The interference of uptake of thallium-201 in cultured rat myocardial cells with existence of potassium related pharmaceuticals--a preliminary report.
Thallium-201 myocardial perfusion imaging is wildly used to detect and assess the extent of jeopardized myocardial ischemia in the coronary artery disease and the viability of myocardium post infarction. In recent years, there has been a great deal of pharmacological development of blockers and openers of potassium channel. In this study, we will discuss the interference of uptake of thallium-201 ion in cultured neonatal rat myocytes with existence of a variety of pharmacological agents. The cultures of neonatal rat myocardial cells were incubated with different agents such as potassium chloride, sodium-potassium ATPase pump inhibitor (ouabain), cesium compound, variable potassium channel blockers (4 AP, TEA and glibenclamide) and their openers (minoxidil, and cromakalim). The radioactivity of intracellular thallium-201 that could enter rat myocardial cells was detected by gamma counter sixty minutes after thallium-201 was added. In this study we found that thallium and potassium ions behave in an analogous manner in cultured rat myocardial cells. Both 2.5 mM and 5 mM concentration of extracellular potassium ion significantly result in reduction of thallium-201 ion influx in rat myocardial cells. 0.5 mM ouabain, an inhibitor of sodium-potassium ATPase pump, reduced about 40% of influx of thallium-201 ion in cultured rat myocardial cells via active transport. Combination of both potassium ion and ouabain inhibit most of thallium-201 ions influx in myocardial cells, but it is not completely inhibited. Cesium, a potassium antagonist, also interferes with the uptake of thallium-201 in cultured rat myocytes in our study. The most interesting finding in our investigation is that potassium channel blockers such as TEA and glibenclamide, inhibit the influx of thallium-201 in myocytes. However, potassium channel openers have no overt effect on influx of thallium-201 in cultured rat myocytes. We indirectly observe about 60% of influx of thallium-201 ion into cultured rat myocardial cells via active sodium-potassium ATPase pump. Potassium, cesium and potassium channel blockers, such as TEA and glibenclamide, inhibited the different percentage of influx of thallium-201 in cultured rat myocardial cells in this study.
Chen
Y W
YW
Department of Nuclear Medicine, Kaohsiung Medical University Hospital, Taiwan.
Yeh
J L
JL
Huang
Y C
YC
Chen
I J
IJ
Huang
Y F
YF
Liu
G C
GC
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D009206:Myocardium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013794:Thallium Radioisotopes / Q000493:pharmacokinetics*
D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D013794:Thallium Radioisotopes; D011189:Potassium Chloride; D000255:Adenosine Triphosphate