Effects of rosiglitazone on altered electrical left ventricular papillary muscle activities of diabetic rat.
The action potential configuration of the left ventricular papillary muscle as well as the rosiglitazone-dependent changes in ventricular papillary muscle action potential amplitude were studied, and the duration was studied and compared in both healthy and diabetic rats. In this study, we used four groups: (1) nondiabetic control animals (C), (2) rosiglitazone-treated nondiabetic control animals (C+RSG), (3) diabetic animals (D), and (4) rosiglitazone-treated diabetic animals (D+RSG). Diabetes was induced by a single intravenous (i.v.) injection of streptozotocin (STZ). Conventional microelectrode techniques were applied to record action potentials after the establishment of diabetes (8 weeks after STZ treatment). Resting membrane potential (RMP) was decreased significantly in both RSG-treated C and D rats (from -70.2 +/- 0.7 to -63.2 +/- 0.7 and from -69.2 +/- 0.4 to -61.2 +/- 0.4). C+RSG and D+RSG groups showed increase in action potential amplitude compared with C and D groups (from 67.1 +/- 0.8 to 68.2 +/- 0.5 and from 67.1 +/- 0.8 to 80.1 +/- 0.8 and from 68.2 +/- 0.5 to 79.3 +/- 0.3) Depolarization time was significantly prolonged in diabetic rats (12.1 +/- 0.4 to 27.5 +/- 0.9). However, this prolongation in D+RSG group was significantly lower according to D group (from 27.5 +/- 0.9 to 19.2 +/- 0.7). There was no difference between C and C+RSG rats (12.1 +/- 0.4 to 11.6 +/- 0.2). Half repolarization time was also prolonged in diabetic rats (17.5 +/- 0.6 to 59.9 +/- 1.0). Moreover, D+RSG rats showed a slight and statistically insignificant difference according D rats (59.9 +/- 1.0 to 55.9 +/- 1.7). C+RSG rats showed a slight significant increase in half repolarization time compared with C group (17.5 +/- 0.6 to 29.4 +/- 0.7). Treatment of rats with RSG markedly decreased insulin resistance and also increased insulin sensitivity of the heart. Our data suggest that the beneficial effects of RSG treatment on the electrical activities of the diabetic rat papillary appear to be due to the diminished K+ currents, partially related to the decrease of hyperglycemia.
Kavak
Servet
S
Department of Biophysics, Faculty of Medical, Cukurova University, 01330 Adana, Turkey. skavak@cu.edu.tr
Emre
Mustafa
M
Tetiker
Tamer
T
Kavak
Tuyana
T
Kolcu
Zekeriya
Z
Günay
Ismail
I
D000200:Action Potentials / Q000187:drug effects*; D000704:Analysis of Variance; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000503:physiopathology*; D004558:Electric Stimulation; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D066298:In Vitro Techniques; D007333:Insulin Resistance; D008297:Male; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D000077154:Rosiglitazone; D013311:Streptozocin; D045162:Thiazolidinediones / Q000494:pharmacology*; D016276:Ventricular Function
D007004:Hypoglycemic Agents; D015221:Potassium Channels; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D013311:Streptozocin