections of 25-micrometer diameter microspheres had minimal effect on either the clinical status or serum values of the dogs. Histologic examination revealed the majority of the microspheres lodged within the capillary beds of the glomeruli, and little change to the kidneys. However, injections of 50-micrometer diameter microspheres caused significant increases in serum concentrations of urea nitrogen and creatinine. Histologically, the larger microspheres obstructed afferent arterioles and small arteries, which caused diffuse glomerular necrosis and nephron damage. With doses ranging from 1 to 3 million microspheres/dog, a correlation between the quantity of microspheres injected and severity of renal damage was observed. The optimal dose for producing a model of moderate renal disease was determined to be 1.8 million microspheres/dog (0.9 million microspheres/kidney). During long-term studies, microsphere-injected dogs fed a moderately restricted protein ration remained relatively azotemic, compared with control dogs on the identical ration. During the 5-month postsurgical period, the serum urea nitrogen concentration averaged 18.41 +/- 1.59 mg/dl (mean +/- SE) for the microsphere-injected dogs vs 9.31 +/-0.38 for the control dogs (P < 0.001). Similarly, the mean serum creatinine value was significantly higher (P = 0.020) for the microsphere-injected dogs, compared with the controls (1.23 +/- 0.12 mg/dl vs 0.94 +/- 0.03). In addition, the difference in mean endogenous creatinine clearance rates was statistically significant (microsphere-injected 1.02 0.05 ml/min/kg, vs control 1.53 +/- 0.06, P < 0.001).

The growth hormone (GH) secretagogue activity of variable dosages of clonidine (16.5, 50, 150, and 450 microgram/kg of body weight), given orally mixed with the daily food ration, was evaluated in young and old dogs. Significant (P < 0.05) increase in plasma GH concentration was detected at all dosages tested in young dogs and in response to all but the lowest dose tested in the old dogs fed the clonidine-containing diet. Old dogs had plasma GH concentration that exceeded that of young dogs when higher doses of clonidine were used. A clonidine (100 microgram/kg)-supplemented diet was fed to middle-aged dogs twice daily for 30 days. Significant (P < 0.01) increase of plasma GH concentration was observed on the first day of the feeding trial, but was undetectable by day 30. After feeding the clonidine-enhanced diet for 30 days, the effects on thymic morphology were variable, and there was no effect on plasma thymulin titer. Clonidine-fed dogs had significantly increased lymphocyte blastogenic responsiveness to mitogens, compared with that of control dogs, when evaluated as stimulation index.