Myocardial potassium balance associated with regional ischaemia in the pig: effects of beta-adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods.
The effects of beta-adrenoceptor blockade, duration of ischaemia and preceding ischaemic periods on ischaemia-induced changes in myocardial K+ balance were studied in 12 open-chest pigs. Coronary venous blood was directed through a shunt from the coronary sinus to the right atrium. Continuous recordings of arterial, shunt blood [K+] and shunt flow enabled us to compute myocardial K+ balance during and after consecutive 2-, 2-, 5-, 10- and 2-min periods of regional ischaemia separated by 30 min of reperfusion. beta-adrenoceptor blockade (propranolol 1 mg kg-1 i.v.) given between the first and second ischaemic period did not alter the effects of 2 min ischaemia on myocardial K+ balance. Total K+ losses induced by 2, 5 and 10 min of ischaemia were 67.1 (40.6-93.3), 106.7 (69.4-176.8) and 192.2 (117.7-332.6) mumol 100 g-1, respectively. Thus, the plateau observed in extracellular [K+] between 2 and 10 min of regional ischaemia could, at least partly, be explained by continuous drainage of K+ from ischaemic myocardium into the surrounding normally perfused tissue. The total K+ loss induced by the second and last 2-min ischaemic period were 67.1 (40.6-93.3) and 35.6 (23.1-53.6) mumol 100 g-1 (P less than 0.001), respectively. This reduction shows that ion homeostasis during ischaemia was greatly changed in myocardium which had been 'preconditioned' and 'stunned' by 5 plus 10 min of ischaemia. Total amount, maximal rate and duration of post-ischaemic K+ reuptake increased with the duration of the preceding ischaemia. Moreover, K+ re-uptake after 2 min of ischaemia and the number of sarcolemmal Na/K pumps ([3H]ouabain binding), were normal in stunned myocardium. From these observations we conclude that progressive stimulation of the Na/K-pump occurred when ischaemia was prolonged from 2 to 10 min, and that Na/K-pump function was preserved in stunned myocardium.
University of Oslo, Institute for Experimental Medical Research, Ullevål Hospital, Norway.
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D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active; D002395:Catecholamines / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism*; D005260:Female; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism; D012756:Sheep; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000187:drug effects
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium