Epidemiologic relations were evaluated between plasma concentrations of nutrients and cardiovascular diseases. A total of 220 cats were assessed: 144 cats with noninduced acquired heart disease and 76 clinically normal cats. Plasma was assayed for taurine, alpha-tocopherol, selenium, retinol, and total cholesterol and triglycerides concentrations. Cardiovascular disease groups included dilated cardiomyopathy (n = 53), left ventricular hypertrophy (n = 28), hyperthyroidism (n = 11), and uncertain classification (n = 52). In cats with dilated cardiomyopathy, mean plasma taurine concentration was the lowest of that in cats of any group, being only 38% of the value in healthy cats; females had less than half the mean value of males. Tocopherol concentration was 20% lower than normal, and retinol concentration was 40% higher than normal. Total cholesterol concentration was 36% lower than normal. Triglycerides concentration was higher in these cats than in any other group-twice the value recorded in healthy cats and 67% higher than that in hyperthyroid cats. In cats with hypertrophic cardiomyopathy, almost 15% had mean plasma taurine concentration < 30 micromol/L. Retinol concentration was 15% higher, and triglycerides concentration was 54% higher than normal. Approximately 27% of hyperthyroid cats had mildly decreased plasma taurine concentration. Hyperthyroid cats had the lowest tocopherol and cholesterol values; both were at least 30% lower than normal. Retinol concentration was 30% higher than Approximately 14% of cats with uncertain classification had mildly decreased plasma taurine concentration. Plasma retinol and triglycerides concentrations were higher than normal in 25 and 38% of these cats, respectively. Plasma selenium concentration, compared between healthy cats and cats with cardiac disease, was not significantly different. This observation may not be meaningful, however, in light of the limited number of cats in which selenium was assessed.

Introduction: The clinical symptoms of portosystemic shunts (PSSs) and hepatic microvascular dysplasia (HMD) – portal vein hypoplasia (PVH) in dogs are similar. PSSs are abnormal vascular connections between the portal vein system and systemic veins. HMD is a very rare developmental vascular anomaly, recognisable during histopathological examination. The study aim was to assess the prevalence of HMD–PVH and hepatocellular and vascular pathologies in the liver. Material and Methods: Liver biopsies from 140 dogs (of different breeds and both sexes) arousing clinical suspicion of PSS were examined histopathologically. Results: An initial PSS diagnosis was confirmed in 125 dogs (89.29%). HMD–PVH was found in 12.32% of dogs, as an isolated disease in 9.29%, especially in Yorkshire terriers, and with extrahepatic PSS in 6.67%. Histopathological analysis of muscles around sublobular veins showed that HMD cases presented hypertrophy or hypertrophy with fibrosis. In 2.17% of all dogs with liver vascular developmental disorders calcification was visible around vessels (without correlation by degenerative changes in those vessels), suggesting prior onset of deep metabolic disorders. Clinical suspicion of PSS was also formed upon quite different pathological processes in young dogs. Conclusion: Histopathological findings diagnosed the type of vascular anomalies (PSS or HMD–PVH) or other pathological changes conclusively, therefore detailed hepatic histopathology is an indispensable component of the clinical diagnostic process.

Clinically healthy pigs used in research are assumed to have normal cardiac structure and function. Subclinical cardiac abnormalities may adversely affect the responses being measured in these experiments. The gross and histologic lesions observed in hearts collected from a Canadian abattoir between 2012 and 2015 indicated an unexpectedly high prevalence of cardiac abnormalities: 75% (297/396) of the hearts examined had such lesions. The ratios of total heart weight to body weight and of right ventricle weight to body weight were significantly greater for the hearts with lesions than for the hearts with no lesions, which suggests that cardiac remodeling, particularly hypertrophy, had occurred. The large percentage of hearts with cardiac remodeling from asymptomatic market pigs demonstrates an increased probability that subclinical cardiac abnormalities may exist in research pigs, especially those accessed through commercial channels. Researchers should be aware of this likelihood if subclinical cardiac abnormalities could adversely affect their experimental findings.

OBJECTIVE To histologically evaluate and compare features of myofibers within the elongated soft palate (ESP) of brachycephalic and mesocephalic dogs with those in the soft palate of healthy dogs and to assess whether denervation or muscular dystrophy is associated with soft palate elongation. SAMPLE Soft palate specimens from 24 dogs with ESPs (obtained during surgical intervention) and from 14 healthy Beagles (control group). PROCEDURES All the soft palate specimens underwent histologic examination to assess myofiber atrophy, hypertrophy, hyalinization, and regeneration. The degrees of atrophy and hypertrophy were quantified on the basis of the coefficient of variation and the number of myofibers with hyalinization and regeneration. The specimens also underwent immunohistochemical analysis with anti-neurofilament or anti-dystrophin antibody to confirm the distribution of peripheral nerve branches innervating the palatine myofibers and myofiber dystrophin expression, respectively. RESULTS Myofiber atrophy, hypertrophy, hyalinization, and regeneration were identified in almost all the ESP specimens. Degrees of atrophy and hypertrophy were significantly greater in the ESP specimens, compared with the control specimens. There were fewer palatine peripheral nerve branches in the ESP specimens than in the control specimens. Almost all the myofibers in the ESP and control specimens were dystrophin positive. CONCLUSIONS AND CLINICAL RELEVANCE These results suggested that palatine myopathy in dogs may be caused, at least in part, by denervation of the palatine muscles and not by Duchenne- or Becker-type muscular dystrophy. These soft palate changes may contribute to upper airway collapse and the progression of brachycephalic airway obstructive syndrome.

Objective: To identify cardiac mechanisms that contribute to adaptation to high altitudes in Tibetan antelope (Pantholops hodgsonii). Animals: 9 male Tibetan antelope and 10 male Tibetan sheep (Ovis aries). Procedures: Tibetan antelope and Tibetan sheep inhabiting a region with an altitude of 4,300 m were captured, and several cardiac variables were measured. Expression of genes for atrial natriuretic peptide, brain natriuretic peptide, and calcium-calmodulin–dependent protein kinase II δ was measured via real-time PCR assay. Results: Ratios of heart weight to body weight for Tibetan antelope were significantly greater than those of Tibetan sheep, but ratios of right-left ventricular weights were similar. Mean ± SD baseline heart rate (26.33 ± 6.15 beats/min) and systolic arterial blood pressure (97.75 ± 9.56 mm Hg) of antelope were significantly lower than those of sheep (34.20 ± 6.57 beats/min and 130.06 ± 17.79 mm Hg, respectively). The maximum rate of rise in ventricular pressure in antelope was similar to that in Tibetan sheep, but after exposure to air providing a fraction of inspired oxygen of 14.6% or 12.5% (ie, hypoxic conditions), the maximum rate of rise in ventricular pressure of the antelope increased significantly to 145.1% or 148.1%, respectively, whereas that of the sheep decreased to 68.4% or 70.5%, respectively. Gene expression of calcium-calmodulin–dependent protein kinase II δ and atrial natriuretic peptide, but not brain natriuretic peptide, in the left ventricle of the heart was significantly higher in antelope than in sheep. Conclusions and Clinical Relevance: Hearts of the Tibetan antelope in this study were well adapted to high-altitude hypoxia as shown by higher heart weight ratios, cardiac contractility in hypoxic conditions, and expression of key genes regulating cardiac contractility and cardiac hypertrophy, compared with values for Tibetan sheep.

Objective—To determine effects of various concentrations of retinoic acid (RA) or a synthetic RA receptor antagonist (LE135) on equine chondrocytes or bone marrow—derived equine mesenchymal stem cells (BMDMSCs) in monolayer cultures. Sample—Articular cartilage and BMDMSCs from 5 clinically normal horses. Procedures—Monolayers of chondrocytes cultured in standard media and of BMDMSCs cultured in chondrogenic media were treated with RA at concentrations of 0, 0.1, 1, or 10μM or LE135 at concentrations of 0, 0.1, 1, or 10μM on day 0. On days 7 and 14, samples were analyzed for DNA concentration, chondrocyte morphology or features consistent with chondrogenesis (ie, chondral morphology [scored from 0 to 4]), and gene expression of collagen type Ia (CI), collagen type II (CII), and aggrecan. Results—Chondrocytes treated with RA had more mature chondral morphology (range of median scores, 3.0 to 4.0) than did untreated controls (range of median scores, 0.5 to 0.5). Chondrocytes treated with LE135 did not sustain chondrocyte morphology. All BMDMSCs had evidence of chondral morphology or high CII:CI ratio. Retinoic acid (1 or 10μM) or LE135 (10μM) treatment decreased DNA content of BMDMSC cultures. At 0.1 and 1μM concentrations, LE135 weakly but significantly increased chondral morphology scores, compared with untreated controls, but lack of aggrecan expression and lack of increased CII:CI ratio, compared with that of controls, did not affect chondrogenesis. Conclusions and Clinical Relevance—RA promoted maturation and hypertrophy in chondrocytes but not BMDMSCs in monolayer cultures. Deficiency or blockade of RA may prevent hypertrophy and maturation of differentiated chondrocytes.

While heart failure is a primary cause of death for many in-transit-loss (ITL) pigs, the underlying cause of these deaths is not known. Cardiomyopathies are considered a common cause of heart failure in humans and often have a genetic component. The objective of this study was to determine if genes associated with cardiomyopathies could be identified in ITL pigs. Samples from the hearts of pigs that died during transport to an abattoir in Ontario, Canada were collected and genotyped along with samples from pigs that did not die during transport (ILT hearts: n = 149; non-ITL/control hearts: n = 387). Genome-wide analyses were carried out on each of the determined phenotypes (gross cardiac lesions) using a medium density single nucleotide polymorphism (SNP) chip and 500 kb windows/regions for analysis, with 250 kb regions of overlap. The distribution derived by a multidimensional scaling (MDS) analysis of all phenotypes demonstrated a lack of complete separation between phenotypes of affected and unaffected animals, which made diagnosis difficult. Although genetic differences were small, a few genes associated with dilated cardiomyopathy (DCM) and arrhythmogenic right ventricular cardiomyopathy (ARVM) were identified. In addition, multiple genes associated with cardiac arrhythmias and ventricular hypertrophy were identified that can possibly result in heart failure. The results of this preliminary study did not provide convincing evidence that a single, heritable cardiomyopathy is the cause of heart failure in ITL pigs.

We have examined distribution and expression of caveolin-3 (cav-3), one of three caveolin isoforms from 16-wks-old spontaneously hypertensive rats (SHR) compared with age-matched control wistar-kyoto (WKY) rats. The expression of cav-3 was increased, whereas expression of PKB/Akt and calcineurin (Cn) was not changed in cardiac tissues of SHR compared to WKY rats. Interestingly, expression of cav-3, PKB/Akt and Cn were decreased in plasma membrane fraction in SHR compared to WKY rats. In H9c2 cardiomyoblast cells treated with phenylephrine (50 μM, 48hr) or isoproterenol (10 μM, 48hr), the expression of cav-3 was markedly enhanced compared to nontreated cells.

Severe hypertension (greater than 180 mmHg) develops in spontaneously hypertensive rats (SHR) after 12 wk-oldhowever, it is not clear whether what kinds of molecular mechanism leads to altered cardiac performance following developmental stages in SHR. Also, although the effect of calcineurin (Cn) to promote cardiomyocyte hypertrophy in vivo and in vitro is established, its overall necessity as a hypertrophic mediator is currently an area of ongoing debate. Thus, we have examined i) body weight and blood pressure, ii) differences of expression and distribution of signaling molecules such as Cn, protein kinase B/Akt (PKB/Akt), and extracellular signal-regulated kinase (ERK) between SHR and their agematched control Wistar-Kyoto (WKY) rats following developmental stages.

OBJECTIVE To investigate cardiac structural and functional changes by tissue Doppler imaging (TDI) and strain imaging in dogs with spontaneous type 1 diabetes mellitus. ANIMALS 30 client-owned dogs, of which 10 had normotensive type 1 diabetes mellitus and 20 were healthy. PROCEDURES All dogs underwent physical examination, laboratory analyses, standard echocardiography, and TDI. RESULTS On TDI and strain imaging, transmitral peak early diastolic velocity (E)-to-tissue Doppler–derived peak early diastolic velocity at basal segment (E') of septum ratio, E:lateral E’ ratio, and septal tissue Doppler–derived peak late diastolic velocity at basal segment (A') were significantly higher and the septal E':A’ ratio and lateral longitudinal strain were significantly lower for diabetic dogs than for control dogs. Furthermore, in diabetic dogs, serum glucose and fructosamine concentrations after a 12-hour period of food withholding were positively correlated with regional systolic functional variables (septal and lateral longitudinal strain) and left ventricular filling pressure indices (E:septal E’ and E:lateral E’ ratios) but were negatively correlated with diastolic functional variables (E:transmitral peak late diastolic velocity and septal and lateral E':A’ ratios). CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that myocardial function in diabetic dogs may be altered before the development of clinical heart-associated signs and that the change may be more readily detected by TDI and strain imaging than by conventional echocardiography. In addition, findings indicated that hyperglycemia could have detrimental effects on myocardial function, independent of hypertension, other cardiac diseases, and left ventricular hypertrophy, in dogs with type 1 diabetes.