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

• Published in: Acta diabetologica 2000, Vol.37 (3), p.119-124
• Main Authors: HOWARTH, F. C, QURESHI, M. A, LAWRENCE, P, ADEGHATE, E
• Format: Article
• Language: English
• Subjects: Animals; Associated diseases and complications; Biological and medical sciences; Blood Glucose - metabolism; Body Weight; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Heart Ventricles - ultrastructure; Insulin - blood; Male; Medical sciences; Microscopy, Electron; Muscle Contraction - drug effects; Muscle Contraction - physiology; Myocardium - ultrastructure; Papillary Muscles - ultrastructure; Rats; Rats, Wistar; Tropical medicine
• ISSN: 0940-5429; 1432-5233
• DOI: 10.1007/s005920070013

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.