Chronic effects of streptozotocin-induced diabetes on the ultrastructure of rat ventricular and papillary muscle

Abstract

Contractile dysfunctions have been demonstrated in different experimental models of diabetes which have similar characteristics to many of the abnormalities found in the clinical setting. Administration of streptozotocin (STZ) to young adult rats induces beta-cell necrosis of the pancreas which gives rise to hypoinsulinaemia and hyperglycaemia, features which are also seen in untreated type 1 clinical diabetes. We have investigated the chronic effects of STZ-induced diabetes on contraction in rat ventricular myocytes and ultrastructure of cardiac muscle. Diabetes was induced in male Wistar rats (230-270 g) with a single injection of STZ (60 mg kg(-1)). At 2 and 10 months after STZ treatment, the amplitude of contraction was larger in diabetic compared to control myocytes. Time to peak contraction was significantly longer at 2 months but appeared to normalise at 10 months after STZ treatment. In contrast, time to half relaxation of contraction was not significantly different after 2 months but was significantly reduced at 10 months after STZ treatment compared to control. Transmission electron microscope examination of cardiac muscle showed that the ultrastructure of cardiac muscle, especially structures associated with contraction, were not greatly altered after STZ treatment. Sarcomere lengths were not significantly different in papillary or ventricular muscle at 4 or 8 months after STZ treatment compared to control. Our data provide evidence that morphological defects in contractile myofilaments and associated structures cannot explain contractile dysfunctions seen in ventricular myocytes from STZ-treated animals.

Regional effects of streptozotocin-induced diabetes on shortening and calcium transport in epicardial and endocardial myocytes from rat left ventricle

“…Resting cell length was similar in EPI and ENDO myocytes from STZ-treated rats and controls. These results are consistent with previous studies that have variously demonstrated unchanged resting cell length, width, and the calculated cell volume in myocytes isolated from whole ventricle from STZ-treated rats compared to controls (Howarth et al 2000(Howarth et al , 2002Hamouda et al 2015). However, differences have been reported in other regional cell measurements.…”

“…These results are consistent with previous studies that have variously demonstrated unchanged resting cell length, width, and the calculated cell volume in myocytes isolated from whole ventricle from STZ‐treated rats compared to controls (Howarth et al. , ; Hamouda et al. ).…”

Cod liver oil supplementation improves cardiovascular and metabolic abnormalities in streptozotocin diabetic rats

“…In fact, the cardiac content of noradrenaline and noradrenaline turnover, uptake, synthesis and release have been demonstrated to all be enhanced in diabetic cardiomyopathy (Ganguly etal 1987), which might lead to down-regulation of cardiac b-adrenoceptors, resulting in a deficiency in b 1adrenoceptor-mediated stimulation. As reported previously, we also found that diabetes results in an increased responsiveness of papillary muscle to noradrenaline and isoprenaline (Austin & Chess-Williams 1992;Howarth et al 2000). The mechanisms of contrary responsiveness of diabetic atria and papillary muscle to b-adrenoceptor agonists are not known, but similar controversial findings were reported previously (Dinçer et al 1998).…”

Effect ofPiper sarmentosumExtract on the Cardiovascular System of Diabetic Sprague-Dawley Rats: Electron Microscopic Study

“…These findings are consistent with previous reports that also showed loss of myofibrils in the diabetic cardiomyocytes. In addition, the researchers pointed out that there were no changes in sarcomere length related to DM [25]. However, the sarcomere length was not measured in the present study.…”