Association of hyponatremia and hyperglycemia with outcome in dogs with congestive heart failure

Objective: To evaluate plasma sodium and glucose concentrations in dogs with congestive heart failure (CHF) prior to treatment and evaluate the differences between survivors and non‐survivors. Design: Retrospective study. Animals: Fifty‐nine dogs with CHF prior to receiving cardiac medication. Interventions: None. Measurements and main results: The mean plasma sodium concentration in dogs with CHF was below the reference range (144–156 mmol/L) and significantly lower (P=0.009) in non‐survivors (141±6 mmol/L) compared with survivors (147±4 mmol/L). The mean plasma glucose concentration was above the reference range (76–117 mg/dL) and significantly higher (P=0.004) in non‐survivors (128±52 mg/dL) compared with survivors (100±13 mg/dL). Forty‐four percent of non‐survivors had concurrent low plasma sodium and high plasma glucose concentrations, whereas no survivors had both abnormalities (P<0.0001). Conclusions: Lower plasma sodium and higher plasma glucose are associated with a worse outcome in dogs with CHF.     

Mesh-like vascular changes in copper deficiency-induced rat cardiomyopathy

The pathological effects of copper deficiency (COD) are well known. However, the pathogenesis of cardiomyopathy resulting from COD remains unclear. In this study, aimed to elucidate the pathogenesis of COD-induced cardiomyopathy by examining the morphology of the cardiovascular system in copper-deficient rats using histopathology, immunohistochemistry, and scanning and transmission electron microscopy. Changes detected in the myocardium and interstitium were consistent with those reported for COD. Morphological changes included mesh-like changes in the capillary endothelial cells that appear to be a novel finding in COD-induced cardiomyopathy. These changes are hypothesized to result from abnormal vascular remodeling following damage to the basement membrane and due to the mechanical effects of myocardial contractions. Although cardiomyopathy may be associated with microcirculatory disorders arising from these lesions, further investigations are necessary to demonstrate a causal relationship between the pathogenesis of cardiomyopathy and the contribution of these lesions to disease progression.     

Papillary muscle measurements in cats with normal echocardiograms and cats with concentric left ventricular hypertrophy

BACKGROUND: Papillary muscle hypertrophy can occur in conjunction with, or as the only indication of, hypertrophic cardiomyopathy or other diseases that result in left ventricular concentric hypertrophy (LVCH). Assessment of papillary muscle size is usually subjective because objective measures have not been reported. HYPOTHESIS: The study hypothesis was that papillary muscle dimensions are different between normal cats and cats with LVCH. ANIMALS: Echocardiograms from 44 normal cats and 40 cats with LVCH were included in the study. METHODS: All measurements were taken from the right parasternal short-axis view at the level of the papillary muscles at end-diastole. Three methods were used to assess papillary muscle size: the area subtraction method, the direct area trace method, and the diameter method. Measurements were compared between cat groups and method comparisons were made among methods for area determination. RESULTS: Cats with LVCH were older and had significantly greater left ventricular septal and free wall thicknesses and larger left atrial measurements than normal cats (P < .0006). Papillary muscle measurements were significantly greater by all measurement methods in cats with LVCH than in cats with normal echocardiograms (P < .0001). The area subtraction method and direct area trace method showed moderate agreement. CONCLUSIONS AND CLINICAL IMPORTANCE: Papillary muscle measurements were larger for LVCH cats than normal cats; however, some overlap was present. The establishment of these objective measures adds to the echocardiographic examination of cats.     

加味生脉补心丹对2型糖尿病大鼠心肌损伤的保护作用

目的 探讨加味生脉补心丹（以下简称BXD）对自发性非肥胖2型糖尿病Goto-kakisaki （GK）大鼠心肌损伤的保护作用。方法 8~9周龄雄性Wistar大鼠8只作为空白组,另将40只糖尿病模型GK大鼠按随机数字表将大鼠分为5组,分别为：模型组、西药组（格列齐特缓释片组）、BXD低剂量组、BXD中剂量组、BXD高剂量组。各组大鼠按治疗方法给药10周后处死,腹主动脉采血检测空腹血糖（FPG）、糖化血红蛋白（HbAlc）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）,取左心室行心肌组织HE染色、PAS染色观察病理改变,免疫组化测定心肌凋亡相关蛋白Bax、Bcl-2的表达。结果 与空白组比较,模型组FPG、HbAlc显著升高（P<0.01）,SOD、GSH-Px均显著降低（P<0.01）,MDA显著升高（P<0.01）;HE染色可见心肌组织水肿坏死、纤维溶解断裂;PAS染色可见大量糖原物质沉积;免疫组化示心肌组织Bax表达增多、Bcl-2表达减少（P<0.01）。与模型组比较,BXD低剂量组FPG降低（P<0.05）,西药组和BXD中、高剂量组FPG均显著降低（P<0.01）;西药组HbAlc显著降低（P<0.01）,BXD高剂量组HbAlc降低（P<0.05）;西药组与BXD高剂量组SOD、GSH-Px均显著升高（P<0.01）、MDA含量均降低（P<0.05）;西药组、BXD高剂量组Bax表达显著减少（P<0.01）,西药组及BXD中剂量组、高剂量组Bcl-2表达显著增多（P<0.01）。结论 BXD对GK大鼠心肌损伤具有保护作用,其机制可能是通过增强抗氧化能力、抑制心肌细胞凋亡,从而起到心肌保护作用。     

Serum nitrate and nitrite in dogs with spontaneous cardiac disease

The purpose of this study was to determine whether nitric oxide (NO) concentrations are high in dogs with chronic valvular disease (CVD) and dilated cardiomyopathy (DCM) compared to healthy controls and to determine whether NO concentrations are correlated with type of cardiac disease, disease severity, medical therapy, or serum tumor necrosis factor (TNF) and interleukin-1 (IL-1). Blood was collected from 32 dogs with DCM, from 10 dogs with CVD, and from 10 healthy controls. Indirect determination of NO concentrations was performed by a commercial photoabsorbance assay that uses a Greiss reagent to measure the concentration of nitrite and nitrate (NN), end products of NO metabolism. TNF and IL-1 activities were measured by bioassay. Mean NN concentrations were significantly higher in dogs with heart disease (median, 4.57 microM; range, 0.00-31.05 microM) than in controls (median, 0.00 microM; range, 0.00-6.16 microM; P = .04). NN concentrations in dogs with cardiac disease were not correlated with type or severity of cardiac disease, medication type, or TNF and IL-1 concentrations. NN concentrations were inversely correlated with fractional shortening. The results of this study suggest that metabolites of NO are increased in some dogs with cardiac disease, but these increases appear to be independent of disease severity, TNF and IL-1 concentrations, and type of pharmacologic intervention.     

Effect of thyroid hormone supplementation on survival of euthyroid dogs with congestive heart failure due to systolic myocardial dysfunction: a double-blind, placebo-controlled trial

Nineteen euthyroid dogs of 12 breeds with echocardiographic signs of dilated cardiomyopathy (DCM) and radiographic and clinical signs of congestive heart failure (CHF) were evaluated in a randomised, double-blind, and placebo-controlled study. The dogs received either thyroxine or placebo as an adjunct to digoxin, furosemide and propranolol. The group assignment of individual dogs and serum concentrations of thyroid hormones remained unknown to owners and investigators during the entire study period. Dogs were evaluated clinically and with electrocardiography (ECG), thoracic radiography, echocardiography and measurement of total thyroxine (tT4) and thyroid stimulating hormone (TSH) before beginning of the trial, and then one week, 2 months, 6 months and yearly after initial examination, and, when applicable, at the time of euthanasia. End-point of the study was euthanasia (n = 17) due to severe congestive heart failure or sudden death (n = 2). Survival times ranged from 17 to 1030 days (median 187 days) in the placebo group, and from 18 to 1000 days (median 73 days) in the treatment group. There was no statistically significant difference in survival times between the treatment group and the placebo group (p = 0.46). Post mortem and histopathologic examinations revealed the attenuated wavy fiber type of DCM in 11 dogs, and myocardial infarcts, arteriosclerosis and chronic valvular disease in one dog. In conclusion, there was a wide range in survival times of dogs treated with digoxin, furosemide and propranolol. Adding thyroid hormones to the treatment did not significantly influence survival.     

Syncope secondary to transient atrioventricular block in a German shepherd dog with dilated cardiomyopathy and atrial fibrillation

This case report describes transient atrioventricular block as the etiology for syncopal events in a 6-year-old male German shepherd dog with atrial fibrillation and dilated cardiomyopathy. The arrhythmia diagnosis was obtained via Holter monitoring. Medical treatment with a sustained-release preparation of theophylline, as an additive to the standard congestive heart failure treatment (benazepril, furosemide and pimobendan) may have contributed to temporary remission of the syncopal events. However, the congestive heart failure progressed and the dog was euthanized. Veterinarians should be aware of the possibility of transient atrioventricular block causing syncope in dogs with DCM and AF and should be careful in empirically lowering the ventricular response rate if these dogs present with syncopal episodes.     

Suramin alleviates hypertrophic scar in mice by inhibiting fibroplasia and inflammatory response

AIM: To investigate the therapeutical effect of suramin on hypertrophic scar (HPS) and its mechanism. METHODS: After the mouse model of HPS was established by mechanical stretching, the suramin solution at low dose (5 mg/kg) and high dose (10 mg/kg) was applied onto the scar site caused by mechanical load in mice by transdermal administration once a day for 10 d. The degree of scar hyperplasia was observed by macroscopy. The scar cross-sectional area and scar elevation index in the HPS tissues were evaluated by hematoxylin-eosin (HE) staining. The expression levels of transforming growth factor-β1 (TGF-β1) and interleukin-6 (IL-6) in HPS tissues were detected by immumohistochemical staining. The expression level of α-smooth muscle actin (α-SMA) in HPS tissues was detected by immunofluorescence staining, RT-qPCR and Western blot. The levels of tumor necrosis factor-α (TNF-α), IL-6, IL-10 and TGF-β1 in the HPS tissues were measured by ELISA. RESULTS: Macroscopic observation showed that the surface areas of scar in the HPS mice after treatment with suramin at low and high doses were significantly reduced (P<0.01). HE staining results showed that the scar cross-sectional area and the scar elevation index of HPS mice after treatment with suramin at low and high doses were significantly reduced (P<0.05 or P<0.01). The results of immunofluorescence staining, RT-qPCR and Western blot showed that the number of α-SMA positive cells and the mRNA and protein expression of α-SMA in scar tissues of HPS mice after treatment with suramin at low and high doses were significantly decreased (P<0.05 or P<0.01). The results of immunohistochemical staining showed that the expression levels of TGF-β1 and IL-6 in scar tissues of HPS mice after treatment with suramin at low and high doses were significantly reduced (P<0.01). The results of ELISA showed that the levels of TNF-α, IL-6, IL-10 and TGF-β1 in the scar tissues of HPS mice after treatment with suramin at low and high doses were significantly reduced (P<0.01). CONCLUSION: Suramin inhibits the formation of HPS, which may be related to the inhibition of fibroplasia and reduction of local inflammatory response.