Effects of Volatile Anesthetics on the Intracellular Calcium Transient and Calcium Current in Cardiac Muscle Cells

1991 ◽  
pp. 97-107 ◽  
Author(s):  
Zeljko J. Bosnjak
Keyword(s):  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Calcium Current ◽  
Calcium Transient ◽  
Muscle Cells ◽  
Volatile Anesthetics ◽  
Cardiac Muscle Cells ◽  
Intracellular Calcium Transient

Effect of membrane potential changes on the calcium transient in single rat cardiac muscle cells

Science ◽  
1987 ◽  
Vol 238 (4832) ◽  
pp. 1419-1423 ◽  
Author(s):  
M. Cannell ◽  
Berlin ◽  
W. Lederer
Keyword(s):  
Membrane Potential ◽  
Cardiac Muscle ◽  
Calcium Transient ◽  
Muscle Cells ◽  
Cardiac Muscle Cells

Effects of Sevoflurane on the Intracellular Ca2+Transient in Ferret Cardiac Muscle

2000 ◽  
Vol 93 (6) ◽  
pp. 1500-1508 ◽  
Author(s):  
Anna E. Bartunek ◽  
Philippe R. Housmans
Keyword(s):  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Negative Inotropic Effect ◽  
Calcium Transient ◽  
Ventricular Myocardium ◽  
Peak Force ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Intracellular Calcium Transient

Background Sevoflurane depresses myocardial contractility by decreasing transsarcolemmal Ca2+ influx. In skinned muscle fibers, sevoflurane affects actin-myosin cross-bridge cycling, which might contribute to the negative inotropic effect. It is uncertain to what extent decreases in Ca2+ sensitivity of the contractile proteins play a role in the negative inotropic effect of sevoflurane in intact cardiac muscle tissue. The aim of this study was to assess whether sevoflurane decreases myofibrillar Ca2+ sensitivity in intact living cardiac fibers and to quantify the relative importance of changes in myofibrillar Ca2+ sensitivity versus changes in myoplasmic Ca2+ availability by sevoflurane. Methods The effects of sevoflurane 0-4.05% vol/vol (0-1.5 minimum alveolar concentration [MAC]) on isometric and isotonic variables of contractility and on the intracellular calcium transient were assessed in isolated ferret right ventricular papillary muscles microinjected with the Ca2+-regulated photoprotein aequorin. The intracellular calcium transient was analyzed in the context of a multicompartment model of intracellular Ca2+ buffers in mammalian ventricular myocardium. Results Sevoflurane decreased contractility, time to peak force, time to half isometric relaxation, and the [Ca2+]i transient in a reversible, concentration-dependent manner. Increasing [Ca2+]o in the presence of sevoflurane to produce peak force equal to control increased intracellular Ca2+ transient higher than control. Conclusions Sevoflurane decreases myoplasmic Ca2+ availability and myofibrillar Ca2+ sensitivity in equal proportions except at 4.05% vol/vol (1.5 MAC), where Ca2+ availability is decreased more. These changes are at the basis of the negative inotropic effect of sevoflurane in mammalian ventricular myocardium.

Abstract 5403: Protein Kinase C-Induced Troponin I Phosphorylation Causes Changes in Cardiac Contractile Function but not the Intracellular Calcium Transient

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jonathan A Kirk ◽  
Stephen H Smith ◽  
Guy A MacGowan ◽  
Sanjeev G Shroff
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Troponin I ◽  
Contractile Function ◽  
Calcium Transient ◽  
Kinase C ◽  
Intracellular Calcium Transient ◽  
Muscle Contractile

Both intracellular calcium transients ([Ca] i ) and myofilament properties determine cardiac muscle contractile force. Transgenic mouse models created to perturb specific myofilament proteins often cause a compensatory change in [Ca] i , which confounds the assessment of myofilament structure-function relationships. We have created a new transgenic mouse that has all three protein kinase C (PKC) phosphorylation sites on cardiac troponin I (cTnI) mutated to glutamic acid, rendering these sites constitutively pseudo-phosphorylated. Our goal was to determine the effects of this mutation on cardiac muscle contractile function and whether these effects would be concurrent with changes in the [Ca] i . Two sets of studies were conducted: skinned muscle fiber experiments to characterize the steady-state force-pCa relationships at sarcomere lengths of 1.9 and 2.3 μm and right ventricular papillary muscle experiments to characterize the peak developed force (F dev )-muscle length (L) relationships and [Ca] i (fura-5F calcium dye, emission: 510 nm, excitation: 340 and 380 nm, R = [emission fluorescence 340 ]/[emission fluorescence 380 ]). In skinned fibers, there was a significant decrease in maximally activated force (i.e., force at pCa 4.33) in transgenic mice (Wild-Type, WT (n = 7): 64.4± 8.0, Transgenic, TG (n = 6): 42.6±6.8 mN•mm −2 , P = 0.004), without any changes in calcium sensitivity or cooperativity (Hill coefficient). In intact papillary muscles, TG mice showed a decrease in F dev and slowed relaxation for all muscle lengths examined (F dev @ 100% L max , WT (n = 5): 9.3±3.5, TG (n = 6): 4.2±1.6 mN•mm −2 , P = 0.005; dF/dt min @ 100% L max , WT: −136±32, TG: −74±38 mN•mm −2 •s −1 , P = 0.002). In contrast, [Ca] i was unaltered in TG mice at all muscle lengths examined ([Ca] i amplitude as quantified by R systole / R diaastole , WT: 1.62±0.07, TG: 1.48±0.22; [Ca] i relaxation rate d R /dt min , WT: −96±37, TG: −64±30 s −1 ). Thus, PKC-induced TnI phosphorylation affects cardiac muscle contraction (reduced force magnitude and slowed relaxation) via changes in the myofilament properties (activation and/or crossbridge dynamics), and these contractile effects are not related to any changes in the intracellular calcium transient.

THE EFFECTS OF ACUPUNCTURE ON CARDIAC MUSCLE CELLS AND BLOOD PRESSURE IN SPONTANEOUS HYPERTENSIVE RATS

2004 ◽  
Vol 29 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Hung-Chien Wu ◽  
Jaung-Geng Lin ◽  
Chun-Hsien Chu ◽  
Yung-Hsien Chang ◽  
Chung-Gwo Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Hypertensive Rats ◽  
Cardiac Muscle Cells
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