Literature DB >> 3998332

The conduction and cardiac sympathetic systems: metabolic aspects.

W Kübler, A Schömig, J Senges.   

Abstract

Compared with the myocardium, glycolytic enzymes are reduced by 50% and mitochondrial enzymes and space by 70% in the conduction system of the calf heart. In addition, on the basis of adenosine triphosphate activities energy demands are reduced by more than 50%; this is in parallel with the reduction in myofibrillar space. The increased tolerance of the conduction system against ischemia can be explained by a reduction of energy demands and a higher proportion of (anaerobic) glycolytic as opposed to aerobic mitochondrial energy production. Among the structures of the conduction system, the sinoatrial and atrioventricular nodes are markedly susceptible to hypoxia in contrast to atrial conduction and ventricular conduction by way of the His-Purkinje system. In the isolated perfused rat heart, an increased net release of noradrenaline during the first 10 minutes of ischemia is only noted after sympathetic stimulation. During this phase, catecholamine overflow is limited by the activity of the neuronal reuptake. At a later second phase, from 15 to 40 minutes after the onset of ischemia, the mechanism of noradrenaline net release is carrier-mediated efflux inhibited by neuronal uptake blocking agents. During the third phase of ischemia, after about 40 minutes, spontaneous noradrenaline release is greatly augmented, probably as a result of leakage caused by membrane damage.

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Year:  1985        PMID: 3998332     DOI: 10.1016/s0735-1097(85)80548-9

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  6 in total

1.  Ultrastructural effects induced by global ischaemia on the AV node compared with the working myocardium. A qualitative and morphometric investigation on the canine heart.

Authors:  P A Schnabel; J Richter; M M Gebhard; G Mall; A Schmiedl; H J Clavien; H J Bretschneider
Journal:  Virchows Arch A Pathol Anat Histopathol       Date:  1990

Review 2.  Genetic causes of human heart failure.

Authors:  Hiroyuki Morita; Jonathan Seidman; Christine E Seidman
Journal:  J Clin Invest       Date:  2005-03       Impact factor: 14.808

3.  Response of the border zone to myocardial infarction in rats.

Authors:  G Olivetti; R Ricci; C Beghi; G Guideri; P Anversa
Journal:  Am J Pathol       Date:  1986-12       Impact factor: 4.307

4.  The ultrastructural effects of global ischaemia on Purkinje fibres compared with working myocardium: a qualitative and morphometric investigation on the canine heart.

Authors:  P A Schnabel; J Richter; A Schmiedl; B Ramsauer; U Bartels; M M Gebhard; G Mall; H J Bretschneider
Journal:  Virchows Arch A Pathol Anat Histopathol       Date:  1991

5.  Transgenic mouse model of ventricular preexcitation and atrioventricular reentrant tachycardia induced by an AMP-activated protein kinase loss-of-function mutation responsible for Wolff-Parkinson-White syndrome.

Authors:  Jasvinder S Sidhu; Yadavendra S Rajawat; Tapan G Rami; Michael H Gollob; Zhinong Wang; Ruiyong Yuan; A J Marian; Francesco J DeMayo; Donald Weilbacher; George E Taffet; Joanna K Davies; David Carling; Dirar S Khoury; Robert Roberts
Journal:  Circulation       Date:  2004-12-20       Impact factor: 29.690

6.  Anatomical Variations in the Sinoatrial Nodal Artery: A Meta-Analysis and Clinical Considerations.

Authors:  Jens Vikse; Brandon Michael Henry; Joyeeta Roy; Piravin Kumar Ramakrishnan; Wan Chin Hsieh; Jerzy A Walocha; Krzysztof A Tomaszewski
Journal:  PLoS One       Date:  2016-02-05       Impact factor: 3.240

  6 in total

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