Effects of damaging the endocardial surface on the mechanical performance of isolated cardiac muscle.

Brutsaert, Dirk L.; Meulemans, Ann; Sipido, Karin R.; Sys, Stanislas U.

doi:10.1161/01.res.62.2.358

Cited by 247 publications

(107 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This procedure results in characteristic endocardial damage ( Figure 1) but does not damage subjacent myocardium either morphologically (determined by light microscopy and transmission electron microscopy) or functionally as assessed by maximal contractile performance at high extracellular calcium concentrations. 15 Similar changes in twitch performance are produced when the endocardium is damaged by gentle mechanical abrasion. 15 The integrity of the myocardium after either of these procedures is also indicated by an unaltered maximum velocity of unloaded shortening.…”

Section: Removal Of Functional Endocardiummentioning

confidence: 90%

“…The lower end of the muscle was held by a phosphor-bronze clip, and the upper tendinous end was attached to an electromagnetic lengthtension measuring and controlling transducer. 15 Muscles were stimulated electrically at 12 beats/min and by a voltage approximately 10% above threshold by rectangular pulses of 5-msec duration through two longitudinally arranged platinum electrodes. After stabilization for 2-3 hours at 290 C and with 2.5 mM Ca2+, experiments were performed at Lmax (the muscle length at which active force development was maximal) in Ringer's solution containing 1.25 mM ionized Ca2+ at 350 C.…”

Section: Cardiac Muscle Preparationsmentioning

confidence: 99%

“…15 Muscles were subsequently allowed to stabilize for at least 30 minutes. This procedure results in characteristic endocardial damage ( Figure 1) but does not damage subjacent myocardium either morphologically (determined by light microscopy and transmission electron microscopy) or functionally as assessed by maximal contractile performance at high extracellular calcium concentrations.…”

Section: Removal Of Functional Endocardiummentioning

confidence: 99%

“…We have recently shown that the endocardial endothelium can modulate the peak contractile performance and relaxation of subjacent myocardium in isolated mammalian cardiac muscle. 15 The presence of an intact endocardial endothelium results in a characteristic modulation of twitch contractions-a delayed onset of isometric tension decline and a concomitant increase in peak isometric tension but without any significant change in maximum velocity of unloaded shortening (Vmax) -particularly at a physiologic extracellular ionized calcium concentration (1.25 mM) and physiologic temperatures (35-37°C). This typical inotropic response differs from most other inotropic responses that also affect Vmax and that, in general, shorten twitch duration.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Myocardial inotropic responses to aggregating platelets and modulation by the endocardium.

1989

Self Cite

View full text Add to dashboard Cite

Ventricular mural thrombi complicate many cardiac diseases. The endocardial endothelium can modulate the mechanical performance of subjacent myocardium and mediate responses to certain physiopharmacologic agents. We studied the effects of aggregating platelets on the contractile performance of isolated cardiac muscle. The role of the endocardium was investigated by selectively damaging it by very brief (1 second) exposure to 1% Triton X-100 in some muscle preparations before experiments. Cat papillary muscles (n =54) were attached to an electromagnetic length-tension transducer in organ baths containing Krebs-Ringer solution (1.25 mM Ca2', 350 C), and stimulated electrically at 0.2 Hz. Homologous washed platelets (final concentration 3 x 10/l) aggregated spontaneously on addition to baths. Mechanical performance increased significantly more in muscles with damaged endocardium than in intact muscles (p<0.05); total peak isometric twitch tension increased by 31.8+7.8% (with damaged endocardium) and 11.8+2.6% (with intact endocardium), and peak isotonic twitch shortening increased by 36.7±7.8% (with damaged endocardium) and 9.6±2.0% (with intact endocardium). Increases in maximum velocity of unloaded shortening were similar in both muscle groups. Time to half isometric twitch tension decline decreased in intact muscles (3.6+1.0%/lo) but increased in Triton-treated muscles (2.5±1.3%, p=0.003 for difference between groups). The inotropic response to platelets in muscles with intact endocardium was unaltered by pretreatment of muscles with indomethacin (10 ,M) or by stimulation of platelet aggregation with thrombin (0.1 unit/ml). ATP (.10 ,M) produced significantly larger responses in muscles without intact endocardium compared with those with (p<0.05), at 50 puM increasing twitch tension by 14.0+3.4% (with damaged endocardium) and 4.7±2.8% (with intact endocardium). Responses to ADP (0.1-100 ,uM) were similar in the presence or absence of endocardium. 5-Hydroxytryptamine (.10 ,M) also produced significantly greater inotropic effects in Tritontreated muscles (p<0.01), at 30 ,uM increasing twitch tension by 107.3±19.5% (with damaged endocardium) compared with 37.3+±8.6% (with intact endocardium). 5-Hydroxytryptamine delayed isometric relaxation in Triton-treated muscles but induced an earlier onset in intact muscles. These results show that an intact endocardium diminishes and modulates myocardial contractile responses to aggregating platelets. This action was not dependent upon the production of prostacyclin. Inotropic responses to ATP and 5-hydroxytryptamine (but not ADP) were also reduced in the presence of an intact endocardium. In the intact heart, these responses could contribute to nonuniformity of contractile performance and therefore impair cardiac hemodynamic output. (Circulation 1989;79:1315-1323 V nentricular mural thrombi frequently occur in cardiac diseases such as ischemic heart disease and dilated and restrictive cardiomyopathies,1-5 often with spontaneous variations in size and shape.5 Like atrial thro...

show abstract

Section: Removal Of Functional Endocardiummentioning

confidence: 90%

Section: Cardiac Muscle Preparationsmentioning

confidence: 99%

Section: Removal Of Functional Endocardiummentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Myocardial inotropic responses to aggregating platelets and modulation by the endocardium.

1989

Self Cite

View full text Add to dashboard Cite

show abstract

“…Selective removal of the endocardial endothelium was performed according to the methodology described by Brutsaert and collaborators (Brutsaert et al, 1988). Briefly, this consisted in the immersion of the papillary muscles in a 0.5% solution of Triton X-100 during 1 s, followed by an abundant washout.…”

Section: Experimental Protocolsmentioning

confidence: 99%

Negative inotropic effect of selective AT2 receptor stimulation and its modulation by the endocardial endothelium

Castro-Chaves¹,

Soares²,

Fontes‐Carvalho³

et al. 2008

European Journal of Pharmacology

View full text Add to dashboard Cite

Angiotensin II is an octapeptide whose effects are mediated by two types of receptors. AT 1 receptors are responsible for the vasoconstrictor, positive inotropic and growth promoting properties, while AT 2 receptors have been linked to vasodilator and anti-mitogenic properties. In this study we investigated the effects of selective AT 2 receptor stimulation on myocardial contractility and lusitropy. Effects of selective AT 2 receptor activation were evaluated in rabbit right papillary muscles (n = 96) by adding increasing concentrations of H-9395, an AT 2 receptor agonist, alone or in presence of a selective AT 1 receptor antagonist (ZD-7155), or alternatively, by adding increasing concentrations of angiotensin II in presence of ZD-7155. In the latter conditions, selective AT 2 receptor activation was also performed in presence of NG-nitro-L-Arginine, indomethacin, proadifen, hydroxocobalamin, apamin plus charybdotoxin, Hoe-140 or PD-123,319, as well as, after endocardial endothelium removal. Selective AT 2 stimulation induced a negative inotropic and lusitropic effect in the first three protocols. This effect was completely abolished after selective removal of the endocardial endothelium and blunted in presence of Hoe-140, hydroxocobalamin, apamin plus charybdotoxin and PD-123,319, but maintained in presence of NG-nitro-L-Arginine, indomethacin or proadifen. Selective AT 2 receptor stimulation induces a negative inotropic and lusitropic effect, which is modulated by endocardial endothelium and mediated by bradykinin B 2 receptors through NO release and calcium dependent potassium channels activation. Such findings may help to better understand the therapeutic effects of selective AT 1 antagonists, which are increasingly used for treating cardiovascular diseases.

show abstract

Endothelial isoform of nitric oxide synthase in rat heart increases during development

Ursell

Mayes

1996

Anat. Rec.

View full text Add to dashboard Cite

Effects of damaging the endocardial surface on the mechanical performance of isolated cardiac muscle.

Cited by 247 publications

References 20 publications

Myocardial inotropic responses to aggregating platelets and modulation by the endocardium.

Myocardial inotropic responses to aggregating platelets and modulation by the endocardium.

Negative inotropic effect of selective AT2 receptor stimulation and its modulation by the endocardial endothelium

Endothelial isoform of nitric oxide synthase in rat heart increases during development

Contact Info

Product

Resources

About