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Prevalence of enteropathic Escherichia coli in dogs with acute and chronic diarrhoea.

Samples of faeces from 57 dogs with acute diarrhoea, 82 dogs with chronic diarrhoea, 34 clinically healthy household dogs and 88 kennelled control dogs were analysed by hybridisation, using DNA probes to detect enteropathogenic Escherichia coli (EPEC) and enterotoxigenic E coli (ETEC), verocytotoxin-producing E coli (VTEC), enterohaemorrhagic E coli (EHEC), enteroinvasive E coli (EIEC) and enteroaggregative E coli (EAggEC). Samples of duodenal juice from 60 of the 82 dogs with chronic diarrhoea were also examined. Significantly more of the dogs with diarrhoea were excreting EPEC (acute 35.1 per cent, chronic 31.7 per cent) and VTEC (acute 24.6 per cent, chronic 28 per cent) than the kennelled dogs (EPEC 17.1 per cent, VTEC 0 per cent) or the household control dogs (EPEC 6 per cent, VTEC 5.9 per cent). Enteropathic E coli was also detected in the duodenal juice of 23 of 60 (38.3 per cent) of the dogs with chronic diarrhoea. The EPEC attaching and effacing A (eaeA) gene and the verocytotoxin 1 (VR1) gene coding for VTEC were often found together. There was good agreement between in vitro studies and hybridisation for the detection of eaeA and VT1. Isolates from the dogs with diarrhoea adhered significantly more to Hep-2 cells, and VT1-positive strains from the dogs with diarrhoea consistently killed more than 50 per cent of Vero cells.

Acute Disease↗

Hypotonic and isotonic aerosols increase bronchial reactivity in basenji-greyhound dogs.

Because basenji-greyhound dogs have greater bronchial reactivity to a range of inhaled stimuli than mongrel dogs do, and because bronchial hyperreactivity to nonspecific stimuli is characteristic of asthma, we asked whether basenji-greyhound dogs have greater bronchial reactivity to hypotonic and isotonic aerosols than mongrel dogs do. We assessed bronchial reactivity by measuring both the total pulmonary resistance and the bronchial response to an acetylcholine aerosol, before and after delivery of hypotonic and isotonic aerosols. Bronchial reactivity as measured by a change in total pulmonary resistance increased 9-fold after delivery of hypotonic and 5-fold after delivery of isotonic aerosols in 5 anesthetized basenji-greyhound dogs, but not in 3 similarly challenged mongrel dogs (p less than 0.01). Bronchial reactivity as measured by an increased bronchial response to acetylcholine aerosol increased 3-fold in basenji-greyhound dogs but not in mongrel dogs. Thus, hypotonic and isotonic aerosols increase bronchial reactivity in basenji-greyhound dogs. We also asked whether vagal or nonvagal pathways are involved in the increase in total pulmonary resistance induced by a hypotonic aerosol. Both vagal and nonvagal pathways appear to be involved, since blockade of the vagal pathway by intravenously administered atropine only partially inhibited the bronchoconstriction induced by a hypotonic aerosol (54%). Disodium cromoglycate, which inhibits vagal and nonvagal pathways, partially inhibited the bronchoconstriction (57%), but even in combination with atropine, did not completely inhibit it (68%). Our observations in basenji-greyhound dogs are similar to results in asthmatic subjects, suggesting that basenji-greyhound dogs are useful experimental animals in which to study the mechanisms by which hypotonic and isotonic aerosols increase bronchial reactivity.

Aerosols↗

Multifocal retinitis in New Zealand sheep dogs.

Thirty-nine percent of 1,448 working sheep dogs were affected with varying degrees of multifocal retinal disease on ophthalmoscopic examination. Lesions consisted of localized areas of hyperreflexia in the tapetal fundus, often associated with hyperpigmentation. Severely affected animals had widespread hyperreflexia with retinal vascular attenuation. Only 6% of 125 New Zealand dogs raised in urban environment were similarly affected. Both eyes of 70 dogs from New Zealand were examined histologically. Forty-seven of 70 dogs had ocular inflammatory disease. Ten other dogs had noninflammatory eye disease, and 13 dogs had normal eyes. Histologically, eyes with inflammatory disease were divided into three categories: Dogs 3 years of age or less with active inflammatory disease of the retina, uvea, and vitreous. Four dogs in this group had migrating nematode larvae identified morphologically as genus Toxocara. Diffuse retinitis and retinal atrophy in conjunction with localized retinal necrosis and choroidal fibrosis. Dogs in this category were severely, clinically affected. Chronic, low-grade retinitis with variable retinal atrophy. Most dogs in this category were over 3 years of age, and many were visually functional. The existence of a definable spectrum of morphological changes associated with inflammation, suggests that Toxocara sp. ocular larva migrans may be the cause of a highly prevalent, potentially blinding syndrome of working sheep dogs in New Zealand.

Animals↗

Necrotizing meningoencephalitis of Maltese dogs.

The clinical and pathologic features of five young Maltese dogs with a necrotizing meningoencephalitis were studied and compared with published reports of the necrotizing meningoencephalitis of Pug dogs. The ages of the Maltese dogs ranged from 9 months to 4 years. Four dogs were male, and one was female. The dogs had a history of seizures with or without other neurologic signs for 3 days to 20 weeks prior to death. Cerebrospinal fluid examination in three dogs revealed a pleocytosis and elevated levels of protein. At necropsy, the cerebrum was asymmetrically swollen in four dogs, with a loss of distinction between the gray and white matter and mild to moderate asymmetrical dilation of the lateral ventricles. Histologically, there was extensive necrosis and nonsuppurative inflammation of the cerebral gray and white matter, overlying meninges, and adjacent thalamus and hippocampus. The 4-year-old dog had the longest duration of clinical signs and had little inflammation but extensive atrophy of affected areas, with astrocytosis. The clinical course and pathologic changes in these Maltese dogs are indistinguishable from those in reported cases of necrotizing meningoencephalitis of Pug dogs, indicating that this lesion is probably not unique to Pug dogs.

Animals↗

Evaluation of low sodium:potassium ratios in dogs.

The results of general chemistry profiles of canine patients from Angell Memorial Animal Hospital, Boston, Massachusetts, during 1993 were reviewed for low (<24) serum sodium:potassium (Na:K) ratios. Thirty-seven dogs had low Na:K ratios. The medical records for 34 these patients were available and sufficiently complete to identify conditions that were associated with low Na:K ratios. Of these 34 dogs, 8 (24%) had hypoadrenocorticism, and 14 had renal disease. Twenty-two of the 34 (65%) had Na:K ratios between 24 and 20. Of these 22 dogs, 9 (41%) had renal or urinary tract disease, and 2 (9%) had hypoadrenocorticism. Other diagnoses in this group included pancreatic disease (3), disseminated neoplasia (3), circulatory disturbance (2), pyometra (1), mushroom poisoning (1), and behavior problem (1). Eight of 34 dogs had Na:K ratios between 19.9 and 15. Of these 8 dogs, 4 (50%) had urinary tract disease, 2 had hypoadrenocorticism, 1 had pancreatic disease, and 1 had severe anemia and hypoproteinemia due to severe parasitism. All of the 4 dogs with Na:K ratios <15 had hypoadrenocorticism, and 1 of these 4 had concurrent renal failure. In all dogs, serum potassium concentration was above the laboratory's reference range, but sodium was below the laboratory's reference range in only 18 dogs (53%). Two of the 8 (25%) dogs with hypoadrenocorticism had serum sodium concentrations within the laboratory's reference range. In this population, low Na:K ratios were invariably associated with hyperkalemia but not always with hyponatremia. Although numerous conditions were associated with a low Na:K ratio, renal disease was the most common. Hypoadrenocorticism was present in only 13% of dogs with Na:K ratios between 24 and 15 but was present in all dogs with Na:K ratios <15.

Adrenal Insufficiency↗

Pet dogs owned by lupus patients are at a higher risk of developing lupus.

The aim of this study is to determine whether pet dogs owned by patients with systemic lupus erythematosus (SLE) are at a higher risk of developing SLE. Diagnosis of canine SLE was mainly based on the 11 diagnostic criteria for human SLE and two marked immunological features of canine SLE. Among 59 pet dogs owned by 37 SLE patients, 11 (18.64%) were ANA positive, and three (5.08%) had SLE. In contrast, of 187 pet dogs owned by non-SLE households, nine (4.81%) were ANA positive, and none (0%) had SLE. Among 650 outpatient dogs registered in the veterinary hospital, 34 (5.23%) were ANA positive, and six (0.92%) had SLE. Frequency of ANA and SLE among pet dogs owned by SLE patients was significantly higher than in pet dogs owned by non-SLE households (P = 0.001 for ANA; P = 0.013 for SLE) and in outpatient dogs (P < 0.001 for ANA; P = 0.032 for SLE). With respect to canine SLE development, the relative risk or risk ratio (R) of human SLE contact varied from 5.5 (compared with outpatient dogs) to near the infinite (compared with dogs owned by non-SLE households). The prevalence of canine SLE among pet dogs of SLE patients was therefore estimated to be 508 per 10 000 [95% confidence interval (95% CI), 0-1068]. In conclusion, pet dogs with human SLE contact were at a higher risk of developing SLE. Our results indicate that a common environmental factor or zoonotic agent may be involved in the development of human and canine SLE.

Animals↗

Parathyroid hormone (PTH)-related protein, PTH, and 1,25-dihydroxyvitamin D in dogs with cancer-associated hypercalcemia.

Circulating N-terminal PTH-related protein (PTHrP), N-terminal PTH, and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in normal dogs and dogs with cancer-associated hypercalcemia (CAH), parathyroid adenomas, and miscellaneous tumors. PTHrP was undetectable (less than 1.8 pM) in normal dogs and increased in dogs with CAH due to adenocarcinomas derived from apocrine glands of the anal sac (44.9 +/- 27 pM), lymphoma (8.3 +/- 4.4 pM), and miscellaneous carcinomas (13.3 +/- 11.4 pM). The PTHrP concentration decreased in dogs with lymphoma and anal sac adenocarcinomas after successful treatment of CAH. The PTHrP concentration had a significant linear correlation with total serum calcium in dogs with anal sac adenocarcinomas and hypercalcemia, but not in dogs with lymphoma and hypercalcemia. Serum N-terminal PTH concentrations were usually in the normal range (12-34 pg/ml) for all groups of dogs except dogs with parathyroid adenomas (83 +/- 38 pg/ml). The serum PTH concentration increased after successful treatment of CAH. Serum 1,25-(OH)2D concentrations were decreased, normal, or increased in dogs with CAH, and 1,25-(OH)2D levels decreased after treatment of CAH. In summary, circulating concentrations of PTHrP are consistently increased in dogs with CAH, and PTHrP appears to play an important role in the induction of hypercalcemia.

Adenoma↗

Serum creatine kinase activities in dogs with dirofilariasis.

Total serum creatine kinase (CK) and its isozyme activities were determined in dogs with dirofilariasis. Before heartworm removal, total CK and isozyme activities in dogs of the mild group were not different from those in dogs of the heartworm-free group. BB activity was higher in dogs of the hemoptysis group. Dogs of the ascites group displayed a mild increase in MM activity. In dogs of the caval syndrome (CS) group, total CK and MM activities were highest among the heartworm-free and heartworm-infected dogs, and MM isozyme accounted for most (75%) of total CK activity. MB and BB activities were also higher. However, there were no significant differences in CK activities between the surviving and non-surviving cases. In dogs with pulmonary heartworm disease (mild and ascites groups), MM activity correlated significantly with the number of heartworms (r = 0.45), hematocrit value (Ht, r = -0.40), serum alanine aminotransferase (ALT, r = 0.42) and lactate dehydrogenase (LDH, r = 0.46) activities, mean pulmonary arterial pressure (r = 0.64) and total pulmonary resistance (r = 0.50). In dogs with CS, MM activity did not correlate with any parameter, but BB activity correlated with the number of heartworms at the right atrium (r = 0.61), Ht (r = -0.53), ALT (r = 0.80), LDH (r = 0.73) and serum urea nitrogen (r = 0.47). At 1 week after heartworm removal, BB and MM activity decreased in dogs of the hemoptysis and ascites groups, respectively. In dogs of the CS group, total CK and MM isozyme activities decreased markedly (P less than 0.01) regardless of their prognosis.

Airway Resistance↗

Comparison of laboratory data in dogs with heartworm caval syndrome surviving and nonsurviving after surgical treatment.

Laboratory data in 47 dogs with caval syndrome (CS) surviving after surgical HW removal compared with those in 15 dogs with CS which died after the treatment. The number of HWs removed in surviving dogs was significantly greater than in nonsurviving dogs. The Ht value was significantly higher in nonsurviving dogs than in surviving dogs. Plasma enzyme activities ranged widely from normal to extremely high levels, and there were no significant differences in plasma enzyme activities between the surviving and nonsurviving dogs. Serum total protein, and plasma triglyceride, creatinine, glucose, calcium, sodium (Na) and chloride (Cl) levels were much similar between the HW-free and surviving dogs, but significantly different between the HW-free and nonsurviving dogs. Plasma urea nitrogen, uric acid and potassium levels were higher, and plasma Na and Cl levels were lower in nonsurviving dogs than in surviving dogs.

Animals↗

Heart rate modulation by sympathetic nerves in dogs with heart failure.

To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (control dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma catecholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure.

Animals↗

Clinical availability of urinary N-acetyl-beta-D-glucosaminidase index in dogs with urinary diseases.

Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was examined in healthy dogs and dogs with urinary diseases, and its clinical usefulness as an indicator of urinary diseases was discussed. Twenty-eight healthy dogs and 20 dogs with urinary diseases were used. Urinary NAG activity was measured using p-nitrophenyl N-acetyl-beta-D-glucosaminide as substrate, and expressed as units per gram of urinary creatinine (NAG index). Urinary NAG index in urine of healthy dogs was 3.2+/-2.4 U/g, and NAG index in the dogs with chronic renal failure or lower urinary tract infection accompanied by pyelonephritis was higher than that in healthy dogs. However, the dogs with lower urinary tract infection without pyelonephritis showed normal values of NAG index. Some dogs with diabetic mellitus showed elevated values of NAG index when control of blood sugar was not successful. Increase of NAG index was observed in some dogs with pyometra before increases of BUN and serum creatinine concentration. Therefore, NAG index in urine seems to be a good indicator for urinary diseases in dogs.

Acetylglucosaminidase↗

Evaluation of cytokine messenger RNA expression in peripheral blood mononuclear cells from dogs with canine demodicosis.

Using RT-PCR and semi-quantitative PCR, mRNA expression for canine interferon (IFN)-gamma, interleukin (IL)-2, IL-4, IL-5, IL-10, tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta in peripheral blood mononuclear cells (PBMCs) was examined in dogs with or without demodicosis. mRNA expression for IFN-gamma as well as TNF-alpha in dogs with demodicosis (localized (LD) and generalized (GD)) was slightly lower than those in dogs without demodicosis (healthy controls). Expression of IL-5 mRNA in dogs with demodicosis was higher than that in control dogs, but there were no significant differences in IL-4 and IL-10 mRNA expression levels among the three groups. On the other hand, expression levels of TGF-beta mRNA in dogs with GD were higher than those in control dogs and dogs with LD. The expression levels of IL-5 and TGF-beta mRNA decreased in all three dogs with GD which showed resolution of the clinical signs. Taken together, these results suggest that the Th2-like response in PBMCs from dogs with demodicosis is up-regulated, and that subsequent increased expression of IL-5 and TGF-beta mRNA in dogs with GD is reversible after treatment. Therefore, these cytokines, particularly IL-5, might be a useful clinical index of the clinical course in demodicosis. Also, increased TGF-beta mRNA expression might be a key factor for revealing the difference in the mechanism of onset between LD and GD.

Animals↗

Oral flora of mongrel and beagle dogs with periodontal disease.

The plaque flora was studied in adult mongrel and beagle dogs with periodontal disease. Gingival plaque from maxillary premolars was removed and cultured on various growth media. The flora in all dogs was composed of mostly anaerobic gram negative rods. Bacteroides asaccharolyticus was found in the highest proportion of plaque samples from mongrel dogs, and decomposed hydrogen peroxide suggesting catalase activity. Fusobacterium nucleatum was found in higher proportion in the plaque of beagle dogs as compared to B. asaccharolyticus. With the increasing numbers of obligative anaerobic gram negative organisms such as B. asaccharolyticus, the proportions of Streptococcus, Enterococcus and Staphylococcus decreased in the dogs with periodontal disease. The salivary flora was different from the plaque flora of the dogs with periodontal disease. It was constant regardless with the disease. The salivary flora of beagle dogs with the healthy gingiva was different from that of mongrel dogs. Enterococcus, Lactobacillus, Eubacterium and black-pigmented Bacteroides (BPB, mainly B. asaccharolyticus) were higher proportion in the flora of beagle dogs as compared to mongrel dogs, while Fusobacterium, Enterobacteriaceae, yeast and molds were lower in the flora. The results reveal that B. asaccharolyticus and F. nucleatum are common pathogens and uniquely contribute to the development of gingival inflammation in dog.

Animals↗

Increased erythrophagocytic activity of macrophages in dogs with Babesia gibsoni infection.

To elucidate the mechanism of anemia caused by Babesia gibsoni infection in dogs, the erythrophagocytic activity of macrophages in infected dogs was investigated in vitro. In the present study, macrophages obtained from peripheral blood (PB-macrophages) and bone marrow (BM-macrophages) of splenectomized dogs with chronic B. gibsoni infection were examined. The BM-macrophages in the splenectomized dogs with chronic babesiosis exhibited an increased erythrophagocytic activity compared with those from splenectomized, non-infected dogs. In the infected dogs, erythrophagocytic activities of macrophages against both auto- and iso-erythorcytes from normal dogs were almost the same. Administration of an anti-protozoal drug, diminazene diaceturate, resulted in a decrease of the erythrophagocytic activity of BM-macrophages associated with an increase of the hematocrit value in splenectomized dogs with chronic babesiosis. In splenectomized dogs with acute babesiosis, erythrophagocytic activity of BM-macrophages was also elevated. Such a phenomenon was not, however, observed in splenectomized dogs with onion-induced hemolytic anemia. These results suggest that the erythrophagocytic ability of macrophages in the infected dogs might be accelerated by parasites per se through an unknown mechanism, resulting in severe anemia in spite of low parasitemia.

Anemia↗

Prevalence of Neospora caninum antibodies in dogs from dairy cattle farms in Parana, Brazil.

Serum samples from 134 dogs from 22 cattle dairy farms in the northern region of Parana State, Brazil, were tested for antibodies to Neospora caninum in an indirect fluorescent antibody test. Antibodies (> or = 1:50) to N. caninum were found in 29 (21.6%) of the 134 dogs, and seropositive dogs were found on 14 (63.6%) of the 22 dairy cattle farrms. The antibody titers of dogs were 1:50 (3 dogs), 1:100 (7 dogs), 1:200 (7 dogs), 1:400 (6 dogs), and > or = 1:800 (6 dogs). The low prevalence (9%) in < 1-yr-old dogs compared with the 2- to 3-fold higher prevalence in older dogs (17-29%) suggests postnatal exposure to N. caninum infection.

Animals↗

The efficacy of L-Deprenyl in dogs with pituitary-dependent hyperadrenocorticism.

Ten dogs with pituitary-dependent hyperadrenocorticism (PDH) received 2 mg/kg of L-Deprenyl once daily for 6 months. Monthly patient assessment consisted of evaluation of the owner's daily observation protocol, a standardized owner questionnaire, physical examination, CBC, biochemical profile, determination of the urine cortisol/creatinine ratio (UC/C), low-dose dexamethasone suppression (LDDS) test, corticotropin releasing hormone (CRH) test, and adrenal ultrasonography. At the beginning and the end of the study, an adrenocorticotropic hormone (ACTH) stimulation test and computed tomography also were performed. Two dogs developed neurologic signs and 2 dogs developed acute pancreatitis. An increase in activity, decrease in polyphagia, and decrease in panting were reported by 6, 4, and 2 owners, respectively. Seven owners believed that water intake decreased, but this was confirmed in only 3 dogs. Water intake increased in 2 dogs and remained unchanged in 5 dogs. The condition of the hair coat and skin improved in 2 dogs, worsened in 3, and remained unchanged in 5. Urine specific gravity, urine osmolality, ACTH test results, UC/C, and adrenal gland size did not change significantly throughout the study. In 4 of 8 dogs, LDDS was abnormal at the start of the study but normal at the end of the study, and in 2 dogs, the opposite occurred. Marked individual variation was noted in the CRH test, with a tendency for smaller increases in ACTH toward the end of the study. A marked increase in hypophyseal tumor size occured in 4 dogs. Treatment with L-Deprenyl resulted in improvement, deterioration, and stagnation of clinical signs in 2, 4, and 4 dogs, respectively. The results of this study indicate that L-Deprenyl cannot be recommended as the sole treatment for canine PDH.

Adrenal Glands↗

Disturbed vasopressin release in 4 dogs with so-called primary polydipsia.

Primary polydipsia is characterized by a marked increase in water intake and secondary polyuria, and in dogs often is described as a behavioral problem or a psychological disorder. We describe 4 dogs with primary polydipsia, diagnosed on the basis of a modified water deprivation test, in which further examination included serial measurements of urine osmolality (UOsm) and plasma vasopressin (VP) measurements during water deprivation and hypertonic saline infusion. The dogs, ranging in age from 4 months to 4 years, all were presented for evaluation of polyuria and polydipsia. Physical examination, routine blood chemistry, and urinalysis disclosed no specific cause for the polyuria and polydipsia. During serial measurements UOsm spontaneously reached high concentrations in 2 dogs, whereas in the other 2 dogs UOsm also fluctuated but on no occasion exceeded 1,000 mosm/kg. Primary polydipsia was diagnosed when UOsm exceeded 1,000 mosm/kg at the end of the modified water deprivation test and plasma osmolality did not exceed the upper limit of the reference range during testing. During water deprivation, plasma VP concentrations remained relatively low. The VP response to hypertonic saline infusion was abnormal, with an increased threshold value in 3 dogs, an increased sensitivity in 2 dogs, and an exaggerated response in 1 dog. It is concluded that some dogs fulfilling current criteria for primary polydipsia produce concentrated urine spontaneously throughout the day in a pattern similar to what has been observed in healthy pet dogs. This finding can be regarded as diagnostic and precludes the need for a water deprivation test. During water deprivation testing, all 4 dogs produced highly concentrated urine in the face of low basal plasma VP concentrations. The observed abnormal VP release in response to hypertonic stimulation may be interpreted as a primary disturbance in the regulation of VP secretion, although it might also be the result of overhydration caused by a primary abnormality in drinking behavior.

Animals↗

Transvenous embolization of small patent ductus arteriosus with single detachable coils in dogs.

Transvenous embolization of small patent ductus arteriosus (PDA; < or = 4 mm) with a single detachable coil was attempted in 24 dogs (median age 5.7 months, range, 2.6-65.5 months; median body weight 5.5 kg, range, 1.5-30.0 kg). Angiographic imaging of the duct and pressure measurements were made before and after embolization. The minimal ductal diameter was 2.7 +/- 0.7 mm. In all dogs, a single coil was employed regardless of residual shunting. Ten dogs (PDA minimal diameter range, 1.5-2.2 mm) received a 5-mm coil, and 14 dogs (PDA minimal diameter range, 2.9-3.6 mm) received a 8-mm coil. After coil embolization the angiographic shunt grade decreased significantly (n = 20, P < .001). Residual shunts were assessed by angiography 15 minutes after and by Doppler echocardiography 1-3 days and 3 months after the intervention. In the dogs treated with the 5-mm coils the residual shunt rate was low (0%, 10%, and 0% for angiography and Doppler echocardiography at 1-3 days and 3 months, respectively), in contrast to the dogs treated with the 8-mm coils (91%, 79%, and 67% for angiography and Doppler echocardiography at 1-3 days and 3 months, respectively). After 3 months, no residual murmur was found in dogs treated with the 5-mm coils (0/7), in contrast to murmurs in 5 of 12 (42%) dogs treated with the 8-mm coils. Despite incomplete closure in these dogs, volume loading of the left heart decreased in all dogs. Pulmonic or aortic coil embolism did not occur. Analysis of initial results shows that single detachable coil embolization is possible in all dogs with a small PDA (< or = 4 mm), but only very small PDA (< or = 2.5) could be treated effectively, and for the moderate PDA (2.6-4.0 mm) longer coils or multiple coils may be necessary to achieve complete occlusion.

Angiography↗