The effect of taurine supplementation on the renin-angiotensin-aldosterone system of dogs with congestive heart failure.

The role of taurine in the treatment of congestive heart failure (CHF) in dogs without systemic deficiency is unexplored. Taurine might have beneficial cardiac effects aside from deficit replacement. We hypothesized that oral taurine supplementation administered to dogs with naturally-occurring CHF would suppress the renin-angiotensin aldosterone system (RAAS). Oral taurine was administered to 14 dogs with stable CHF. Serum biochemical variables, blood taurine concentrations, and comprehensive analysis of RAAS variables were compared before and 2 weeks after taurine supplementation added to background furosemide and pimobendan therapy for CHF. Whole blood taurine concentrations increased after supplementation (median 408 nMol/mL, range 248-608 before and median 493 nMol/mL, range 396-690 after; P = .006). Aldosterone to angiotensin II ratio (AA2) was significantly decreased after taurine supplementation (median 1.00, range 0.03-7.05 before and median 0.65, range 0.01-3.63 after; P = .009), but no other RAAS components significantly differed between timepoints. A subset of dogs showed marked decreases in RAAS metabolites after supplementation and these dogs were more likely to have been recently hospitalized for CHF treatment than dogs that did not show marked decreases in classical RAAS metabolites. Overall, taurine only lowered AA2 in this group of dogs, however, response heterogeneity was noted, with some dogs showing RAAS suppression.

Prospective study of dilated cardiomyopathy in dogs eating nontraditional or traditional diets and in dogs with subclinical cardiac abnormalities.

BACKGROUND: Recent studies have investigated dogs with presumed diet-associated dilated cardiomyopathy (daDCM), but prospective studies of multiple breeds are needed. HYPOTHESIS/OBJECTIVES: To evaluate baseline features and serial changes in echocardiography and cardiac biomarkers in dogs with DCM eating nontraditional diets (NTDs) or traditional diets (TDs), and in dogs with subclinical cardiac abnormalities (SCA) eating NTD. ANIMALS: Sixty dogs with DCM (NTD, n = 51; TDs, n = 9) and 16 dogs with SCA eating NTDs. METHODS: Echocardiography, electrocardiography, and measurement of taurine, cardiac troponin I, and N-terminal pro-B-type natriuretic peptide were performed in dogs with DCM or SCA. Diets were changed for all dogs, taurine was supplemented in most, and echocardiography and cardiac biomarkers were reassessed (3, 6, and 9 months). RESULTS: At enrollment, there were few differences between dogs with DCM eating NTDs or TDs; none had low plasma or whole blood taurine concentrations. Improvement in fractional shortening over time was significantly associated with previous consumption of a NTD, even after adjustment for other variables (P = .005). Median survival time for dogs with DCM was 611 days (range, 2-940 days) for the NTD group and 161 days (range, 12-669 days) for the TD group (P = .21). Sudden death was the most common cause of death in both diet groups. Dogs with SCA also had significant echocardiographic improvements over time. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with DCM or SCA previously eating NTDs had small, yet significant improvements in echocardiographic parameters after diet changes.

Use of computed tomography and radiation therapy planning software to develop a novel formula for body surface area calculation in dogs.

BACKGROUND: Body surface area (BSA) can reflect metabolic rate that might normalize dosing of chemotherapeutics across widely variable weights within a species. The current BSA formula for dogs lacks height, length, and body condition. HYPOTHESIS: Computed tomography (CT) imaging will allow inclusion of morphometric variables in allometric modeling of BSA in dogs resulting in an improved formula for BSA estimation. ANIMALS: Forty-eight dogs from 4 institutions with whole-body CT images. METHODS: Retrospective and prospective case series. Body surface area was contoured using whole-body CT scans and radiation therapy planning software. Body length and height were determined from CT images and also in 9 dogs by physical measurement. Nonlinear regression was used to model the BSA data sets using allometric equations. Goodness-of-fit criteria included average relative deviation, mean standard error, Akaike information criterion, and r2 (derived from the r-value generated by regression models). RESULTS: Contoured BSA differed from the current formula by -9% to +19%. Nonlinear regression on untransformed data yielded BSA = 0.0134 × body weight [kg]∧ 0.4746 × length (cm)∧ 0.6393 as the best-fit model. Heteroscedasticity (increasing morphometric variability with increasing BSA) was an important finding. CONCLUSIONS AND CLINICAL IMPORTANCE: Computed tomography-derived BSA was used to incorporate body length into a novel BSA formula. This formula can be applied prospectively to determine whether it correlates with adverse events attributed to chemotherapy.

A spectrum of exercise training reduces soluble Aß in a dose-dependent manner in a mouse model of Alzheimer's disease.

Physical activity has long been hypothesized to influence the risk and pathology of Alzheimer's disease. However, the amount of physical activity necessary for these benefits is unclear. We examined the effects of three months of low and high intensity exercise training on soluble Aß40 and Aß42 levels in extracellular enriched fractions from the cortex and hippocampus of young Tg2576 mice. Low (LOW) and high (HI) intensity exercise training animals ran at speeds of 15m/min on a level treadmill and 32 m/min at a 10% grade, respectively for 60 min per day, five days per week, from three to six months of age. Sedentary mice (SED) were placed on a level, non-moving, treadmill for the same duration. Soleus muscle citrate synthase activity increased by 39% in the LOW group relative to SED, and by 71% in the HI group relative to LOW, indicating an exercise training effect in these mice. Soluble Aß40 concentrations decreased significantly in an exercise training dose-dependent manner in the cortex. In the hippocampus, concentrations were decreased significantly in the HI group relative to LOW and SED. Soluble Aß42 levels also decreased significantly in an exercise training dose-dependent manner in both the cortex and hippocampus. Five proteins involved in Aß clearance (neprilysin, IDE, MMP9, LRP1 and HSP70) were elevated by exercise training with its intensity playing a role in each case. Our data demonstrate that exercise training reduces extracellular soluble Aß in the brains of Tg2576 mice in a dose-dependent manner through an up-regulation of Aß clearance.