Key result
Diabetes blunts TEA-induced ventricular repolarization prolongation, with a ~15-ms smaller increment versus controls.
Why the study?
The effects of tetraethylammonium on ventricular repolarization in diabetic myocardium and the modifying role of rosiglitazone were unclear.
Does rosiglitazone modify TEA-sensitive ventricular repolarization in streptozotocin-induced diabetic rats?
Does rosiglitazone modify TEA-sensitive ventricular repolarization in streptozotocin-induced diabetic rats?
Diabetes causes profound baseline prolongation of ventricular repolarization in an animal model, which is modified but not normalized by rosiglitazone despite improvements in glycemic control.
Answers are grounded in this paper and cite their sources.
Diabetes-associated repolarization prolongation in rat myocardium may heighten arrhythmia risk; leaves open clinical translation and rosiglitazone effects.
OBJECTIVE: To examine ventricular action-potential responses to tetraethylammonium (TEA), a non-selective potassium-channel blocker, in streptozotocin-induced diabetic rats and determine whether rosiglitazone modifies these responses. MATERIALS AND METHODS: Male Wistar rats were assigned to Control (C), Control plus Rosiglitazone (C+RSG), Diabetic (D), or Diabetic plus Rosiglitazone (D+RSG) groups. Diabetes was induced with streptozotocin (45 mg/kg, intravenous). Resting membrane potential (RMP), action potential amplitude (APA), and half-repolarization time (½RT) were recorded from isolated left ventricular papillary muscles before and after TEA administration (2 mmol/L). RESULTS: At week 8, blood glucose was 563 ± 29 mg/dL in diabetic rats and 98 ± 6 mg/dL in controls (p < 0.001). Rosiglitazone reduced the diabetic value to 336 ± 25 mg/dL (p < 0.05 vs. D). TEA increased ½RT from 18 ± 1 to 38 ± 2 ms in controls (+20 ms) and from 60 ± 3 to 65 ± 3 ms in diabetic myocardium (+5 ms). Diabetic preparations had higher post-TEA ½RT because repolarization was prolonged at baseline; however, the absolute TEA-associated increment was smaller than in controls. TEA also increased APA in untreated control and diabetic preparations. CONCLUSION: Diabetes was associated with marked baseline prolongation of ventricular repolarization. The smaller absolute ½RT increment in diabetic myocardium does not support enhanced TEA responsiveness. Because TEA is non-selective, the findings reflect an integrated response to TEA-sensitive potassium conductances rather than dysfunction of a specific current subtype. Rosiglitazone modified selected electrophysiological responses without normalizing diabetic repolarization.
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Kavak et al. (2026) studied Streptozotocin-induced diabetes mellitus (n=32). Tetraethylammonium vs. Baseline (pre-exposure) was evaluated on Half-repolarization time (½RT). Diabetes was associated with marked baseline prolongation of ventricular repolarization, and the absolute half-repolarization time increment following tetraethylammonium exposure was smaller in diabetic myocardium (+5 ms) compared to controls (+20 ms).
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