Positive inotropic effect of Streptococcus faecalis in isolated cardiac muscle

1994 ◽  
Vol 267 (6) ◽  
pp. H2450-H2461 ◽  
Author(s):  
I. E. Schoemaker ◽  
S. U. Sys ◽  
L. J. Andries ◽  
J. M. Meyers ◽  
S. R. Pattyn ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Positive Inotropic Effect ◽  
Mechanical Performance ◽  
Bacterial Colonization ◽  
Ringer Solution ◽  
Inotropic Effect ◽  
Maximal Velocity ◽  
Acute Effects ◽  
Before And After ◽  
Isometric Twitch

Infective endocarditis is caused by bacterial colonization of the endocardium. Because endocardium modulates mechanical performance of subjacent myocardium, we studied acute effects of bacteria on isolated cardiac muscle and on the functional role of the endocardium. Bacteria, grown in broth at 37 degrees C, were added at increasing concentrations (10(2) to 10(6) bacteria/ml) to cat papillary muscles in Krebs-Ringer solution (1.25 mM Ca2+, 35 degrees C). The endocardial surface was damaged by exposing muscles to a stream of dry air for 30 s. Streptococcus (Enterococcus) faecalis induced significant increases in total peak isometric twitch tension (TT) and maximal velocity of unloaded shortening (Vmax) and significant decreases in time to TT (TtTT) and time to half isometric twitch tension decline (RT 1/2), both before and after removal of endocardial endothelium. This response could also be elicited with bacterial filtrate, after boiling the filtrate or after extracting the polysaccharides from it with KIO4. Increasing Ca2+ concentrations progressively reduced the response to the filtrate. Propranolol slightly, although not significantly, diminished the effects on TT and Vmax while abolishing the effects on TtTT and on RT 1/2. By contrast, Streptococcus bovis and Staphylococcus aureus did not affect TT or Vmax but induced a slight but significant decrease in TtTT at the highest concentration of bacteria. Accordingly, the filtrate of Strep. faecalis induces a positive inotropic effect. The active component is neither a protein nor a polysaccharide, and its effect may be partly beta-adrenoceptor mediated. Strep. bovis and Staph. aureus have negligible acute effects on contractility.

Role of endocardial endothelium in positive inotropic action of vasopressin

1990 ◽  
Vol 259 (4) ◽  
pp. H1148-H1151 ◽  
Author(s):  
I. E. Schoemaker ◽  
A. L. Meulemans ◽  
L. J. Andries ◽  
D. L. Brutsaert
Keyword(s):  
Positive Inotropic Effect ◽  
Ringer Solution ◽  
Isometric Tension ◽  
Inotropic Effect ◽  
Endothelial Surface ◽  
Velocity Of Shortening ◽  
Before And After ◽  
Triton X ◽  
Endocardial Endothelium

We have studied the effects of vasopressin on isolated cat papillary muscle both before and after damaging the endocardium. The experiments were performed in physiological conditions of temperature (35 degrees C) and calcium concentration (1.25 mM Ca2+). Isometric and isotonic twitches as well as maximal unloaded velocity of shortening (Vmax) were measured. In muscles with an intact endocardium (n = 13), vasopressin (10(-12) to 10(-6) M) induced early twitch relaxation with a significant reduction of time to half isometric tension decline and with concomitant significant decrease in peak twitch performance. In a second group of muscles (n = 13) the endocardial endothelial surface was damaged by briefly (1 s) exposing the muscles to a 0.5% Triton X-100 followed by abundant wash with Krebs-Ringer solution, thereby irreversibly decreasing time to half twitch relaxation and peak twitch tension without significantly affecting Vmax. After this intervention, vasopressin had a positive inotropic effect with a significant increase in peak twitch tension and Vmax with no significant changes in twitch duration. Accordingly, in the presence of a functional endocardium, the direct myocardial positive inotropic effect of vasopressin was reversed, with early twitch relaxation and diminished peak twitch performance. At the highest concentrations of vasopressin, vasopressin-induced functional and morphological damage of the endocardium was observed.

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)

Endothelin-Mediated Positive Inotropic Effect Induced by Reactive Oxygen Species in Isolated Cardiac Muscle

1995 ◽  
Vol 76 (5) ◽  
pp. 878-884 ◽  
Author(s):  
Gilles W. De Keulenaer ◽  
Luc J. Andries ◽  
Stanislas U. Sys ◽  
Dirk L. Brutsaert
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Muscle ◽  
Positive Inotropic Effect ◽  
Reactive Oxygen ◽  
Inotropic Effect ◽  
Oxygen Species

ET-1 increases distensibility of acutely loaded myocardium: a novel ETA and Na+/H+exchanger-mediated effect

2003 ◽  
Vol 284 (4) ◽  
pp. H1332-H1339 ◽  
Author(s):  
Adelino F. Leite-Moreira ◽  
Carmen Brás-Silva ◽  
Carla A. Pedrosa ◽  
Amândio A. Rocha-Sousa
Keyword(s):  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Papillary Muscles ◽  
Similar Extent ◽  
Endothelin 1 ◽  
Resting Tension ◽  
Isometric Twitch

This study investigated, in rabbit papillary muscles ( n = 61) and human auricular strips ( n = 7), effects of endothelin-1 (ET-1; 0.1–10 nM) on diastolic myocardial properties. ET-1 (1 nM) was also given in the presence of selective ETA or ETB antagonism, nonselective ETA/ETB antagonism, and Na+/H+ exchanger inhibition. Effects of 6.3 mM Ca2+ were also studied. ET-1 dose dependently increased inotropism. In contrast to baseline, in the presence of ET-1, resting tension (RT) decreased, after an isometric twitch, 3.4 ± 1.4, 6.9 ± 1.5, and 12.5 ± 3.1% with 0.1, 1, and 10 nM, respectively, reflecting an increase in myocardial distensibility. ET-1 effects were abolished with selective ETA as well as with nonselective ETA/ETB antagonism, whereas they were still present with ETB antagonism. Na+/H+ exchanger inhibition abolished ET-1 effects on distensibility, whereas it only partially inhibited positive inotropic effect. Ca2+ increased inotropism to a similar extent to ET-1 (1 nM) but did not affect distensibility. ET-1 therefore increased diastolic distensibility of acutely loaded human and nonhuman myocardium. This effect is mediated by ETA receptors, requires Na+/H+ exchanger activation, and cannot be elicited by Ca2+.

200 years of digitalis: the emerging central role of the sodium ion in the control of cardiac force

1985 ◽  
Vol 249 (5) ◽  
pp. C367-C378 ◽  
Author(s):  
C. O. Lee
Keyword(s):  
Cardiac Muscle ◽  
Time Course ◽  
Positive Inotropic Effect ◽  
Quantitative Relationship ◽  
Complete Recovery ◽  
Contractile Force ◽  
Inotropic Effect ◽  
Parallel Increase ◽  
Small Rise ◽  
High Concentrations

Digitalis has been used therapeutically for two centuries, but the mechanism by which it enhances the ability of cardiac muscle to produce force (the positive inotropic effect) has not been fully elucidated. The major controversy concerns the question of whether the inhibition of the Na+-K+ pump by digitalis, particularly at low (therapeutic) concentrations, increases the intracellular Na+ concentration and thus is causally related to the positive inotropic effect. Na+-selective microelectrodes, introduced recently, have made it possible to measure small changes in intracellular Na+ activity (aiNa) in beating preparations of cardiac muscle and, in particular, to follow the exact time course of change in both aiNa and contractile force during the positive inotropic effect of digitalis. It has been demonstrated that digitalis at low and high concentrations produces a parallel increase in aiNa and in contractile force during the onset of its effect; washout of the drug results in a parallel and complete recovery of aiNa and contractile force. Additional strong evidence for a correlation between the pump inhibition and digitalis inotropy is the fact that the magnitude of increase in aiNa and contractile force produced by digitalis depends on the level of aiNa and therefore on the rate of Na+ extrusion by the Na+-K+ pump. The study on the quantitative relationship between aiNa and contractile force reveals that the force of contraction is a power function of aiNa, such that a small rise in aiNa produces a significant increase in contractile force. Direct measurements of aiNa and intracellular free Ca2+ during digitalis inotropy strongly support the hypothesis that an increase in aiNa raises intracellular Ca2+ via Na+-Ca2+ exchange, thus producing the positive inotropic effect. In conclusion, the recent data available from the simultaneous and continuous measurements of aiNa and contractile force strongly indicate that the inhibition of the Na+-K+ pump is causally related to the positive inotropic effect of digitalis on cardiac muscle.

scholarly journals BINDING SITE OF OUABAIN IN CARDIAC MUSCLE CELL AND ITS POSITIVE INOTROPIC EFFECT IN CAT

1971 ◽  
Vol 21 (3) ◽  
pp. 423-425 ◽  
Author(s):  
Sumiko FUJINO ◽  
Shunsaku KAWAGISHI ◽  
Noriyasu EGUCHI ◽  
Mamoru TANAKA
Keyword(s):  
Cardiac Muscle ◽  
Binding Site ◽  
Muscle Cell ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Cardiac Muscle Cell
Sign in / Sign up

Export Citation Format

Share Document