Contraction–relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium

The two main phases of the mammalian cardiac cycle are contraction and relaxation; however, whether there is a connection between them in humans is not well understood. Routine exercise has been shown to improve cardiac function, morphology, and molecular signatures. Likewise, the acute and chronic changes that occur in the heart in response to injury, disease, and stress are well characterized, albeit not fully understood. In this study, we investigated how exercise and myocardial injury affect contraction–relaxation coupling. We retrospectively analyzed the correlation between the maximal speed of contraction and the maximal speed of relaxation of canine myocardium after receiving surgically induced myocardial infarction, followed by either sedentary recovery or exercise training for 10–12 wk. We used isolated right ventricular trabeculae, which were electrically paced at different lengths, frequencies, and with increasing β-adrenoceptor stimulation. In all conditions, contraction and relaxation were linearly correlated, irrespective of injury or training history. Based on these results and the available literature, we posit that contraction–relaxation coupling is a fundamental myocardial property that resides in the structural arrangement of proteins at the level of the sarcomere and that this may be regulated by the actions of cardiac myosin binding protein C (cMyBP-C) on actin and myosin.

Effects of cortisol on catabolism of canine myocardium and mitral valve

Cortisol can be thought of as the body's main stress hormone, where it works with specific parts of the brain to control moods, motivations and fears. Cortisol is a hormone that many animals produce too, including dogs - in which it can help control weight, fight infections and keep blood sugar levels in check. However, if the body produces too much cortisol - in humans and in dogs - it can cause many problems. Cushing's syndrome is the name for the condition where dogs produce too much cortisol. The incidence is one or two cases in every 1,000 dogs per year, making it the most common endocrine disorder in dogs. Humans can also be diagnosed with Cushing's syndrome, where excessive exposure to cortisol is known to cause myocardial hypertrophy and cardiac dysfunction. It has also been reported that humans can experience hypertrophy of the cardiomyocytes and an increase in myocardial fibre. A team of researchers based at the Nippon Veterinary and Life Science University in Japan is investigating the cardiovascular effects of hyperglycocorticoidemia. Dr Sachiyo Tanaka is working with Professor Yasushi Hara and Assistant Professor Shuji Suzuki, to conduct research in order to elucidate the histopathological changes that occur in the heart organ when there is hyperglucocorticoidemia.

A Three-Compartment Pharmacokinetic Model to Predict the Interstitial Concentration of Talaporfin Sodium in the Myocardium for Photodynamic Therapy: A Method Combining Measured Fluorescence and Analysis of the Compartmental Origin of the Fluorescence

To evaluate the effectiveness of photodynamic therapy occurring in the interstitial space of the myocardium, we estimated the interstitial concentration of talaporfin sodium in the canine myocardium by constructing a three-compartment pharmacokinetic model based on measured changes in talaporfin sodium plasma concentration and myocardial fluorescence. Differential rate equations of talaporfin sodium concentration in the plasma, interstitial space, and cell compartment were developed with individual compartment volume, concentration, and rate constants. Using measured volume ratios based on histological examinations, we defined that the myocardial fluorescence consisted of the linear addition of fluorescence generated from these three compartments. The rate constants were obtained by fitting to minimize the sum of the squared errors between the measured talaporfin sodium concentrations and the calculated concentrations divided by the number of data points using the conjugate gradient method in MATLAB. We confirmed that this fitting operation may be appropriate, because a coefficient of determination between the measured talaporfin sodium changes and the calculated concentrations using our equations was 0.99. Consequently, to estimate the interstitial concentration in the canine myocardium, we propose a three-compartment pharmacokinetic model construction methodology using measured changes in talaporfin sodium plasma concentration and changes in myocardial fluorescence.