Abstract
The effects of temperature on cardiac cells have been previously explored. It is well characterised that on single cell level the action potential measured at room temperature has longer duration compared with that obtained at body temperature. The duration of the AP (APD) is a parameter which is related to the ability of cells to cope with faster pacing rates. APD prolongation by drug or disease condition may lead to arrhythmia. However so far, the comparison has been done mostly on data obtained at body and room temperature. One common explanation for the prolongation of the APD at room temperature is the slower kinetics of underlying ion channels, exchangers and pumps (please check for pump).We measured AP from live cardiac ventricular slices after incubating in ice cold solution for over 60min. The AP from rabbit cardiac tissue slices, were measured shortly after transfer into body temperature solution. These AP exhibit a very short APD (e.g. 89.6ms APD, 6min after warming up). Only after incubation in body temperature of about 1h or more, the AP shape and duration are back to the values under control conditions (205+/-21ms, at 2Hz pacing). The mechanisms for the changes in AP are still not clear however an impaired ion gradient control and subsequently increased intracellular sodium concentration could be responsible for these changes.The temperature effects of ice cold solution are of different origin compared to the reduction to room temperature settings. This could be one of the main reasons why implanted hearts can adapt to the new environment without exhibiting prolonged AP, once coming from cold incubation. However, further investigations are needed to explain the effects in total.
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