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Titolo:
The effects of tubulin-binding agents on stretch-induced ventricular arrhythmias
Autore:
Parker, KK; Taylor, LK; Atkinson, B; Hansen, DE; Wikswo, JP;
Indirizzi:
Vanderbilt Univ, Dept Phys & Astron, Living State Phys Grp, Nashville, TN 37235 USA Vanderbilt Univ Nashville TN USA 37235 Phys Grp, Nashville, TN 37235 USA Vanderbilt Univ, Sch Med, Dept Internal Med, Div Cardiol, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 v Cardiol, Nashville, TN 37212 USA
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1-2, volume: 417, anno: 2001,
pagine: 131 - 140
SICI:
0014-2999(20010406)417:1-2<131:TEOTAO>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONTRACTION-EXCITATION FEEDBACK; INSITU CANINE HEARTS; MECHANOELECTRICAL FEEDBACK; HYPERTROPHIED CARDIOCYTES; CARDIAC-HYPERTROPHY; MICROTUBULES; MYOCARDIUM; TAXOL; FAILURE; CA2+;
Keywords:
arrhythmia; mechanics; cytoskeleton; microtubule;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Wikswo, JP Vanderbilt Univ, Dept Phys & Astron, Living State Phys Grp, Box1807 Stn B, Nashville, TN 37235 USA Vanderbilt Univ Box 1807 Stn B Nashville TN USA 37235 37235 USA
Citazione:
K.K. Parker et al., "The effects of tubulin-binding agents on stretch-induced ventricular arrhythmias", EUR J PHARM, 417(1-2), 2001, pp. 131-140

Abstract

Stretch-activated ion channels have been identified as transducers of mechanoelectric coupling in the heart, where they may play a role in arrhythmogenesis. The role of the cytoskeleton in ion channel control has been a topic of recent study and the transmission of mechanical stresses to stretch-activated channels by cytoskeletal attachment has been hypothesized. We studied the arrhythmogenic effects of stretch in 16 Langendorff-perfused rabbit hearts in which we pharmacologically manipulated the microtubular network of the cardiac myocytes, Group 1 (n = 5) was treated with colchicine, which depolymerizes microtubules, and Group 2 (n = 6) was treated with taxol, which polymerizes microtubules. Stretch-induced arrhythmias were produced by transiently increasing the volume of a fluid-filled left ventricular balloonwith a volume pump driven by a computer-controlled stepper motor. Electrical events were recorded by a contact electrode which provided high-fidelityrecordings of monophasic action potentials and stretch-induced depolarizations. The probability of eliciting a stretch-induced arrhythmia increased (0.22 +/- 0.11 to 0.62 +/- 0.19, p = 0.001) in hearts treated with taxol (5 muM), whereas hearts treated with colchicine (100 muM) showed no statistically significant change. We conclude that proliferation of microtubules increased the arrhythmogenic effect of transient left ventricle diastolic stretch. This result indicates a possible mode of arrhythmogenesis in chemotherapeutic patients and patients exhibiting uncompensated ventricular hypertrophy. The data would indicate that the cytoskeleton represents a possible target for antiarrhythmic therapies. (C) 2001 Elsevier Science B.V. All rightsreserved.

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Documento generato il 24/11/20 alle ore 22:47:37