Abstract
Hyperkalemic cardioplegic solutions produce cardiac arrest during open heart surgery by depolarizing the sarcolemma. A recognized adverse effect of hyperkalemic cardioplegia is the possible development of ventricular dysfunction believed to be related to intracellular Ca2+ loading, a consequence of K+-induced membrane depolarization. Adenosine has been proposed as an adjunct to hyperkalemic cardioplegic solutions. However, it is not known whether adenosine can affect K+-induced membrane depolarization, and associated intracellular Ca2+ loading. Perforated patch-clamp method, applied to isolated single guinea-pig ventricular myocytes, revealed that adenosine (1 mM) did not significantly reduce the magnitude of K+-induced membrane depolarization (35.7 ± 1.7 v 31.0 ± 1.1 mV in the absence v presence of adenosine). Yet, adenosine significantly slowed the rate of K+-induced membrane depolarization (167 ± 32.8 v 67.9 ± 12.9 mV/min in the absence v presence of adenosine) without directly affecting Ca2+, Na+, and K+ currents. Imposed ramp-pulses, with different rates (ranging from 0.33 to 0.05 V/s), but same magnitude of depolarization (100 mV), demonstrated that reduction in the rate of membrane depolarization decreases net inward Ca2+ current. Indeed, in Fluo-3 loaded ventricular myocytes, imaged by laser confocal microscopy, adenosine (1 mM) prevented K+-induced intracellular Ca2+ loading. The present findings indicate that adenosine slows the rate of K+-induced membrane depolarization, and reduces K+-induced intracellular Ca2+ loading in ventricular myocytes. Such findings support the notion that adenosine may play a cardioprotective role in hyperkalemic cardioplegia.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1193-1202 |
| Number of pages | 10 |
| Journal | Journal of Molecular and Cellular Cardiology |
| Volume | 28 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 1996 |
| Externally published | Yes |
Fingerprint
Keywords
- Adenosine
- Ca
- Cardiomyocyte
- Cardioplegia
- Depolarization
- K
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine
Cite this
Adenosine slows the rate of K+-induced membrane depolarization in ventricular cardiomyocytes : Possible implication in hyperkalemic cardioplegia. / Alekseev, Alexey E.; Jovanović, Aleksandar; López, Jóse R.; Terzic, Andre.
In: Journal of Molecular and Cellular Cardiology, Vol. 28, No. 6, 06.1996, p. 1193-1202.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Adenosine slows the rate of K+-induced membrane depolarization in ventricular cardiomyocytes
T2 - Possible implication in hyperkalemic cardioplegia
AU - Alekseev, Alexey E.
AU - Jovanović, Aleksandar
AU - López, Jóse R.
AU - Terzic, Andre
PY - 1996/6
Y1 - 1996/6
N2 - Hyperkalemic cardioplegic solutions produce cardiac arrest during open heart surgery by depolarizing the sarcolemma. A recognized adverse effect of hyperkalemic cardioplegia is the possible development of ventricular dysfunction believed to be related to intracellular Ca2+ loading, a consequence of K+-induced membrane depolarization. Adenosine has been proposed as an adjunct to hyperkalemic cardioplegic solutions. However, it is not known whether adenosine can affect K+-induced membrane depolarization, and associated intracellular Ca2+ loading. Perforated patch-clamp method, applied to isolated single guinea-pig ventricular myocytes, revealed that adenosine (1 mM) did not significantly reduce the magnitude of K+-induced membrane depolarization (35.7 ± 1.7 v 31.0 ± 1.1 mV in the absence v presence of adenosine). Yet, adenosine significantly slowed the rate of K+-induced membrane depolarization (167 ± 32.8 v 67.9 ± 12.9 mV/min in the absence v presence of adenosine) without directly affecting Ca2+, Na+, and K+ currents. Imposed ramp-pulses, with different rates (ranging from 0.33 to 0.05 V/s), but same magnitude of depolarization (100 mV), demonstrated that reduction in the rate of membrane depolarization decreases net inward Ca2+ current. Indeed, in Fluo-3 loaded ventricular myocytes, imaged by laser confocal microscopy, adenosine (1 mM) prevented K+-induced intracellular Ca2+ loading. The present findings indicate that adenosine slows the rate of K+-induced membrane depolarization, and reduces K+-induced intracellular Ca2+ loading in ventricular myocytes. Such findings support the notion that adenosine may play a cardioprotective role in hyperkalemic cardioplegia.
AB - Hyperkalemic cardioplegic solutions produce cardiac arrest during open heart surgery by depolarizing the sarcolemma. A recognized adverse effect of hyperkalemic cardioplegia is the possible development of ventricular dysfunction believed to be related to intracellular Ca2+ loading, a consequence of K+-induced membrane depolarization. Adenosine has been proposed as an adjunct to hyperkalemic cardioplegic solutions. However, it is not known whether adenosine can affect K+-induced membrane depolarization, and associated intracellular Ca2+ loading. Perforated patch-clamp method, applied to isolated single guinea-pig ventricular myocytes, revealed that adenosine (1 mM) did not significantly reduce the magnitude of K+-induced membrane depolarization (35.7 ± 1.7 v 31.0 ± 1.1 mV in the absence v presence of adenosine). Yet, adenosine significantly slowed the rate of K+-induced membrane depolarization (167 ± 32.8 v 67.9 ± 12.9 mV/min in the absence v presence of adenosine) without directly affecting Ca2+, Na+, and K+ currents. Imposed ramp-pulses, with different rates (ranging from 0.33 to 0.05 V/s), but same magnitude of depolarization (100 mV), demonstrated that reduction in the rate of membrane depolarization decreases net inward Ca2+ current. Indeed, in Fluo-3 loaded ventricular myocytes, imaged by laser confocal microscopy, adenosine (1 mM) prevented K+-induced intracellular Ca2+ loading. The present findings indicate that adenosine slows the rate of K+-induced membrane depolarization, and reduces K+-induced intracellular Ca2+ loading in ventricular myocytes. Such findings support the notion that adenosine may play a cardioprotective role in hyperkalemic cardioplegia.
KW - Adenosine
KW - Ca
KW - Cardiomyocyte
KW - Cardioplegia
KW - Depolarization
KW - K
UR - http://www.scopus.com/inward/record.url?scp=0030004698&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030004698&partnerID=8YFLogxK
U2 - 10.1006/jmcc.1996.0110
DO - 10.1006/jmcc.1996.0110
M3 - Article
C2 - 8782061
AN - SCOPUS:0030004698
VL - 28
SP - 1193
EP - 1202
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
SN - 0022-2828
IS - 6
ER -