scholarly journals Predominant Negative Inotropic Effect of UTP on Dog Cardiac Muscle

1984 ◽  
Vol 35 (3) ◽  
pp. 334-337 ◽  
Author(s):  
Shigetoshi CHIBA ◽  
Miyoharu KOBAYASHI ◽  
Masahiro SHIMOTORI ◽  
Yasuyuki FURUKAWA
Keyword(s):  
Cardiac Muscle ◽  
Negative Inotropic Effect ◽  
Inotropic Effect

A comparison of cyclopiazonic acid and ryanodine effects on cardiac muscle relaxation

1993 ◽  
Vol 265 (4) ◽  
pp. H1364-H1372 ◽  
Author(s):  
N. Pery-Man ◽  
D. Chemla ◽  
C. Coirault ◽  
I. Suard ◽  
B. Riou ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Muscle Relaxation ◽  
Cyclopiazonic Acid ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Control Group ◽  
Total Force ◽  
Uptake Inhibition ◽  
Relaxant Effect ◽  
Isometric Twitch

We investigated cardiac muscle behavior after inhibition of either sarcoplasmic reticulum (SR) Ca2+ release or SR Ca2+ uptake. Mechanics of 35 rat papillary muscles were studied after either ryanodine 10(-7) M (n = 11) or cyclopiazonic acid (CPA) 10(-5) M (n = 14) and compared with a control group containing the solvent alone (n = 10). We measured the maximum extent of shortening (delta L) of the preloaded twitch (delta Lp), and the normalized total force (TF) of the full isometric twitch (TFi). The peak lengthening velocity (Vl) of the preloaded twitch (Vlp) and the normalized negative peak force derivative of the fully isometric twitch (-DFi) tested the lusitropic state. With the influence of shortening and/or load on relaxation taken into account, analysis of relaxation was performed using 1) Vlp-to-delta Lp and magnitude of -DFi-to-TFi ratios and 2) slopes of the Vl-delta L and magnitude of -DF-TF relationships over the entire continuum of load. Ca(2+)-release inhibition with ryanodine induced a negative inotropic effect and a decrease in Vlp from 2.7 +/- 0.2 to 1.4 +/- 0.2 Lmax/S, where Lmax is the initial length at the peak of the length-active tension curve (P < 0.001). The Vlp-to-delta Lp ratio and the slope of the Vl-delta L relationship were preserved, indicating that ryanodine was devoid of intrinsic relaxant effect under isotonic conditions. Ca(2+)-uptake inhibition with CPA had no inotropic effect but decreased Vlp from 2.9 +/- 0.1 to 2.2 +/- 0.1 Lmax/s (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Some Effects of Caffeine and Quinidine on Sarcoplasmic Reticulum of Skeletal and Cardiac Muscle

1973 ◽  
Vol 51 (7) ◽  
pp. 499-503 ◽  
Author(s):  
William R. Thorpe
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Myocardial Contractility ◽  
Gastrocnemius Muscle ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Experimental Conditions

Sarcoplasmic reticulum (SR) was prepared from the gastrocnemius muscle and the heart of freshly killed rabbits. It was found that the skeletal SR actively bound significantly more calcium than did the cardiac SR under the same experimental conditions. The effect of caffeine and quinidine on the release of calcium actively bound by both cardiac and skeletal SR was studied. Quinidine (10−3 M) released 4.1% of the calcium bound by skeletal SR and 27.7% of that bound by cardiac SR. Similarly, caffeine (20 mM) released 10.5% and 34.3% of the calcium bound by skeletal and cardiac SR, respectively. It is suggested that both caffeine and quinidine could produce contracture of skeletal muscle by acting on the SR and that caffeine could stimulate myocardial contractility through its action on the cardiac SR. However, it is unlikely that quinidine exerts its negative inotropic effect on the heart through its calcium releasing action on the cardiac SR.

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.

Effects of 2,3-butanedione monoxime on sarcoplasmic reticulum of saponin-treated rat cardiac muscle

1993 ◽  
Vol 265 (5) ◽  
pp. H1493-H1500 ◽  
Author(s):  
D. S. Steele ◽  
G. L. Smith
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Adenine Nucleotides ◽  
Direct Action ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Butanedione Monoxime ◽  
Net Release

We have studied the effects of 2,3-butanedione monoxime (BDM) on the sarcoplasmic reticulum (SR) of saponin-treated rat cardiac trabeculae. Rapid application of 20 mM caffeine released Ca2+ from the SR, which was detected using the fluorescent Ca2+ indicator indo 1. The amplitude of the caffeine-induced Ca2+ transient was used as an index of the Ca2+ content of the SR before, during, and after exposure to various concentrations of BDM. BDM (1-5 mM) had little effect on caffeine-induced Ca2+ release. At these levels of BDM, force was inhibited predominantly by a direct action of BDM on the myofilaments. However, with higher concentrations (5-30 mM), BDM caused a concentration-dependent decrease in the amount of Ca2+ released from the SR in response to caffeine. This action of BDM may contribute to the negative inotropic effect of the drug in intact cardiac preparations by reducing the amount of Ca2+ available for release during systole. Rapid application of BDM induced a net release of Ca2+ from the SR. Both BDM and caffeine-induced Ca2+ releases were abolished following treatment of the muscle with 10 microM ryanodine. BDM failed to release Ca2+ in the absence of ATP or after substitution of ATP with nonhydrolyzable adenine nucleotides. In contrast, caffeine released Ca2+ in the absence of ATP. The possible involvement of the Ca(2+)-uptake pump in the action of BDM on the SR is discussed.

Effect of ryanodine on cardiac muscle

1963 ◽  
Vol 204 (6) ◽  
pp. 975-978 ◽  
Author(s):  
Winifred G. Nayler
Keyword(s):  
Cardiac Muscle ◽  
Ethylenediaminetetraacetic Acid ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Ventricular Muscle ◽  
Tyrode Solution

Ryanodine (1 x 10–8 m) exerted a negative inotropic effect on toad ventricular muscle. The amplitude of contractions recorded from ryanodine-depressed ventricles were enhanced by raising the rate of stimulation, by increasing the extracellular Ca++ concentration, and by the addition of caffeine. The negative inotropic effect of ryanodine was reversed following perfusion with Tyrode solution containing 4 mm ethylenediaminetetraacetic acid.

scholarly journals Neuregulin-1 Induces a Negative Inotropic Effect in Cardiac Muscle

Circulation ◽  
2004 ◽  
Vol 109 (3) ◽  
pp. 324-326 ◽  
Author(s):  
Katrien Lemmens ◽  
Paul Fransen ◽  
Stanislas U. Sys ◽  
Dirk L. Brutsaert ◽  
Gilles W. De Keulenaer
Keyword(s):  
Cardiac Muscle ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Neuregulin 1

The negative inotropic effect of esmolol on isolated cardiac muscle

2005 ◽  
Vol 39 (4) ◽  
pp. 250-254 ◽  
Author(s):  
P. Arlock ◽  
B. Wohlfart ◽  
T. Sjöberg ◽  
S. Steen
Keyword(s):  
Cardiac Muscle ◽  
Negative Inotropic Effect ◽  
Inotropic Effect

Rat atrial muscle responses with caffeine: dose–response, force frequency, and postrest contractions

1992 ◽  
Vol 70 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Brian R. MacIntosh ◽  
Philip Posner ◽  
John Lobo ◽  
Randy Harms
Keyword(s):  
Cardiac Muscle ◽  
Low Frequency ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Response Force ◽  
Force Frequency ◽  
State Contraction ◽  
Frequency Of Stimulation ◽  
Negative Inotropic Response ◽  
Muscle Responses

Caffeine has been reported to have a positive and (or) a negative inotropic effect on cardiac muscle. In this study, the force-frequency and postrest characteristics of rat atrium were studied in the presence of caffeine (1.0–10 mM) to see if the interval between beats affected the response of cardiac muscle to caffeine. When stimulation frequency was 0.5 or 2.0 Hz, there was a positive followed by a negative inotropic response with 1, 5, or 10 mM caffeine. Incomplete relaxation occurred under these circumstances, giving rise to contracture. At low frequency of stimulation (0.1 Hz) caffeine had only a negative inotropic effect, and this effect was greater with 1 mM caffeine than with 5 mM caffeine. In the absence of caffeine, when stimulation at 0.5 or 3 Hz was interrupted, a pause of 2–20 s resulted in potentiation. When caffeine was present (2.0 mM), postrest potentiation was severely attenuated, but the steady-state contraction amplitude within the range 0.5–3.0 Hz was not different. These results are consistent with the hypothesis that caffeine induces a leak of Ca2+ from the sarcoplasmic reticulum, and this Ca2+ is extruded from the cell, possibly by Na+/Ca2+ exchange. Sarcoplasmic reticular uptake of Ca2+ and the translocation to release sites appear not to be affected by caffeine within 1–5 mM concentrations.Key words: contractility, excitation–contraction coupling, contraction, cardiac, rest potentiation.

Sign in / Sign up

Export Citation Format

Share Document