Direct Effect of Halothane and Isoflurane on the Function of the Sarcoplasmic Reticulum in Intact Rabbit Atria

1990 ◽  
Vol 72 (4) ◽  
pp. 694-698 ◽  
Author(s):  
Hirochika Komai ◽  
Ben F. Rusy
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Direct Effect ◽  
Intact Rabbit ◽  
Rabbit Atria

scholarly journals Role of Reduced Sarco-Endoplasmic Reticulum Ca2+-ATPase Function on Sarcoplasmic Reticulum Ca2+ Alternans in the Intact Rabbit Heart

2021 ◽  
Vol 12 ◽  
Author(s):  
Lianguo Wang ◽  
Rachel C. Myles ◽  
I-Ju Lee ◽  
Donald M. Bers ◽  
Crystal M. Ripplinger
Keyword(s):  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Optical Mapping ◽  
Cyclopiazonic Acid ◽  
Rabbit Heart ◽  
Intracellular Ca ◽  
Cardiac Alternans ◽  
Intact Rabbit ◽  
Rapid Ventricular Pacing ◽  
Serca Inhibition

Sarcoplasmic reticulum (SR) Ca2+ cycling is tightly regulated by ryanodine receptor (RyR) Ca2+ release and sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ uptake during each excitation–contraction coupling cycle. We previously showed that RyR refractoriness plays a key role in the onset of SR Ca2+ alternans in the intact rabbit heart, which contributes to arrhythmogenic action potential duration (APD) alternans. Recent studies have also implicated impaired SERCA function, a key feature of heart failure, in cardiac alternans and arrhythmias. However, the relationship between reduced SERCA function and SR Ca2+ alternans is not well understood. Simultaneous optical mapping of transmembrane potential (Vm) and SR Ca2+ was performed in isolated rabbit hearts (n = 10) using the voltage-sensitive dye RH237 and the low-affinity Ca2+ indicator Fluo-5N-AM. Alternans was induced by rapid ventricular pacing. SERCA was inhibited with cyclopiazonic acid (CPA; 1–10 μM). SERCA inhibition (1, 5, and 10 μM of CPA) resulted in dose-dependent slowing of SR Ca2+ reuptake, with the time constant (tau) increasing from 70.8 ± 3.5 ms at baseline to 85.5 ± 6.6, 129.9 ± 20.7, and 271.3 ± 37.6 ms, respectively (p < 0.05 vs. baseline for all doses). At fast pacing frequencies, CPA significantly increased the magnitude of SR Ca2+ and APD alternans, most strongly at 10 μM (pacing cycle length = 220 ms: SR Ca2+ alternans magnitude: 57.1 ± 4.7 vs. 13.4 ± 8.9 AU; APD alternans magnitude 3.8 ± 1.9 vs. 0.2 ± 0.19 AU; p < 0.05 10 μM of CPA vs. baseline for both). SERCA inhibition also promoted the emergence of spatially discordant alternans. Notably, at all CPA doses, alternation of SR Ca2+ release occurred prior to alternation of diastolic SR Ca2+ load as pacing frequency increased. Simultaneous optical mapping of SR Ca2+ and Vm in the intact rabbit heart revealed that SERCA inhibition exacerbates pacing-induced SR Ca2+ and APD alternans magnitude, particularly at fast pacing frequencies. Importantly, SR Ca2+ release alternans always occurred before the onset of SR Ca2+ load alternans. These findings suggest that even in settings of diminished SERCA function, relative refractoriness of RyR Ca2+ release governs the onset of intracellular Ca2+ alternans.

Osmoregulation of atrial myocytic ANP release: osmotransduction via cross-talk between L-type Ca2+ channel and SR Ca2+ release

2004 ◽  
Vol 287 (5) ◽  
pp. R1101-R1109 ◽  
Author(s):  
Jing Yu Jin ◽  
Jin Fu Wen ◽  
Dan Li ◽  
Kyung Woo Cho
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cross Talk ◽  
Physiological Role ◽  
Dependent Manner ◽  
Channel Activity ◽  
Concentration Dependent Manner ◽  
The Cross ◽  
Rabbit Atria

Hyperosmolality has been known to increase ANP release. However, its physiological role in the regulation of atrial myocytic ANP release and the mechanism by which hyperosmolality increases ANP release are to be defined. The purpose of the present study was to define these questions. Experiments were performed in perfused beating rabbit atria. Hyperosmolality increased atrial ANP release, cAMP efflux, and atrial dynamics in a concentration-dependent manner. The osmolality threshold for the increase in ANP release was as low as 10 mosmol/kgH2O (∼3%) above the basal levels (1.55 ± 1.71, 17.19 ± 3.11, 23.15 ± 5.49, 54.04 ± 11.98, and 62.00 ± 13.48% for 10, 20, 30, 60, and 100 mM mannitol, respectively; all P < 0.01). Blockade of sarcolemmal L-type Ca2+ channel activity, which increased ANP release, attenuated hyperosmolality-induced increases in ANP release (−13.58 ± 4.68% vs. 62.00 ± 13.48%, P < 0.001) and cAMP efflux but not atrial dynamics. Blockade of the Ca2+ release from the sarcoplasmic reticulum, which increased ANP release, attenuated hyperosmolality-induced increases in ANP release (13.44 ± 7.47% vs. 62.00 ± 13.48%, P < 0.01) and dynamics but not cAMP efflux. Blockades of Na+-K+-2Cl− cotransporter, Na+/H+ exchanger, and Na+/Ca2+ exchanger had no effect on hyperosmolality-induced increase in ANP release. The present study suggests that hyperosmolality regulates atrial myocytic ANP release and that the mechanism by which hyperosmolality activates ANP release is closely related to the cross-talk between the sarcolemmal L-type Ca2+ channel activity and sarcoplasmic reticulum Ca2+ release, possibly inactivation of the L-type Ca2+ channels.

Mechanisms of cardiodepression by an Na+–H+ exchange inhibitor methyl-N-isobutyl amiloride (MIA) on the heart: lack of beneficial effects in ischemia–reperfusion injuryThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigators' Forum.

2007 ◽  
Vol 85 (1) ◽  
pp. 67-78 ◽  
Author(s):  
Harjot K. Saini ◽  
Vijayan Elimban ◽  
A. Tanju Ozcelikay ◽  
Naranjan S. Dhalla
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Function ◽  
Atpase Activity ◽  
Direct Effect ◽  
Positive Inotropic Effect ◽  
Ischemia Reperfusion ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Beneficial Effects ◽  
Intracellular Ca

Although Na+–H+ exchange (NHE) inhibitors such as methyl-N-isobutyl amiloride (MIA) are known to depress the cardiac function, the mechanisms of their negative inotropic effect are not completely understood. In this study, isolated rat hearts were perfused with MIA to study its action on cardiac performance, whereas isolated subcellular organelles such as sarcolemma, myofibrils, sarcoplasmic reticulum, and mitochondria were treated with MIA to determine its effect on their function. The effect of MIA on intracellular Ca2+ mobilization was examined in fura-2-AM-loaded cardiomyocytes. MIA was observed to depress cardiac function in a concentration-dependent manner in HCO3–-free buffer. On the other hand, MIA had an initial positive inotropic effect followed by a negative inotropic effect in HCO3–-containing buffer. MIA increased the basal concentration of intracellular Ca2+ ([Ca2+]i) and augmented the KCl-mediated increase in [Ca2+]i. MIA did not show any direct effect on myofibrils, sarcolemma, and sarcoplasmic reticulum ATPase activities; however, this agent was found to decrease the intracellular pH, which reduced the myofibrils Ca2+-stimulated ATPase activity. MIA also increased Ca2+ uptake by mitochondria without having any direct effect on sarcoplasmic reticulum Ca2+ uptake. In addition, MIA did not protect the hearts subjected to mild Ca2+ paradox as well as ischemia–reperfusion-mediated injury. These results suggest that the increase in [Ca2+]i in cardiomyocytes may be responsible for the initial positive inotropic effect of MIA, but its negative inotropic action may be due to mitochondrial Ca2+ overloading as well as indirect depression of myofibrillar Ca2+ ATPase activity. Thus the accumulation of [H+]i as well as occurrence of intracellular and mitochondrial Ca2+ overload may explain the lack of beneficial effects of MIA in preventing the ischemia–reperfusion-induced myocardial injury.

A Reproducible Selective Stain for Cardiac Sarcoplasmic Reticulum

1974 ◽  
Vol 32 ◽  
pp. 214-215
Author(s):  
R. A. Waugh ◽  
J. R. Sommer
Keyword(s):  
Complex System ◽  
Electron Microscope ◽  
Sarcoplasmic Reticulum ◽  
Transmission Electron Microscope ◽  
Electron Microscopic ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Transmission Electron

Cardiac sarcoplasmic reticulum (SR) is a complex system of intracellular tubules that, due to their small size and juxtaposition to such electron-dense structures as mitochondria and myofibrils, are often inconspicuous in conventionally prepared electron microscopic material. This study reports a method with which the SR is selectively “stained” which facilitates visualizationwith the transmission electron microscope.

Anchorfibers and the Topography of Junctional SR

1977 ◽  
Vol 35 ◽  
pp. 582-583
Author(s):  
James Junker ◽  
Joachim R. Sommer
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Single Filament ◽  
Relaxation Cycle ◽  
10 Nm Filaments ◽  
Junctional Sarcoplasmic Reticulum

Junctional sarcoplasmic reticulum (JSR) in all its forms (extended JSR, JSR of couplings, corbular SR) in both skeletal and cardiac muscle is always located at the Z - I regions of the sarcomeres. The Z tubule is a tubule of the free SR (non-specialized SR) which is consistently located at the Z lines in cardiac muscle (1). Short connections between JSR and Z lines have been described (2), and bundles of filaments at Z lines have been seen in skeletal (3) and cardiac (4) muscle. In opossum cardiac muscle, we have seen bundles of 10 nm filaments stretching across interfibrillary spaces and adjacent myofibrils with extensions to the plasma- lemma in longitudinal (Fig. 1) and transverse (Fig. 2) sections. Only an occasional single filament is seen elsewhere along a sarcomere. We propose that these filaments represent anchor fibers that maintain the observed invariant topography of the free SR and JSR throughout the contraction-relaxation cycle.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.

Electron Probe Analysis of Muscle

1982 ◽  
Vol 40 ◽  
pp. 398-401
Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Resting State ◽  
Binding Sites ◽  
Electron Probe ◽  
Frog Skeletal Muscle ◽  
Electron Probe Analysis ◽  
Probe Analysis

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.

Facial Likability and Smiling Enhance Cooperation, but Have No Direct Effect on Moralistic Punishment

2016 ◽  
Vol 63 (5) ◽  
pp. 263-277 ◽  
Author(s):  
Laura Mieth ◽  
Raoul Bell ◽  
Axel Buchner
Keyword(s):  
Conditional Probability ◽  
Direct Effect ◽  
Prisoner's Dilemma ◽  
Prisoner’S Dilemma ◽  
Prisoner’S Dilemma Game ◽  
Costly Punishment ◽  
Prisoner's Dilemma Game ◽  
Moralistic Punishment

Abstract. The present study serves to test how positive and negative appearance-based expectations affect cooperation and punishment. Participants played a prisoner’s dilemma game with partners who either cooperated or defected. Then they were given a costly punishment option: They could spend money to decrease the payoffs of their partners. Aggregated over trials, participants spent more money for punishing the defection of likable-looking and smiling partners compared to punishing the defection of unlikable-looking and nonsmiling partners, but only because participants were more likely to cooperate with likable-looking and smiling partners, which provided the participants with more opportunities for moralistic punishment. When expressed as a conditional probability, moralistic punishment did not differ as a function of the partners’ facial likability. Smiling had no effect on the probability of moralistic punishment, but punishment was milder for smiling in comparison to nonsmiling partners.

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