Voltage-sensitive dye RH421 increases contractility of cardiac muscle

1998 ◽  
Vol 76 (12) ◽  
pp. 1146-1150 ◽  
Author(s):  
Yuanna Cheng ◽  
David R Wagoner ◽  
Todor N Mazgalev ◽  
Patrick J Tchou ◽  
Igor R Efimov
Keyword(s):  
Imaging Techniques ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Motion Artifacts ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Voltage Sensitive Dye ◽  
Cell Shortening ◽  
Rat Hearts ◽  
Butanedione Monoxime

Voltage-sensitive dyes and imaging techniques have proved to be indispensable tools for use in in vitro electrophysiological studies. To avoid motion artifacts in optical recordings, electromechanical uncouplers such as 2,3-butanedione monoxime (BDM) are required. In this study, we sought to determine whether the voltage-sensitive dye RH421 had an effect on the contractility of heart muscle, either alone or in the presence of BDM. Ventricular contractility was studied in (i) isolated rat myocytes and (ii) Langendorff-perfused rat hearts under control conditions, and during perfusion with RH421 or RH421 + BDM. The following results were obtained. (i) The amplitude of cell shortening increased progressively from 6.24 ± 0.64 to 9.95 ± 1.02 µm during 15 min of superfusion with 5 µM RH421 (n = 11), and further increased to 12.54 ± 0.97 µm during washout. In seven cells first perfused with 15 mM BDM and then with 15 mM BDM + 5 µM RH421, the amplitude of the cell shortening first decreased from 5.17 ± 0.51 to 0.41 ± 0.19 µm, then the amplitude increased to 2.63 ± 0.25 µm. (ii) Left ventricular pressure (LVP) of the heart (n = 7) was reduced by 15 mM BDM from 60.7 ± 2.5 to 2.8 ± 0.5 mmHg (1 mmHg = 133.3 Pa). LVP increased to 12.8 ± 1.1 mmHg during subsequent perfusion with 10 µM RH421 in the presence of BDM and did not change (LVP = 12.4 ± 2.4 mmHg) during washout of the dye. Therefore, RH421 increased the contractility of rat hearts and isolated myocytes with and without BDM.Key words: voltage-sensitive dye RH421, 2,3-butanedione monoxime, left ventricular pressure, cell shortening, contractility.

Cardiac Effects of Postconditioning Depend Critically on the Duration of Reperfusion and Reocclusion Episodes

2010 ◽  
Vol 13 (1) ◽  
pp. 52 ◽  
Author(s):  
Bruno Botelho Pinheiro ◽  
Alfredo In�cio Fiorelli ◽  
Otoni Moreira Gomes ◽  
Borut Gersak
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ischemic Postconditioning ◽  
Ventricular Pressure ◽  
Maximum Speed ◽  
P Value ◽  
Rat Hearts ◽  
Stabilization Period ◽  
Isolated Rat

Objective: The objective of the present study was to evaluate the effects of ischemic postconditioning on left ventricular function in isolated rat hearts.Methods: The hearts of 24 Wistar rats were were isolated, perfused immediately, and distributed into 3 groups: GI, control (n = 8); GII, three 10-second cycles of postconditioning (n = 8); and GIII, three 30-second cycles of postconditioning (n = 8). After a 15-minute stabilization period, all hearts underwent 20 minutes of global ischemia following 20 minutes of reperfusion. At times t0 (control), t5, t10, t15, and t20 (0, 5, 10, 15, and 20 minutes of reperfusion, respectively), we recorded the heart rate, coronary flow, systolic pressure, +(dP/dt)max (maximum speed of increase in the left ventricular pressure), and -(dP/dt)max (maximum speed of decrease in the left ventricular pressure). Data were analyzed by a 1-way analysis of variance, followed by the Tukey test; a P value .05); however, statistically significant differences in +(dP/dt)max between GII and GI and between GII and GIII occurred at t20 (GI, 1409.0 415.1 mm Hg/s; GII, 1917.3 403.0 mm Hg/s; GIII, 1344.8 355.8 mm Hg/s) (GII versus GI, P = .04; GII versus GIII, P = .02).Conclusion: Ischemic postconditioning with three 10-second cycles of reperfusion/reocclusion was demonstrated effective for preserving +(dP/dt)max in isolated rat hearts that underwent 20 minutes of ischemia following 20 minutes of reperfusion.

Muscle metaboreflex control of ventricular contractility during dynamic exercise

2006 ◽  
Vol 290 (2) ◽  
pp. H751-H757 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jong-Kyung Kim ◽  
Noreen F. Rossi ◽  
Larry W. Stephenson ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Rate Of Change ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Muscle Metaboreflex ◽  
Ventricular Elastance ◽  
Pressure Volume Relationship

When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicit reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP), termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance ( Emax), the slope of the end-systolic pressure-volume relationship, such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure. During both mild and moderate exercise, MMR activation increased Emax to 159.6 ± 8.83 and 155.8 ± 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise.

Endogenous adenosine inhibits catecholamine contractile responses in normoxic hearts

1986 ◽  
Vol 251 (2) ◽  
pp. H455-H462 ◽  
Author(s):  
J. G. Dobson ◽  
R. W. Ordway ◽  
R. A. Fenton
Keyword(s):  
Adenosine Deaminase ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Contractile Responses ◽  
Beta Adrenoceptor ◽  
Isolated Hearts ◽  
Endogenous Adenosine ◽  
Rat Hearts ◽  
Pressure Development

The importance of endogenous myocardial adenosine in attenuating catecholamine-elicited contractile responses was investigated in perfused oxygenated rat hearts. Perfusion of the isolated hearts with adenosine deaminase potentiated the isoproterenol-induced increases of three contractile variables (left ventricular pressure development and rates of both left ventricular pressure development and relaxation). The peak (maximal, within 30 s) and maintained (after 1 min) increases of the contractile variables caused by 10(-8) M isoproterenol were enhanced by 15-22 and 31-43%, respectively. Adenosine deaminase appeared in epicardial surface transudates of similarly perfused hearts, indicating that the enzyme had entered the myocardial interstitial space. Isoproterenol alone elevated the release of adenosine into coronary effluents of isoproterenol-stimulated hearts, and adenosine deaminase prevented the release of the nucleoside. The higher the level of adenosine in the effluent, the greater the reduction of the peak contractile variables. Phenylisopropyladenosine at 10(-8) M prevented the adenosine deaminase potentiation of 10(-9) M isoproterenol-induced contractile responses. The adenosine analogue at 10(-6) M blocked completely the isoproterenol-produced increases in the contractile variables. These results suggest that endogenous adenosine prevents full mechanical responsiveness to beta-adrenoceptor stimulation in the oxygenated myocardium. In addition, the findings support the notion that adenosine serves as an important negative feedback modulator in the oxygenated heart.

Statistical analysis of effect of anoxia on rate of change of ventricular pressure

1982 ◽  
Vol 53 (3) ◽  
pp. 726-730 ◽  
Author(s):  
C. George ◽  
M. T. Kopetzky
Keyword(s):  
Heart Rate ◽  
Analysis Of Variance ◽  
Repeated Measures ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Sprague Dawley

Hearts from 32 male Sprague-Dawley rats were studied to determine effects of anoxia on ventricular contractility. Maximum rate of ventricular pressure changes with time (Pmax) were obtained from simultaneous recordings of right and left ventricular pressure curves. Peak aortic flow and heart rate were measured. Anoxia was produced by 100% N2 respiration. Statistical models were repeated-measures analysis of variance and randomized block factorial analysis of variance. Alpha was 0.05. Heart rate during anoxia was significantly lower than during the 1st min of recovery. Heart rate during both these periods was significantly lower than in preanoxia or the remainder of recovery. Peak aortic flow was not significantly altered. In left ventricles positive Pmax was significantly higher than negative Pmax. In right ventricles positive and negative Pmax were not significantly different. Left ventricular Pmax was significantly depressed during anoxia, whereas right ventricular Pmax was not. Significant differences in pressure developed per mass of tissue was a possible source of variation in right (0.12 +/- 0.002 mmHg/mg) and left (0.16 +/- 0.009 mmHg/mg) ventricular contractile maintenance.

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