No abstract

Type 1 diabetes (T1D) leads to ischemic heart disease and diabetic cardiomyopathy. We tested the hypothesis that T1D differently affects the contractile function of the left and right ventricular free walls (LV, RV) and the interventricular septum (IS) using a rat model of alloxan-induced T1D. Single-myocyte mechanics and cytosolic Ca2+ concentration transients were studied on cardiomyocytes (CM) from LV, RV, and IS in the absence and presence of mechanical load. In addition, we analyzed the phosphorylation level of sarcomeric proteins and the characteristics of the actin-myosin interaction. T1D similarly affected the characteristics of actin-myosin interaction in all studied regions, decreasing the sliding velocity of native thin filaments over myosin in an in vitro motility assay and its Ca2+ sensitivity. A decrease in the thin-filament velocity was associated with increased expression of β-myosin heavy-chain isoform. However, changes in the mechanical function of single ventricular CM induced by T1D were different. T1D depressed the contractility of CM from LV and RV; it decreased the auxotonic tension amplitude and the slope of the active tension–length relationship. Nevertheless, the contractile function of CM from IS was principally preserved.

AIM: To identify and describe micro- and ultrastructural thermally induced changes in Bakers cyst wall associated with the duration of unidirectional uniform heating at 70C. MATERIALS AND METHODS: We took one full-thickness fragment from each of the 15 Bakers cysts excised during the operation and divided each fragment into four parts: one was used as a control sample, and the remaining three fragments were placed with the synovial membrane on a thermostat heated to 70C, with exposure times of 60, 120, and 180 seconds. We used light-optical and electron microscopes for the histomorphological examination of the samples. RESULTS: Two layers of Bakers cyst wall were identified: inner (synovial) and outer (fibrous). In samples exposed to heat for 60 seconds, the synovial layer was undamaged. In samples exposed to heat for 120 seconds, thermal damage to the cells of the synovial layer and underlying collagen fibers of the fibrous layer was evident. With a heating duration of up to 180 seconds, histomorphological examination revealed signs of damage reaching the middle of the fibrous layer, and signs of deep disorganization of the collagen fibers of the cyst wall were determined at the electron-microscopic level. DISCUSSION: Using light microscopy of intact sections of the cyst wall, we, like other researchers, identified two layers (synovial and fibrous) of different densities, with blood vessels passing through them. The performed experiment suggests that a clinically significant result using Bakers cyst thermotherapy is achieved when spreading the zone of irreversible coagulation beyond the middle of the fibrous layer of the cyst wall. This, in turn, guarantees damage to the capillary network that provides trophism and proliferation of synoviocytes. The proposed hypothesis corresponds to the paradigm of similar studies on the coagulation of cysts of other localizations. CONCLUSION: The obtained results of the light-optical and electron-microscopic examination of Bakers cyst wall fragments indicate direct dependence of the depth of thermal coagulation on the duration of heating.