TABLE 1.
Factors influencing the time of the shift from flutter to fibrillation
| Factor | Time from beginning of flutter to beginning of fibrillation, min (mean ± SEM) |
|---|---|
| Control | 8.5±1.5 |
| Phorbol 12-myristate 13-acetate | 1.5±0.3* |
| Phorbol 12-myristate 13-acetate plus calphostin C | 6.7±1.5 |
| Phorbol 12-myristate 13-acetate plus leupeptin | 7.5±1.2 |
| Type 1 diabetic model – streptozotocin | 2.1±0.4* |
| Type 1 diabetic model – streptozotocin plus calphostin C | 6.5±1.3 |
| Type 1 diabetic model – streptozotocin plus leupeptin | 6.8±1.8 |
| Type 1 diabetic model – streptozotocin plus AII antagonist | 7.1±1.5 |
| Type 1 diabetic model – streptozotocin plus N-acetyl-leu-leu-norleucinal | 6.5±2.3 |
| Type II diabetic model – OLETF | 2.3±0.9* |
| Control of OLETF – LETO | 8.2±1.2 |
| AII analogue | 1.5±0.6* |
| AII analogue plus AII antagonist | 6.5±1.3 |
| Hypoxia | 2.2±1.2* |
| Protein kinase A activator | 18.1±2.1* |
| Cyclic AMP analogue | 17.2±3.1* |
| Cyclic AMP analogue plus protein kinase A inhibitor | 9.2±1.3 |
| d-sotalol | 15.2±3.5* |
| d-sotalol plus protein kinase A inhibitor | 9.0±2.5 |
| Heptanol | 0.05±0.001* |
Aconitine (0.1 μmol/L) was administrated to the hearts, which were being irrigated on a Langendorff apparatus. The concentrations of the reagents are described in the text.
*
Significant difference, P<0.001 versus the control. AII Angiotensin II; LETO Long-Evans Tokushima Otsuka; OLETF Otsuka Long-Evans Tokushima Fatty