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Effects of rapid cooling on mechanical and electrical responses in ventricular muscle of guinea‐pig.
Author(s) -
Kurihara S,
Sakai T
Publication year - 1985
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1985.sp015650
Subject(s) - stimulation , extracellular , depolarization , contraction (grammar) , chemistry , biophysics , intracellular , membrane potential , muscle contraction , medicine , biochemistry , biology
The effect of rapidly lowering bathing solution temperature from 36.5 +/‐ 0.5 degrees C to various low temperatures was examined in guinea‐pig ventricular muscle to explore the possible role of intracellular Ca2+ store sites in excitation‐contraction coupling. Rapid cooling from 36.5 +/‐ 0.5 degrees C to below 18 degrees C caused contracture (rapid cooling contracture, r.c.c.) with subthreshold depolarization for contraction, if electrical stimulation was applied before cooling. R.c.c. peak tension depended on cooling temperature, and pre‐cooling stimulation frequency and duration. R.c.c. induced after pre‐cooling stimulation was enhanced by increased extracellular Ca2+ ( [Ca2+]o) and decreased by reduction of [Ca2+]o. Co2+ (2‐4 mM) added to the HEPES‐buffered Krebs solution, which suppressed the action potential plateau and inhibited twitch response, did not abolish r.c.c. after pre‐cooling stimulation at high frequency. Reduction of extracellular Na+ concentration ( [Na+]o) before cooling enhanced r.c.c., and even in non‐stimulated preparations, incubation in low [Na+]o below 68.8 mM for 20 min produced r.c.c. R.c.c. was superimposed on the tonic component of the K+ contracture, after a quiescent preparation has been depolarized beyond ‐40 mV by addition of solid KCl to normal Krebs solution. The relation between r.c.c. tension and membrane potential was shifted to the left along the voltage axis by reducing [Na+]o and shifted to the right by decreasing [Ca2+]o. Results suggest that well‐developed intracellular Ca2+ store sites could sequester enough Ca2+ to generate tension by an energy‐dependent process which had been loaded mainly by a voltage‐dependent Na+‐Ca2+ exchange mechanism and Ca2+ current, and that rapid cooling could cause Ca2+ release from the intracellular store sites with little contribution to membrane excitation in the guinea‐pig ventricular muscle.