| Autor: |
Krohn, Edzard, Stinner, Benno, Fleckenstein, Martin, Gebhard, Martha, Bretschneider, Hans |
| Zdroj: |
Pflügers Archiv: European Journal of Physiology; 1989, Vol. 415 Issue 3, p269-275, 7p |
| Abstrakt: |
The effects of the cardioplegic solution HTK on membrane potential (E) and intracellular K and Na activities (a, a) were studied in sheep cardiac Purkinje fibres by means of conventional and ion-selective microelectrodes. HTK contains (mM): Na 15, K 10, Ca 0, Mg 4, histidine 180, (1) In control conditions E was −74.3±3.3 mV ( n=25), awas 116.4±4.1 mM ( n=7) and awas 8.2±1.4 mM ( n=15). (2) Exposure to HTK led to a depolarization to −59.7±3.6 mV ( n=25) which exceeded by about 5-7 mV that induced in a Tyrode solution of 10 mM K and in a modified HTK solution supplemented by 2 mM Ca ( n=6). (3) Addition of 0.5 mM barium eliminated the difference in the steady-state depolarization. (4) HTK superfusion increased ato 120.1±4.4 mM ( n=7) and decreased ato 3.9±0.9 mM ( n=15). (5) The decrease in awas insensitive to amiloride (1 mM) and to external alkalization but was slightly increased by addition of 2 mM calcium. (6) When the calcium in Tyrode solution was lowered from 2.0 mM to 0.05 mM, ahardly decreased during subsequent exposure to unmodified HTK and it increased in the presence of 0.1 mM dihydroouabain. We propose the hypothesis (1) that the difference in membrane depolarization between HTK and a 10 mM K-Tyrode is caused by a decrease in K conductance by the HTK solution and (2) that the adecline mainly results from a coupled Ca influx via Na-Ca exchange due to a delayed washout of external calcium. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink