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去甲肾上腺素、钾与超速抑制

Norepinephrine, potassium and overdrive suppression.

作者信息

Pliam M B, Krellenstein D J, Brooks C M, Vassalle M

出版信息

Basic Res Cardiol. 1977 Jan-Feb;72(1):34-45. doi: 10.1007/BF01906299.

DOI:10.1007/BF01906299
PMID:843320
Abstract

The influence of norepinephrine on ventricular overdrive suppression and attendant potassium shifts has been studied in isolated perfused canine hearts with complete atrioventricular block. It was found that: 1) there is a potassium loss during the drive and a potassium uptake after the drive); 2) reducing the driving rate from 240 to 120/min decreases potassium loss; 3) norepinephrine increases potassium uptake and spontaneously beating ventricles and during the recovery from 120/min drive; 4) norepinephrine enhances K loss during and after a 240/min drive; 5) norepinephrine shortens the overdrive pause under all the conditions tested; 6) in ventricles driven at a constant rate, norepinephrine causes a small loss of ptoassium; 7) reserpinized hearts show a small potassium loss during drive and a larger potassium uptake after drive; yet, the suppression is longer; 8) norepinephrine increases K loss with drive and decreases overdrive suppression in reserpinized hearts; 9) norepinephrine enhances the increase in oxygen consumption caused by overdrive; and 10) norepinephrine antagonizes the depressant effect of high [K]0 on automaticity. It is concluded that norepinephrine shortens the pause independently of potassium levels and antagonizes the inhibittory influence of high K. The effect or norepinephrine on K movements depends on the ventricular rate and such rate-dependence is related to oxygen availability with respect to the increased metabolic demand.

摘要

在具有完全房室传导阻滞的离体灌注犬心脏中,研究了去甲肾上腺素对心室超速抑制及伴随的钾离子转移的影响。结果发现:1)在超速驱动期间有钾离子丢失,驱动后有钾离子摄取;2)将驱动频率从240次/分钟降至120次/分钟可减少钾离子丢失;3)去甲肾上腺素可增加钾离子摄取,在自发搏动的心室以及从120次/分钟驱动恢复期间也是如此;4)去甲肾上腺素在240次/分钟驱动期间及之后会增加钾离子丢失;5)在所有测试条件下,去甲肾上腺素都会缩短超速驱动后的停顿时间;6)在以恒定频率驱动的心室中,去甲肾上腺素会导致少量钾离子丢失;7)经利血平处理的心脏在驱动期间显示少量钾离子丢失,驱动后钾离子摄取量更大;然而,抑制时间更长;8)去甲肾上腺素在经利血平处理的心脏中会随着驱动增加钾离子丢失并减少超速驱动抑制;9)去甲肾上腺素会增强超速驱动引起的耗氧量增加;10)去甲肾上腺素可拮抗高[K]0对自律性的抑制作用。得出的结论是,去甲肾上腺素可独立于钾离子水平缩短停顿时间,并拮抗高钾的抑制作用。去甲肾上腺素对钾离子运动的影响取决于心室率,且这种心率依赖性与相对于增加的代谢需求的氧供应有关。

相似文献

1
Norepinephrine, potassium and overdrive suppression.去甲肾上腺素、钾与超速抑制
Basic Res Cardiol. 1977 Jan-Feb;72(1):34-45. doi: 10.1007/BF01906299.
2
Factors affecting overdrive suppression of idioventricular pacemakers and associated potassium shifts.
J Electrocardiol. 1978 Jan;11(1):3-10. doi: 10.1016/s0022-0736(78)80022-3.
3
Role of adenosine on ventricular overdrive suppression in isolated guinea pig hearts and Purkinje fibers.腺苷在离体豚鼠心脏和浦肯野纤维中对心室超速抑制的作用。
Circ Res. 1985 Oct;57(4):517-31. doi: 10.1161/01.res.57.4.517.
4
Overdrive suppression of automaticity in cultured chick myocardial cells.
Am J Physiol. 1980 Jan;238(1):H24-30. doi: 10.1152/ajpheart.1980.238.1.H24.
5
Transient increase in release of adenosine during rapid cardiac pacing; transient effects on overdrive suppression of ventricular automaticity.
Cardiovasc Res. 1987 Jun;21(6):391-8. doi: 10.1093/cvr/21.6.391.
6
The effects of lidocaine and verapamil on overdrive-induced suppression of pacemakers in dogs with complete atrioventricular block.
Jpn Heart J. 1983 May;24(3):449-55. doi: 10.1536/ihj.24.449.
7
The effect of adrenergic enhancement on overdrive excitation.肾上腺素能增强对超速驱动兴奋的影响。
J Electrocardiol. 1976;9(4):335-43. doi: 10.1016/s0022-0736(76)80026-x.
8
Effects of norepinephine, calcium, and rate of discharge on 42K movements in canine cardiac Purkinje fibers.
Circ Res. 1978 Feb;42(2):276-84. doi: 10.1161/01.res.42.2.276.
9
Norepinephrine evoked by potassium depolarization increases interstitial adenosine concentration via activation of ecto-5'-nucleotidase in rat hearts.钾离子去极化诱发的去甲肾上腺素通过激活大鼠心脏的外5'-核苷酸酶增加细胞间腺苷浓度。
J Pharmacol Exp Ther. 2003 May;305(2):719-24. doi: 10.1124/jpet.102.039917. Epub 2003 Feb 11.
10
Mechanisms underlying overdrive suppression and overdrive excitation in guinea pig sino-atrial node.豚鼠窦房结中超速抑制和超速兴奋的潜在机制。
J Biomed Sci. 2006 Sep;13(5):703-20. doi: 10.1007/s11373-006-9089-3. Epub 2006 May 21.

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