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Titolo:
EFFECT OF RYANODINE ON THE INITIATION AND PERPETUATION OF STRETCH-INDUCED ARRHYTHMIAS IN ISOLATED CANINE VENTRICLE
Autore:
JOBE RL; TAYLOR LK; WANG ZF; BERGER CM; STACY GP; HANSEN DE;
Indirizzi:
VANDERBILT UNIV,SCH MED,MED CTR N,DIV CARDIOL,CC-2218 NASHVILLE TN 37232 VANDERBILT UNIV,SCH MED,MED CTR N,DIV CARDIOL NASHVILLE TN 37232
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 5, volume: 36, anno: 1994,
pagine: 1736 - 1744
SICI:
0363-6135(1994)36:5<1736:EOROTI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRACELLULAR CALCIUM TRANSIENTS; ACTIVATED ION CHANNELS; MECHANOELECTRICAL FEEDBACK; ACTION-POTENTIALS; SKELETAL-MUSCLE; PIG-HEART; CONTRACTION; OSCILLATIONS; MECHANISMS; RELEASE;
Keywords:
STRETCH-INDUCED ARRHYTHMIA; VENTRICULAR TACHYCARDIA; RYANODINE; CALCIUM; SARCOPLASMIC RETICULUM; MECHANOELECTRICAL FEEDBACK; ISOLATED CANINE HEART;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
R.L. Jobe et al., "EFFECT OF RYANODINE ON THE INITIATION AND PERPETUATION OF STRETCH-INDUCED ARRHYTHMIAS IN ISOLATED CANINE VENTRICLE", American journal of physiology. Heart and circulatory physiology, 36(5), 1994, pp. 1736-1744

Abstract

Ventricular arrhythmias can be initiated by a mechanism of transient diastolic dilation. To test the hypothesis that Ca2+ release from sarcoplasmic reticulum (SR) is important in initiation of such stretch-induced arrhythmias (SLAs), we studied effects of ryanodine in an isolated canine heart model. Arrhythmias were induced by a computerized ventricular volume servo-pump system that transiently increased left ventricular volume by precise amounts (Delta V) during diastole. The probability of eliciting an SIA (P-SIA) was compared at the minimum Delta V that resulted in P-SIA of greater than or equal to 90% under baseline conditions. Block of SR Ca2+ release with 10(-5) M ryanodine in 11 ventricles produced mild inhibition of SIAs, reducing P-SIA by 19.4% (P = 0.039). Because ryanodine produces leakage of SR Ca2+ at low concentration and block of SR Ca2+ release at high concentration, ryanodine concentration was varied from 10(-9) to 10(-5) M in six ventricles. Ryanodine had minimal effect on P-SIA over this concentration range. In sixventricles with elevated intracellular Ca2+ produced by pretreatment with 0.1-0.3 mu M strophanthidin, 10(-5) M ryanodine did not significantly reduce P-SIA. Probability of inducing ventricular pairs or nonsustained ventricular tachycardia was greater in strophanthidin-treated ventricles than in controls, but induction of these repetitive ventricular beats in the strophanthidin group was virtually abolished by addition of 10(-5) M ryanodine. We conclude that release of SR Ca2+ via ryanodine-sensitive channels slightly enhances ventricular sensitivity toinduction of SIAs, but this process is not critical to initiation of SIAs, because ryanodine did not completely abolish such arrhythmias. This might occur by Ca2+-induced release of SR Ca2+, where triggering Ca2+ is transported via sarcolemmal stretch-activated channels. Oscillatory release of SR Ca2+ appears to be critical, however, in induction of repetitive ventricular beats by stretch under conditions of intracellular Ca2+ overload, because high-grade ventricular arrhythmias are blocked by ryanodine.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:05:38