{'fraction_non_alphanumeric': 0.0337465564738292, 'fraction_numerical': 0.013774104683195593, 'mean_word_length': 5.486607142857143, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effects of Cromakalim and Glibenclamide on ATP‐sensitive Potassium Channels.

The iontropic activity of the heart decreases at low temperatures and this effect maybe related to altered activity of ATP‐sensitive potassium channels (IK‐ATP). These channels are known to open when extracellular ATP is low, inducing a shortening of the action potential duration. Consequently, the high‐energy consuming contraction period is abbreviated, saving scares ATP for survival.A similar mechanism is hypothesized for the effect of low temperature on cardiac function. The purpose of this study is to assess the activity of IK‐ATP in adult cardiac myocyte at normal (37°C) and low (24°C) temperatures. Using conventional patch‐clamp technique in the whole cell configuration, we have recorded IK‐ATP sequentially in control, followed by 100μM Cromakalim (IK‐ATP activator) and 10 μM Glibenclamide (IK‐ATP blocker) at either temperature settings. The cells were depolarized by 10 mV step voltage from a holding potential of −80 mV to +40 mV. At low temperature, there was no significant activation of IK‐ATP by Cromakalim and consequently no effect of Glibenclamide. However at 37°C, there was a significant activation of IK‐ATP that was subsequently blocked by Glibenclamide. The Glibenclamide‐sensitive current had a conductance of 2.57 nS. We conclude that IK‐ATP channels are temperature‐dependent and their activity is significantly reduced at low temperature.