Abstract:
:Ischemia-induced myocardial potassium loss and post-ischemic potassium reuptake was quantitated in 8 open chest pigs during control conditions and during hemodynamic alterations which have been shown to increase steady state sarcolemmal potassium fluxes. Myocardial K+ balance was continuously computed before, during and after a 90 s occlusion of a branch of the circumflex artery during control (CTR), during pacing tachycardia (PACE: 34% increase in heart rate), during proximal aortic constriction (AC; 28% increase in LVSP), and during isoprenaline infusion (ISO; 135% increase in LVdP/dt and 35% increase in heart rate). Ischemia-induced potassium loss increased significantly (40%) during ISO only. Higher basal metabolic rate, increased sarcolemmal K+ conductance, or ischemia-induced depression of a more active Na/K-pump during ISO are possible explanations to why increased K+ loss appeared in this situation. The maximal rate of post-ischemic potassium reuptake was not different from CTR during PACE and ISO, but it was reduced during AC, which might be due to persisting subendocardial ischemia in early reperfusion when ventricular wall stress is high. The extent of potassium restoration was not different from CTR during AC, PACE and ISO.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Aksnes G,Ellingsen O,Rutlen DL,Ilebekk Adoi
10.1016/0022-2828(89)90673-1subject
Has Abstractpub_date
1989-12-01 00:00:00pages
1273-84issue
12eissn
0022-2828issn
1095-8584pii
0022-2828(89)90673-1journal_volume
21pub_type
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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