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A modified ventral fixation for surgical management of atlantoaxial subluxation in 19 dogs.

OBJECTIVE: To describe a modified ventral stabilization technique for surgical management of atlantoaxial subluxation in dogs and to evaluate the outcome. STUDY DESIGN: Retrospective clinical study. SAMPLE POPULATION: Nineteen client-owned dogs. METHODS: Medical records of 19 dogs with a radiographic diagnosis of atlantoaxial subluxation surgically managed by a modified ventral fixation technique (cortical screws, Kirschner wires, polymethylmethacrylate) were reviewed. Data on pre- and post-operative neurologic status, surgical technique, and complications were retrieved. Follow-up evaluation was performed at approximately 1 month. Telephone interview of the owner was used for long-term assessment (median follow-up for 17 surviving dogs was 10.5 months). RESULTS: Adequate reduction and stabilization was achieved in all dogs based on radiographic assessment immediately after surgery. Improved neurologic outcome occurred in 16 dogs at 1 month and in 15 dogs at follow-up; 2 dogs died of post-operative complications within 24 hours of surgery. One dog was euthanatized at the owners' request because of recurrent neck pain associated with implant failure after 1 month. Two dogs required surgery to remove broken and migrated implants, but further stabilization was not necessary. CONCLUSIONS: Adequate stabilization and improved neurologic outcome was achieved in most dogs. However, on account of the small size of the study and the variable neurologic signs of the dogs on admission, the surgical technique described could not be compared to those previously reported. CLINICAL RELEVANCE: The surgical technique described is an effective means of surgical treatment for atlantoaxial subluxation.

Animals↗

Evaluation of the Norberg angle threshold: a comparison of Norberg angle and distraction index as measures of coxofemoral degenerative joint disease susceptibility in seven breeds of dogs.

OBJECTIVE: To evaluate the thresholds of 2 radiographic methods used to determine coxofemoral joint laxity in 7 breeds of dogs. ANIMALS: Three hundred and fifty clinically normal dogs. STUDY DESIGN: Retrospective study. METHODS: Hip radiographs from 7 breeds of dogs were randomly selected from a database. None of the dogs had radiographic evidence of degenerative joint disease (DJD). Distraction index (DI) and Norberg angle (NA) were measured on these radiographs and compared with DI and NA thresholds for diagnosing DJD susceptibility derived from the literature and from evaluated Borzois. Dogs with a NA<105 degrees and a DI of < or =0.32 were considered false-positives and dogs with a NA> or =105 degrees and a DI of >0.32 were considered false-negatives. RESULTS: Mean age of all dogs was 22.9 months. Mean NA for all dogs was 99.37 degrees, and mean DI for all dogs was 0.44. Borzoi mean DI of was significantly less than the mean DI of the other 6 breeds. The highest (most hip laxity) Borzoi DI was 0.32, and the lowest (most hip laxity) Borzoi NA was 99 degrees. False-positive and false-negative diagnoses were identified in 6 of the 7 breeds. CONCLUSIONS: Using the NA threshold of 105 degrees (literature established threshold of susceptibility to DJD) resulted in a high percentage of false-negative and false-positive diagnoses. Breeds like the Labrador Retriever and Rottweiler would have large numbers of hip dysplasia susceptible dogs remain in the breeding population based on this NA threshold. False-positive diagnoses were common in breeds like the Australian Shepherd, Borzoi, and German Shepherd effectively eliminating hip dysplasia nonsusceptible dogs from the breeding population. CLINICAL RELEVANCE: The NA was not an accurate predictor of DJD susceptibility in these 7 breeds of dogs when using a NA threshold of 105 degrees.

Animals↗

Reassessment of AV and VA conduction and AV junctional reentry in the normal dog heart: the role of altered autonomic tone.

The effects of isoproterenol, atropine, and metoprolol on atrioventricular (AV) and ventriculoatrial (VA) conduction were studied in 30 normal dogs under pentobarbital anesthesia using percutaneously introduced catheters. The inducibility of AV junctional reentry was also assessed before and after drug administration. Resting AV conduction was normal in all dogs, but VA conduction was present in only 57%. Isoproterenol facilitated both antegrade and retrograde conduction, with a preferential effect on retrograde conduction. VA conduction was demonstrated after isoproterenol in 91% of dogs. After testing all drugs, VA conduction was demonstrable in at least one study in 97% of dogs. Atropine had less effect than isoproterenol, suggesting that basal vagal tone was not high in this model. Dual AV nodal pathways were detectable in the antegrade direction in four (13%) dogs, and in the retrograde direction in an additional four (13%) dogs. Single AV junctional echoes were inducible with atrial stimulation in one dog with dual antegrade pathways, but were inducible with ventricular stimulation in at least one study in 83% of dogs with intact retrograde conduction. Sustained AV junctional reentry was never induced before or after drug administration. In conclusion, VA electrical continuity is almost always intact in the normal dog, but its demonstration is significantly modified by the autonomic nervous system. Isoproterenol has preferential effects on retrograde conduction and may have selective influence on distal AV nodal conduction. Twenty-six percent of normal dogs have evidence of dual AV nodal pathways. Single AV junctional echoes are inducible with ventricular stimulation in the majority of dogs and are a normal finding. Sustained AV junctional reentry is not inducible in the normal intact dog heart.

Animals↗

Differences in the pathological changes in dogs' hearts after defibrillation with extrapericardial paddles and implanted defibrillator electrodes.

A comparison was made between the pathological changes in the myocardium of eight dogs, each receiving about 90 joules of energy in a series of defibrillation discharges, delivered either between paddles placed against the pericardium (3 dogs) or between implanted Telectronics 040-105 defibrillation patch electrodes (5 dogs). The changes in the myocardium were most pronounced where the paddles had been applied to the pericardium. There was transmural damage beneath the left and right paddle positions and in the surrounding tissues. Extensive subepicardial and subendocardial myocyte damage was obvious histologically in the right ventricle of one of the patch dogs and in all of the paddle dogs. The percentage of damaged myocardial mass, both right ventricular and total involvement, was higher in the three paddle dogs compared with the five patch dogs. There was septal damage in the heart of one paddle dog. Necrosis of the right ventricular wall was observed in three of the patch dogs and in all the three paddle dogs. Scattered necrotic myocytes and some patches of mild necrosis up to 1-mm deep were observed in the left ventricle of the patch dogs (severity score 1-3). The necrosis was more extensive in the paddle dogs, ranging from mild necrosis less than 1-mm deep to marked necrosis incorporating half-to-whole ventricular wall thickness (severity score 3-5).

Animals↗

Epithelial remnants in the crestal periodontium of the dog.

The purpose of this study was to access the effect of age on the epithelial remnants (EPRs) of the crestal periodontal tissues of beagle dogs. The material consisted of 10 beagle dogs; 5 were 1-year-old (young dogs) and 5 were 9-years-old (old dogs). All animals belonged to the same dog colony and had been raised under similar conditions. Since birth, the dogs had been subjected to professional prophylaxis 4x /per year. Biopsies were obtained from the mandibular 3rd and 4th premolar regions and were prepared for histologic analysis. 2 areas, (1) the supracrestal region and (2) the marginal periodontal ligament region, were identified. The supracrestal region was further divided into 4 compartments of equal height. The histologic parameters studied included: the (i) number of EPRs/mm root length; EPR frequency; (ii) size of EPR; (iii) distance between the root surface and the EPR; (iv) distance between the alveolar bone and the EPR; (v) epithelial cell area. The supracrestal region (total and various compartments) of old dogs harbored significantly fewer yet larger EPRs than epithelial remnants of young dogs. Similarly, the EPR's of the periodontal ligament region were significantly larger and closer to the root surface in old dogs compared to young dogs. No difference was noted in the cell area of EPRs between young and old dogs for either region. Epithelial remnants of the supracrestal region in both groups of dogs were somewhat more frequent, larger and positioned further from the root surface than the EPRs of the periodontal ligament region.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Attitudes of dog owners to neutering pets: demographic data and effects of owner attitudes.

A survey of the attitudes of dog owners to desexing male and female dogs was conducted in the Brisbane area. Over 15,800 replies (35% response) were returned for analyses and included both demographic and attitude data. The most common reasons given by owners for not having the dog desexed were that it was unnecessary or they wanted to breed from it or could not afford it or did not agree with it or that the dog was too old or it might get fat. Nearly twice as many male owners agreed that desexing male dogs removed maleness and also more males agreed with the question "Do you equate dog sexuality with human sexuality?" Female owners were more aware than males that their female dogs did not need to have a season (oestrus) or a litter before being desexed. More male owners thought that desexing changed a male or female dog's personality. A disturbing fact was that 61.1% of male owners and 47.3% of female owners would now not have their dog desexed if it had not already been done. More male than female dog owners were ignorant about whether desexing changed personality, made dogs frustrated, or if female dogs should have a season or a litter before desexing. The study showed a gender bias in owner attitudes to all the attitude questions.

Animals↗

Prevalence of Giardia lamblia infection in household dogs.

A total of 1035 household dogs were examined for the presence of Giardia lamblia (G. lamblia) in their feces. Fecal samples from 151 (14.6%) of the dogs were positive for Giardia. The protozoan was more often detected in soft feces (26.4%) than in normal (10.0%) or diarrheic feces (13.7%) (p < 0.001 and p < 0.01, respectively). The forms of the organisms obtained from the 151 dogs were cysts (77.5%), trophozoites (9.9%), or both cysts and trophozoites (12.6%). Dogs kept indoors had a higher prevalence (18.5%) of Giardia than dogs kept outdoors (4.8%) (p < 0.001). Giardia infection was also more prevalent in 1-6 months old puppies (21.7%) compared to other groups (2.4%-7.5%) (p < 0.001). The prevalence of Giardia in dogs originally purchased from pet shops or breeding kennels was extremely high (21.5%) compared to that of dogs from individual households (4.3%) (p < 0.001). With regard to human public health, the high infection rate of Giardia in puppies and dogs kept indoors is a serious problem because G. lamblia in infected dogs may have zoonotic potential. No reports of human giardiasis transmitted from dogs have been made. However, the results of this study suggest that the risk of Giardia transmission from household dogs to humans is not negligible. Pet owners should be taught appropriate hygiene measures to prevent Giardia transmission from dogs to humans.

Animals↗

Dog bite and injury prevention--analysis, critical review, and research agenda.

OBJECTIVES: To analyze Australian dog bite injury data and make international comparisons; to review risk and protective factors relating to the dog, injured person, and environment; and to recommend action for prevention and research. METHODS: Australian dog bite injury data, complemented by detailed Victorian and regional data from routine health records and vital statistics, were analyzed to determine incidence, severity, nature, circumstances, and trends. International comparison data were extracted from published reports. Risk and protective factor studies were selected for review from electronic and bibliographic searches where data were recent, sample sizes substantial, and bias limited. RESULTS: The Australian dog bite death rate (0.004/100,000) is lower than both the United States (0.05-0.07/100,000) and Canadian rates (0.007/100,000). Victorian hospitalized trend rates were stable between 1987 and 1998, but there was a decline for children <5 years (p=0.019) corresponding with a reduction in dog ownership. Children 0-4 years have the highest rate of serious injury, particularly facial. Adults have longer hospitalizations, most frequently for upper extremity injury. Risk factors include: child, males, households with dogs, certain breeds, male dogs, home location, and leashed dog. CONCLUSIONS: Dog bite rates are high and it may therefore be assumed that current preventative interventions are inadequate. Responsible dog ownership, including separating young children from dogs, avoiding high risk dogs, neutering, regulatory enforcement, and standardized monitoring of bite rates are required. Controlled investigations of further risk and protective factors, and validated methods of breed identification, are needed.

Animals↗

Coronary dilation with carotid chemoreceptor stimulation in cardiac-denervated dogs.

The coronary vasodilation that is secondary to carotid chemoreceptor stimulation (CCS) was compared in normal (N) and in cardiac-denervated (CD) conscious dogs. Under base-line conditions, CD only differed from N dogs by greater (P less than 0.01) increases in mean arterial pressure (MAP) with CCS. Coronary blood flow (CBF) increased similarly in N (146 +/- 18%) and CD (126 +/- 15%) dogs, and coronary resistance (CR) fell to a similar extent in N (53 +/- 3%) and CD (43 +/- 5%) dogs. After muscarinic and beta-adrenergic blockade, CCS resulted in similar increases in MAP in N and CD dogs; increases in CBF averaged 122 +/- 15 and 115 +/- 12% in N and CD dogs, respectively. Decreases in CR with CCS averaged 46 +/- 3 and 40 +/- 5% in N and CD dogs, respectively. alpha 1-Adrenergic blockade prevented the increases in MAP with CCS and resulted in smaller (P less than 0.01) increases in CBF, similar in N (77 +/- 13%) and in CD (69 +/- 10%) dogs. CR fell to the same extent in N (40 +/- 4%) and CD (37 +/- 5%) dogs. Additional blockade of alpha 2-adrenergic receptors further limited the increases in CBF with CCS in N (20 +/- 5%) and CD (28 +/- 7%) dogs; decreases in CR were attenuated similarly in N (13 +/- 5%) and CD (21 +/- 5%) dogs. Thus, in conscious dogs, cardiac nerves contribute little to the coronary dilation after carotid chemoreceptor stimulation.

Animals↗

Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction.

We have suggested that among conscious dogs with a healed anterior wall myocardial infarction (MI) a depressed baroreflex sensitivity (BRS) carries a higher risk of developing ventricular fibrillation during a brief ischemic episode associated with an exercise stress test. The clinical and pathophysiological implications of our previous findings prompted the present study, which addressed three major questions: 1) Is, indeed, analysis of BRS after MI a specific and sensitive marker for sudden death-risk stratification? 2) Does MI modify BRS? 3) Does analysis of BRS before MI provide information about outcome during ischemic episodes occurring after MI? An anterior MI was produced in 301 dogs, and 4 weeks later, a 2-minute circumflex coronary artery occlusion beginning during the last minute of an exercise stress test could be performed in 192 animals. Ventricular fibrillation occurred in 106 (55%) dogs (susceptible to sudden death), whereas 86 (45%) dogs (resistant to sudden death) survived. BRS was assessed by the phenylephrine method and was expressed by the regression line relating RR intervals to blood-pressure changes. BRS was significantly lower among susceptible than among resistant dogs (9.1 +/- 6.0 vs. 17.7 +/- 6.5 msec/mm Hg, p less than 0.0001). The risk for sudden death increased from 20% (15 of 73 dogs) for a BRS greater than 15 msec/mm Hg to 91% (62 of 68 dogs) for a BRS less than 9 msec/mm Hg (p less than 0.001). An internal control study in 55 animals showed that BRS was reduced 4 weeks after MI compared with control conditions (13.5 +/- 6.7 vs. 17.8 +/- 6.6 msec/mm Hg, p less than 0.001) and that a reduction occurred in 73% of animals. Susceptible dogs and those that spontaneously died after MI had a lower BRS even before the MI (16.2 +/- 5.9 vs. 22.2 +/- 6.2 msec/mm Hg, p less than 0.001). The risk for sudden death after MI increased from 35% (nine of 26 dogs) for a BRS before MI greater than 20 msec/mm Hg to 85% (17 of 20 dogs) for a BRS before MI less than 14 msec/mm Hg (p less than 0.001). This study demonstrates that the presence of a reduced BRS is associated with a greater susceptibility to ventricular fibrillation during subsequent ischemic episodes. In the majority of dogs, BRS is reduced after an MI. The results in 192 conscious dogs with a healed MI indicate that analysis of BRS is a powerful tool for risk stratification not only after, but even before, the occurrence of an MI.

Animals↗

Coronary blood flow in dogs with contractile dysfunction due to experimental volume overload.

BACKGROUND: Abnormalities in coronary blood flow are responsible for stress-induced reductions in contractile function in pressure overload hypertrophy. Less is known about coronary blood flow in volume overload. In this study, we tested the hypothesis that coronary blood flow abnormalities were responsible for contractile abnormalities in experimental volume overload hypertrophy. METHODS AND RESULTS: We examined coronary blood flow at rest and during pacing in seven dogs with contractile dysfunction secondary to chronic experimental mitral regurgitation (average regurgitant fraction at 3 months, 0.58 +/- 0.05). After 3 months of mitral regurgitation, left ventricular mass had increased from 92 +/- 8 g at baseline to 118 +/- 10 g (p less than 0.002). The slope of the end-ejection stress-volume relation, one of our indexes used to estimate contractile function, had fallen from 5.4 +/- 0.3 at baseline to 3.0 +/- 0.3 at 3 months of mitral regurgitation (p less than 0.001). In the mitral regurgitation dogs, coronary blood flow at rest was similar to that of control dogs (endocardial blood flow: control dogs, 1.33 +/- 0.12 ml/min/g; mitral regurgitation dogs, 1.16 ml/min/g, p = NS; epicardial blood flow at rest: control dogs, 1.30 +/- 0.16 ml/min/g; mitral regurgitation dogs 1.13 +/- 0.2 ml/min/g, p = NS). With pacing-induced stress, coronary blood flow increased appropriately in control and mitral regurgitation dogs. Ultrasonic dimension gauges placed in the endocardium and epicardium demonstrated no further deterioration in ventricular function during pacing in the mitral regurgitation dogs. In a separate group of five control dogs and five dogs with mitral regurgitation and left ventricular dysfunction, coronary blood flow was examined in the conscious closed-chest state at rest, during adenosine infusion, and during rapid atrial pacing (240 beats/min). Blood flow increased similarly in both groups during pacing and adenosine infusion. CONCLUSIONS: We conclude that in dogs with mitral regurgitation that have developed contractile dysfunction, abnormalities in coronary blood flow do not explain the resting contractile dysfunction. Furthermore, studies during pacing-induced stress and coronary vasodilation with adenosine demonstrate that substantial coronary blood flow reserve is present in this type of volume overload hypertrophy.

Animals↗

Effects of diuretics on inner medullary hemodynamics in the dog.

Although the hemodynamic effects of diuretics have been studied extensively, their effects on inner medullary blood flow remain unknown. In the present study, renal hemodynamics, including papillary plasma flow measured by the albumin accumulation technique, and associated alterations in papillary tissue solute content were determined in anesthetized, hydropenic dogs and during euvolemic diuresis induced by furosemide (3 mg/kg plus 2 mg/kg per hr, iv), ethacrynic acid (3 mg/kg plus 2 mg/kg per hr, iv) or chlorothiazide (10 mg/kg plus 10 mg/kg per hr, iv). Renal blood flow increased significantly after furosemide and ethacrynic acid and decreased significantly after chlorothiazide. Sixty minutes after diuretic administration, papillary plasma flow was 10.8 +/- 1.0 (mean +/- SE) in six furosemide- and 11.3 +/- 2.6 ml/min per 100 g in six ethacrynic acid-treated dogs, both significantly lower than in eight normal or eight chlorothiazide-treated dogs [26.4 +/- 2.6 and 26.7 +/- 2.7 ml/min per 100 g, respectively (P less than 0.01)]. A similarly low papillary plasma flow was also noted 10 minutes after diuretic administration in five furosemide and four ethacrynic acid dogs (13.6 +/- 2.3 and 13.4 +/- 1.8 ml/min per 100 g, respectively). In furosemide and ethacrynic acid dogs, papillary osmolality and sodium content were significantly lower than those in normal or chlorothiazide dogs. In normal and chlorothiazide dogs, papillary sodium content was similar, with a significantly reduced papillary osmolality in the latter. At the time papillary plasma flow was measured, extracellular fluid volume was similar among the four groups of dogs; however, plasma renin activity increased significantly in furosemide and ethacrynic acid dogs (P less than 0.01) and remained unchanged in normal and chlorothiazide dogs. Furthermore, papillary plasma flow was restored to normal (25.3 +/- 3.9 ml/min per 100 g) in five dogs in which furosemide was infused during angiotensin II blockage with saralasin, despite a similar diuresis and natriuresis as the other furosemide group. These data demonstrate that after administration of furosemide, ethacrynic acid and chlorothiazide, regulation of papillary plasma flow is independent of renal blood flow, and suggest that angiotensin II may play a role in the reduced papillary plasma flow in furosemide and ethacrynic acid dogs.

Animals↗

Exercise-induced subendocardial dysfunction in dogs with left ventricular hypertrophy.

The effects of treadmill exercise on regional myocardial blood flow and function were examined in 10 adult, conscious dogs with left ventricular hypertrophy (LVH) induced by aortic banding in puppies, which resulted in a left ventricular (LV) weight/body weight ratio of 8.5 +/- 0.3. Data were compared with results from eight control dogs with an LV weight/body weight ratio of 4.9 +/- 0.2. At rest, LV systolic and end-diastolic pressures were significantly greater (p less than 0.01), and mean arterial pressure was significantly less (p less than 0.05) in LVH dogs. Mean myocardial blood flow (control dogs, 0.98 +/- 0.11 ml/min/g; LVH dogs, 1.16 +/- 0.06 ml/min/g) and the transmural blood flow distribution at baseline, as assessed by endocardial/epicardial blood flow ratio (control, 1.35 +/- 0.12; LVH, 1.21 +/- 0.09), were similar in the two groups. During exercise to a target heart rate (240 beats/min), LVH dogs demonstrated greater (p less than 0.01) increases in LV systolic and end-diastolic pressures. In control dogs, as expected, exercise augmented velocity of circumferential fiber shortening (16 +/- 9%) and shortening fraction (15 +/- 5%), but in LVH dogs, exercise reduced the velocity of circumferential fiber shortening (-14 +/- 6%) and shortening fraction (-17 +/- 5%). Exercise also increased full wall thickening (35 +/- 5%), subendocardial wall thickening (66 +/- 10%), and subepicardial wall thickening (44 +/- 9%) in control dogs. In LVH dogs, exercise increased subepicardial wall thickening (31 +/- 9%) and reduced subendocardial wall thickening (-40 +/- 7%); full wall thickening did not change (-11 +/- 9%). This was associated with a fall in endocardial/epicardial flow ratio to 0.72 +/- 0.05 (p less than 0.01) in LVH dogs. The subendocardial dysfunction persisted late into recovery, at a time when the transmural blood flow distribution had returned to baseline; this occurrence suggested myocardial stunning. Thus, in dogs with LVH, selective subendocardial hypoperfusion and profound selective depression in subendocardial wall thickening are observed during exercise. The subendocardial dysfunction persisted into recovery despite resolution of the perfusion abnormality.

Animals↗

Early recovery of regional performance in salvaged ischemic myocardium following coronary artery occlusion in the dog.

Although numerous agents have been shown experimentally to protect ischemic myocardium, a critical unanswered question is whether function is preserved in the salvaged tissue. Accordingly, 38 openchest dogs had measurements of percent segment length shortening (%SS) and velocity of segment length shortening either in midmyocardial or subepicardial and subendocardial ischemic segments before and after 60 min of left anterior descending coronary artery occlusion during 5 h of reperfusion; 10 additional dogs were subjected to 3 h of coronary occlusion followed by 72 h of reperfusion. 15 min after coronary artery occlusion, radiolabeled microspheres were injected into the left atrium for measurement of regional myocardial blood flow, and dogs were treated with 1 mg/kg i.v. (n = 23) of an anti-inflammatory drug, flurbiprofen or an equal volume of saline (n = 25). The ischemic myocardium-at-risk for necrosis was determined by injecting methylene blue dye into the left atrium with the coronary artery reoccluded at the end of the reperfusion period, slicing the left ventricle into thin transverse sections, and measuring the areas of each slice that were not perfused (pink unstained tissue) by methylene blue. The quantity of necrotic tissue in each transverse section was measured by planimetry after incubation of the slices in triphenyltetrazolium chloride, and by direct histological examination in dogs with 72 h of reperfusion. Regional myocardial blood flow of the ischemic segments between the ultrasonic dimension crystals was similar in treated (0.34+/-0.03 ml/min per g) and control dogs (0.35+/-0.03 ml/min per g). In saline-treated control dogs subjected to a l-h coronary occlusion, 17.9+/-1.8% of the myocardium-at-risk became necrotic but in flurbiprofen-treated dogs none of the tissue became necrotic. In saline-treated dogs passive lengthening of the previously ischemic segments persisted through 5 h of reperfusion in all three regions of myocardium after a 1-h coronary occlusion. In flurbiprofen-treated dogs regional function returned to normal within 5 min of reperfusion in both the subendocardium (%SS preocclusion = 17.2+/-2.0%; 5 min reperfusion = 17.8+/-3.1%; P = NS) and in the midmyocardium (%SS preocclusion = 17.8+/-2.2%; 5 min reperfusion = 17.9+/-2.3%; P = NS) and was not significantly different after 5 h of reperfusion from what it was before coronary occlusion. In the subepicardium of treated dogs regional function began to improve within 15 min of drug administration even during coronary occlusion. Regional function was not different from preocclusion values after either 5 min or 5 h of reperfusion (%SS preocclusion = 21.0+/-2.4%; 5 min reperfusion = 20.6+/-3.8%; P = NS). In dogs subjected to 3 h of coronary occlusion and 72 h of reperfusion, the administration of flurbiprofen was also associated with significantly smaller infarcts and a significantly more rapid rate of functional recovery than in control dogs.Thus, it appears that flurbiprofen not only decreased the quantity of necrosis in tissue made ischemic after coronary occlusion and then reperfused, but also allowed more rapid recovery of segmental function in ischemic but nonnecrotic tissue and in tissue with patchy necrosis; such recovery did not occur in equally ischemic myocardium in untreated control dogs. Earlier functional recovery of reversibly injured tissue following prolonged periods of ischemia is an additional important role for agents that protect ischemic myocardium from necrosis.

Animals↗

Pharmacological and toxicological effects of chronic porcine growth hormone administration in dogs.

The purpose of this study was to evaluate the pharmacological and toxicological effects of exogenous GH administration in normal adult dogs. Because porcine GH (pGH) is structurally identical to canine GH, pGH was selected for a 14-wk study in dogs. Thirty-two dogs (< 2 yr) were randomized to 4 groups (4 dogs/sex/group); 1 group was treated with the vehicle and 3 groups received pGH at 0.025, 0.1, or 1.0 IU/kg/day subcutaneously. Daily clinical signs and weekly body weights were recorded. Hematology, serum biochemistry, urinalyses, electrocardiograms, and ophthalmoscopic examinations were done. Serum GH, insulin-like growth factor-1 (IGF-1), insulin, thyroxine (T4), triiodothyronine (T3), and cortisol levels were determined. Necropsies were performed, organs weighed, and tissues were fixed and processed for light microscopic examination. Porcine GH caused increased body weight gain (p < or = 0.05) through the mid dose; the mean weight gains at study termination in mid- and high-dose groups were 2.8 kg and 4.7 kg, respectively, compared to 0.4 kg and 0.8 kg in control and low-dose groups, respectively. Dose-related increased weights of liver, kidney, thyroid, pituitary gland, skeletal muscle, and adrenal gland were noted. In pGH-treated dogs, increased skin thickness seen grossly correlated histologically with increased dermal collagen. There was no gross or histomorphological evidence of edema. There were dose-related increased serum IGF-1 levels (approximately 2-10-fold; p < or = 0.05) that correlated with the elevated serum GH levels in pGH-treated dogs. Also, increased serum insulin levels (p < or = 0.05) through the mid dose were seen throughout the study. In high-dose dogs, the insulin levels remained elevated over 24 hr postdose. The serum glucose levels in fasted dogs remained within the control range and there was no chronic hyperglycemia based on glycosylated hemoglobin levels. Renal glomerular changes, significant polyuria with decreased urine specific gravity, and increased serum insulin levels suggested that the dogs had early insulin-resistant diabetes. There was minimal or no biologically significant effect of pGH on serum T3, T4, and cortisol levels in dogs. Other serum biochemical changes in pGH-treated dogs included decreased urea nitrogen and creatinine, and increased potassium, cholesterol, and triglycerides. Significant increases in serum calcium and phosphorous levels and alkaline phosphatase activity (bone isozyme) correlated with the histological changes in bone. In pGH-treated dogs, there was a dose-related normochromic, normocytic, nonregenerative anemia. The changes described above, except for the anemia, are related to either anabolic or catabolic effects of high doses of GH. Based on this study, it is concluded that the dog is a good model in which to evaluate the safety of GH secretagogues as well as compounds with GH-like activity.

Anemia↗

Effect of training and rest on respiratory mechanical properties in racing sled dogs.

INTRODUCTION: Racing Alaskan sled dogs develop exercise-induced airway inflammation, similar to that reported for elite human athletes participating in cold-weather sports. These human athletes also have airway hyperresponsiveness, but airway function in sled dogs has not been measured. PURPOSE: To compare respiratory mechanical properties in trained, rested Alaskan sled dogs with typical laboratory hounds, and to determine whether subsequent training alters respiratory mechanical properties. METHODS: Nineteen healthy adult Alaskan sled dogs were compared with five healthy adult mixed-breed laboratory hounds. All dogs were rested for at least 4 months before examination. Respiratory mechanical properties were measured while the dogs were anesthetized and ventilated with a piston ventilator. The mean respiratory resistance and compliance measurements for 20 consecutive breaths were used as baseline values immediately before measurement of respiratory reactivity. Respiratory reactivity was the mean of 20 consecutive breaths immediately after the administration of aerosol histamine, expressed as the percentage change in prehistamine measurements. After the initial examinations, the sled dogs were divided into exercised and controls. Exercised dogs were trained for competitive endurance racing. Both groups were examined after 2 and 4 months of training. RESULTS: Alaskan sled dogs had greater respiratory compliance reactivity to histamine (77.47 +/- 8.58% baseline) compared with laboratory dogs (87.60 +/- 9.22% baseline). There was no effect of training on respiratory mechanical properties detected in racing sled dogs. CONCLUSIONS: Racing Alaskan sled dogs have airway dysfunction similar to "ski asthma" that persists despite having 4 months of rest. These findings suggest that repeated exercise in cold conditions can lead to airway disease that does not readily resolve with cessation of exercise.

Aerosols↗

Effects of bromocriptine on corticotrophin, melanotrophin and corticosteroid secretion in dogs with pituitary-dependent hyperadrenocorticism.

Dogs with spontaneous pituitary-dependent hyperadrenocorticism were divided into two groups, one with normal plasma concentrations of alpha-MSH (normal alpha-MSH dogs, n = 26) and the other with high plasma concentrations of alpha-MSH (high alpha-MSH dogs, n = 14), on the presumption that high alpha-MSH concentrations indicated a parent cell of pars intermedia origin. The urinary corticoid/creatinine ratios of the high alpha-MSH dogs were significantly higher than those of the normal alpha-MSH dogs. The percentage decrease of the corticoid/creatinine ratios following dexamethasone administration was significantly higher in the normal alpha-MSH dogs than in the high alpha-MSH dogs. Dexamethasone resistance occurred in both the normal alpha-MSH dogs (4 out of 26) and the high alpha-MSH dogs (7 out of 14), indicating a relative rather than an absolute difference. The short-term effect of orally administered bromocriptine, at a dose (10 micrograms/kg body weight) known to be effective in lowering prolactin concentrations in dogs, was investigated by measuring concentrations of cortisol, ACTH and alpha-MSH in plasma at 4, 6 and 8 h after administration. Significant decreases were observed for cortisol in both groups and for alpha-MSH only in the high alpha-MSH dogs. The effect of 5 days of bromocriptine administration (10 micrograms at 12-h intervals) was assessed by measurements of urinary corticoid/creatinine ratios. Considering both groups as a whole, only the corticoid/creatinine ratios of the high alpha-MSH dogs decreased significantly on the first day of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗

Alterations in thyroid hormone concentrations in healthy sled dogs before and after athletic conditioning.

OBJECTIVE: To determine effects of athletic conditioning on thyroid hormone concentrations in a population of healthy sled dogs. ANIMALS: 19 healthy adult sled dogs. PROCEDURE: Serum concentrations of thyroxine (T4), triiodothyronine (T3), thyroid-stimulating hormone (TSH), free T4 (fT4), free T3 (fT3), and autoantibodies directed against T3, T4, and thyroglobulin were measured in sled dogs that were not in training (ie, nonracing season) and again after dogs had been training at maximum athletic potential for 4 months. RESULTS: Analysis revealed significant decreases in T4 and fT4 concentrations and a significant increase in TSH concentration for dogs in the peak training state, compared with concentrations for dogs in the untrained state. Serum concentrations of T4 and fT4 were less than established reference ranges during the peak training state for 11 of 19 and 8 of 19 dogs, respectively; fT4 concentration was greater than the established reference range in 9 of 19 dogs in the untrained state. CONCLUSIONS AND CLINICAL RELEVANCE: Decreased total T4 and fT4 concentrations and increased serum concentrations of TSH were consistently measured during the peak training state in healthy sled dogs, compared with concentrations determined during the untrained state. Although thyroid hormone concentrations remained within the established reference ranges in many of the dogs, values that were outside the reference range in some dogs could potentially lead to an incorrect assessment of thyroid status. Endurance training has a profound impact on the thyroid hormone concentrations of competitive sled dogs.

Animals↗