{'fraction_non_alphanumeric': 0.02512212142358688, 'fraction_numerical': 0.009769713886950453, 'mean_word_length': 5.128205128205129, '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}}
Differences in ischaemic myocardial potassium leakage after treatment with the calcium antagonist anipamil or the beta-blocker atenolol.

The abilities of the new calcium antagonist anipamil as well as the beta-blocker atenolol to reduce the amount of K+ released into the extracellular space during the first minutes of acute coronary artery occlusion were investigated in anaesthetized pigs. [K+]e was continuously measured epicardially with ion selective electrodes. Immediately after starting an occlusion [K+]e rose steeply from normal plasma levels of 3.5 mmol/l to values about three times as high at the end of the 6-min occlusion. This was reproducible in a second and third occlusion in the untreated control group. In the treatment groups either anipamil (0.5; 1.0 mg/kg) or atenolol (0.3 mg/kg) were injected intravenously 10 min before the second occlusion. Anipamil inhibited K+ loss into the extracellular space dose relatedly and significantly throughout the 6-min occlusion period, whereas atenolol showed no protection. The cardioprotective effect of anipamil was also demonstrated in a third occlusion 60 min post application. This different profile cannot be explained by differences in the ability of the two drugs to lower myocardial oxygen consumption; indeed this was only achieved after atenolol. It is concluded that anipamil exerted a direct protective effect on the cardiac myocyte level during ischaemia.