SPONTANEOUS CONTRACTIONS IN RAT CARDIAC TRABECULAE - TRIGGER MECHANISM AND PROPAGATION VELOCITY

被引:29
作者
DANIELS, MCG [1 ]
TERKEURS, HEDJ [1 ]
机构
[1] UNIV CALGARY,HLTH SCI CTR,FAC MED,DEPT MED,3330 HOSP DR NW,CALGARY T2N 4N1,ALBERTA,CANADA
关键词
D O I
10.1085/jgp.95.6.1123
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
It has previously been observed that spontaneous contractions start in a region of damage of isolated right ventricular trabeculae of rat, propagate along the muscle, and induce triggered arrhythmias (Mulder, B.J.M., P.P. de Tombe, and H.E.D.J. ter Keurs. 1989. J. C, en. Physiol. 93:943-961). The present study was designed to analyze the mechanisms that lead to triggered propagated contractions (TPCs). TPCs were elicited in 29 trabeculae by stimulation with trains (2 Hz; 15-s intervals) at varied number of stimuli (n), lowered temperature (19-21°C and varied [Ca++]0 (1.5-4 mM) in the superfusate. Length (SL) and shortening of sarcomeres in the musde were measured at two sites using laser diffraction techniques; twitch force (Ft) was measured with a silicon strain gauge. Time between the last stimulus in the train and the onset of sarcomere shortening due to a TPC at a site close to the damaged end region (latency) and propagation velocity of the contraction (Vprop) were correlated with F t. For 10 trabeculae, TPCs were calculated to start in the end region itself 586 + 28 ms (mean ± 1 SEM) after the last stimulus of a train (n = 15; [Ca++]0: 1.5 mM), i.e., at the end of or after the rapid release of the damaged end during twitch relaxation. When Ft was increased by increasing either SL prior to stimulation or the afterload during twitches, methods that do not affect intracellular calcium levels, latency decreased, but Vprop remained constant. No TPC occurred when Ft was <20% of maximal Ft. Both increasing [Ca++]o and n increased Ft to a maximum, increased Vprop progressively (maximum Vprop, 17 mm/s), but decreased latency. These observations suggest that initiation of TPCs depends on the force developed by the preceding twitch, and therefore on the degree of stretch and subsequent rapid release of damaged areas in the myocardium, while Vprop along the trabeculae is determined by intracellular calcium concentration. © 1990, Rockefeller University Press., All rights reserved.
引用
收藏
页码:1123 / 1137
页数:15
相关论文
共 36 条
[11]   PRIMARY ROLE OF SARCOPLASMIC-RETICULUM IN PHASIC CONTRACTILE ACTIVATION OF CARDIAC MYOCYTES WITH SHUNTED MYOLEMMA [J].
CHIESI, M ;
HO, MM ;
INESI, G ;
SOMLYO, AV ;
SOMLYO, AP .
JOURNAL OF CELL BIOLOGY, 1981, 91 (03) :728-742
[12]  
CRANEFIELD PF, 1977, CIRC RES, V41, P416
[13]   VELOCITY OF SARCOMERE SHORTENING IN RAT CARDIAC-MUSCLE - RELATIONSHIP TO FORCE, SARCOMERE-LENGTH, CALCIUM AND TIME [J].
DANIELS, M ;
NOBLE, MIM ;
TERKEURS, HEDJ ;
WOHLFART, B .
JOURNAL OF PHYSIOLOGY-LONDON, 1984, 355 (OCT) :367-381
[14]  
FABIATO A, 1985, BASIC RES CARDIOL, V80, P83
[15]   EXCITATION-CONTRACTION COUPLING OF ISOLATED CARDIAC FIBERS WITH DISRUPTED OR CLOSED SARCOLEMMAS - CALCIUM-DEPENDENT CYCLIC AND TONIC CONTRACTIONS [J].
FABIATO, A ;
FABIATO, F .
CIRCULATION RESEARCH, 1972, 31 (03) :293-+
[16]   SPONTANEOUS TENSION OSCILLATIONS IN GUINEA-PIG ATRIAL TRABECULAE [J].
GLITSCH, HG ;
POTT, L .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1975, 358 (01) :11-25
[17]  
GOLOVINA V A, 1986, Biophysics (English Translation of Biofizika), V31, P311
[18]   ACTIVE SHORTENING RETARDS THE DECLINE OF THE INTRACELLULAR CALCIUM TRANSIENT IN MAMMALIAN HEART-MUSCLE [J].
HOUSMANS, PR ;
LEE, NKM ;
BLINKS, JR .
SCIENCE, 1983, 221 (4606) :159-161
[19]  
JANUARY CT, 1988, PHARMACOL REV, V40, P219
[20]   COMPARISON BETWEEN THE SARCOMERE LENGTH-FORCE RELATIONS OF INTACT AND SKINNED TRABECULAE FROM RAT RIGHT VENTRICLE - INFLUENCE OF CALCIUM CONCENTRATIONS ON THESE RELATIONS [J].
KENTISH, JC ;
TERKEURS, HEDJ ;
RICCIARDI, L ;
BUCX, JJJ ;
NOBLE, MIM .
CIRCULATION RESEARCH, 1986, 58 (06) :755-768