Myocardial stretch alters twitch characteristics and Ca2+ loading of sarcoplasmic reticulum in rat ventricular muscle

1992 ◽  
Vol 26 (9) ◽  
pp. 865-870 ◽  
Author(s):  
J. Gamble ◽  
P. B. Taylor ◽  
K. A. Kenno
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Muscle ◽  
Myocardial Stretch ◽  
Twitch Characteristics

Doxorubicin-induced late cardiotoxicity: delayed impairment of Ca2+-handling mechanisms in the sarcoplasmic reticulum in the rat

2000 ◽  
Vol 78 (4) ◽  
pp. 329-338 ◽  
Author(s):  
Akihito Chugun ◽  
Kyosuke Temma ◽  
Toshifumi Oyamada ◽  
Natsuyo Suzuki ◽  
Yoshinori Kamiya ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Left Atrial ◽  
Force Frequency ◽  
Ventricular Muscle ◽  
Doxorubicin Treatment ◽  
Time To Peak ◽  
Atrial Muscle ◽  
Late Cardiotoxicity ◽  
Cardiac Functions ◽  
Rat Hearts

Doxorubicin treatment causes delayed development of cardiotoxicity. Whether the doxorubicin-induced impairment of cardiac functions reverses or progresses with time after the cessation of the treatment was examined. The rats were injected with doxorubicin (2.5 mg/kg, i.v., once a week for 3 weeks) and sacrificed at 1 (1W), 13 (13W), or 18 (18W) weeks after the final doxorubicin administration. The time to peak of twitch contraction observed at 2-Hz stimulation was not altered in left atrial or ventricular muscle preparations isolated from 1W rats, but it was prolonged in those from 13W and 18W rats. The reduction of the magnitude of postrest contraction and the alteration of force-frequency relationships in left atrial muscle preparations in 1W rats were not significant, but were intensified in the 13W and 18W groups. Alterations in the postrest contraction and the force-frequency relationships in ventricular muscle preparations isolated from doxorubicin-treated rat hearts were weaker, but the pattern of alteration was similar to that observed in left atrial muscle preparations. Caffeine-induced contraction observed in skinned fibers that were isolated from the 1W rats was not altered, but it was reduced in the 18W rats. The Ca2+ sensitivity of contractile proteins was not altered in doxorubicin-treated rat hearts in any of the groups. The Kd values estimated from a [3H]ryanodine binding study were not altered, but the Bmax values were significantly lower in the 13W and 18W groups than those observed in control rats. These results suggest that the dysfunction of the sarcoplasmic reticulum progresses after the completion of doxorubicin treatment and contributes to the doxorubicin-induced late cardiotoxicity.Key words: doxorubicin, late cardiotoxicity, rat heart, sarcoplasmic reticulum.

Loading of Calcium and Strontium into the Sarcoplasmic Reticulum in Rat Ventricular Muscle

2000 ◽  
Vol 32 (7) ◽  
pp. 1285-1300 ◽  
Author(s):  
C.Ian Spencer ◽  
Robert J Barsotti ◽  
Joshua R Berlin
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Muscle

The distribution of calsequestrin in rat myocardial sarcoplasmic reticulum

1984 ◽  
Vol 42 ◽  
pp. 712-713
Author(s):  
A. O. Jorgensen ◽  
A. C.-Y. Shen ◽  
K. P. Campbell ◽  
G. Denney
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Muscle ◽  
Myocardial Cells ◽  
Transverse Tubules ◽  
Purkinje Fibers ◽  
Immunofluorescence Localization ◽  
Band Region ◽  
Junctional Sarcoplasmic Reticulum

We have previously identified and purified calsequestrin from canine ventricular muscle. Immunofluorescence localization suggested that cardiac calsequestrin is confined to the lumen of the interior and peripheral junctional sarcoplasmic reticulum (SR) in adult mammalian ventricular myocardial cells. Immunolocalization of calsequestrin in myocardial cells without transverse tubules (chicken ventricular myocardial cells and sheep Purkinje fibers) clearly showed that calsequestrin as predicted was present in the lumen of peripheral junctional SR but absent from the lumen of the network SR. However, in addition calsequestrin was also present in the lumen of the corbular SR, bulbous ends on the network SR mostly confined to the I band region of myocardial cells.

The mechanism of ryanodine action in rabbit ventricular muscle evaluated with Ca-selective microelectrodes and rapid cooling contractures

1987 ◽  
Vol 65 (4) ◽  
pp. 610-618 ◽  
Author(s):  
Donald M. Bers ◽  
John H. B. Bridge ◽  
Kenneth T. MacLeod
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Extracellular Space ◽  
Repetitive Stimulation ◽  
Ventricular Muscle ◽  
Half Time ◽  
Rapid Cooling ◽  
Ca Uptake ◽  
Rabbit Ventricular Muscle ◽  
Independent Assay ◽  
Cellular Ca

Cellular Ca uptake and efflux in rabbit ventricular muscle was measured using double-barreled Ca microelectrodes in the extracellular space. When repetitive stimulation was stopped there was a slow loss of cellular Ca. Upon resumption of stimulation Ca was taken up by the cells. These Ca movements are thought to represent the loss of Ca from the sarcoplasmic reticulum and the cell during rest and the refilling of the sarcoplasmic reticulum during stimulation. Ryanodine (100 nM) greatly enhanced both the efflux of Ca during rest and the uptake of Ca induced by stimulation. These results are consistent with the conclusions drawn below, but they are dependent upon the interpretation that these extracellular Ca depletions are indicative of sarcoplasmic reticulum Ca movements. To examine further this process, contractures induced by rapid cooling to 0 °C were used as an independent assay of sarcoplasmic reticulum Ca content. These rapid cooling contractures were smaller after longer rest intervals (declining with a half time of 1.5 min). In the presence of ryanodine, the rapid cooling contracture immediately after a contraction was greater than that seen under control conditions. However, in the presence of ryanodine these rapid cooling contractures decline as a function of rest duration with a half time of about 1 s. These results suggest that in the presence of ryanodine the sarcoplasmic reticulum can still take up Ca, but that it also loses this Ca very rapidly at the onset of rest. Caffeine (20 mM) inhibits both the extracellular Ca depletions and the rapid cooling contractures that are attributed to the sarcoplasmic reticulum Ca content changes (in the presence or absence of ryanodine). These results suggest the following two actions of ryanodine: (i) inhibition of sarcoplasmic reticulum Ca release into the cytoplasm upon activation, and (ii) enhancement of Ca loss from the sarcoplasmic reticulum upon the termination of stimulation and extrusion from the cell without activation of appreciable tension.

scholarly journals Relationships between the sarcoplasmic reticulum and sarcolemmal calcium transport revealed by rapidly cooling rabbit ventricular muscle.

1986 ◽  
Vol 88 (4) ◽  
pp. 437-473 ◽  
Author(s):  
J H Bridge
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Transport ◽  
Fourier Spectrum ◽  
Papillary Muscles ◽  
Ventricular Muscle ◽  
Relative Index ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Muscle Cooling ◽  
Rabbit Ventricular Muscle

Rabbit right ventricular papillary muscles were cooled from 30 to approximately 1 degree C immediately after discontinuing electrical stimulation (0.5 Hz). This produced a contracture that was 30-50% of the preceding twitch magnitude and required 20-30 s to develop. The contractures were identical in cooling solutions with normal (144 mM) or low (2.0 mM) Na. They were therefore not Na-withdrawal contractures. Contracture activation was considerably slower than muscle cooling (approximately 2.5 s to cool below 2 degrees C). Cooling contractures were suppressed by caffeine treatment (10.0 mM). Rapid cooling did not cause sufficient membrane depolarization (16.5 +/- 1.2 mV after 30 s of cooling) to produce either a voltage-dependent activation of contracture or a gated entry of Ca from the extracellular space. Contractures induced by treating resting muscles with 5 X 10(-5) M strophanthidin at 30 degrees C exhibited pronounced tension noise. The Fourier spectrum of this noise revealed a periodic component (2-3 Hz) that disappeared when the muscle was cooled. Cooling contractures decayed with rest (t1/2 = 71.0 +/- 9.3 s). This decay accelerated in the presence of 10.0 mM caffeine and was prevented and to some extent reversed when extracellular Na was reduced to 2.0 mM. 20 min of rest resulted in a net decline in intracellular Ca content of 1.29 +/- 0.38 mmol/kg dry wt. I infer that cooling contractures are principally activated by Ca from the sarcoplasmic reticulum (SR). The properties of these contractures suggest that they may provide a convenient relative index of the availability of SR Ca for contraction. The rest decay of cooling contractures (and hence the decay in the availability of activating Ca) is consistent with the measured loss in analytic Ca during rest. The results suggest that contraction in heart muscle can be regulated by an interaction between sarcolemmal and SR Ca transport.

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