scholarly journals Staircase, rest contractions, and potentiation in the isolated rat heart

1962 ◽  
Vol 202 (4) ◽  
pp. 636-640 ◽  
Author(s):  
F. L. Meijler
Keyword(s):  
Cycle Length ◽  
Rest Period ◽  
Isolated Rat Heart ◽  
Stimulation Rate ◽  
Rat Hearts ◽  
Constant Rate ◽  
Theoretical Evidence ◽  
The Relationship ◽  
Isotonic Contractions ◽  
Isolated Rat

Variation in amplitude of isotonic contractions of intact isolated rat hearts, following changes in cycle length, were studied. It was found that a staircase-like phenomenon resembling the original Bowditch effect cannot be evoked in a intact mammalian heart without special measures, such as adding acetylcholine to the perfusion fluid. A steady state relation of rate to amplitude of isotonic contractions was demonstrated. Potentiation of contractility can be originated by sudden changes in stimulation rate. A rest period preceding the changes in stimulation rate does not change the potentiation found originally. At a constant rate the amplitude of a contraction is determined by the preceding cycle length. This relation has been called restitution. Theoretical evidence is presented in an attempt to demonstrate that restitution and potentiation are due to the same process. It can be concluded that Bowditch's staircase does not play a role in the relationship between cycle length and contractility in intact hearts and the statement that restitution and potentiation are due to the same process offers an opportunity to describe all effects of changes in cycle length on isotonic contractions as one phenomenon.

Influence of monoamine oxidase inhibitor on contractility of isolated rat hearts

1962 ◽  
Vol 202 (6) ◽  
pp. 1152-1154 ◽  
Author(s):  
F. L. Meijler ◽  
D. Durrer
Keyword(s):  
Monoamine Oxidase ◽  
Cycle Length ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Metabolic Process ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Isotonic Contractions ◽  
Isolated Rat ◽  
Isolated Perfused Rat Hearts

Following the suggestion that monoamine oxidase inhibitor might interfere with potentiation of cardiac contractions, the influence of 1-iso-nicotinyl-2-isopropyl-hydrazide and 1-pivaloyl-2-benzyl-hydrazine on postextrasystolic increase of isotonic contractions in isolated perfused rat hearts was studied. It was found that monoamine oxidase inhibitor did not change the increase in contractility following an interpolated or a noninterpolated premature beat. The metabolic process by which cardiac muscle varies its contractility with varying cycle length remains unknown.

Ischemic preconditioning translocates PKC-δ and -ε, which mediate functional protection in isolated rat heart

1998 ◽  
Vol 275 (6) ◽  
pp. H2266-H2271 ◽  
Author(s):  
Shuji Kawamura ◽  
Ken-Ichi Yoshida ◽  
Toshiro Miura ◽  
Yoichi Mizukami ◽  
Masunori Matsuzaki
Keyword(s):  
Cardiac Function ◽  
Ischemic Preconditioning ◽  
Rat Heart ◽  
Membrane Fraction ◽  
Isolated Rat Heart ◽  
Kinase C ◽  
Rat Hearts ◽  
Pkc Isoforms ◽  
The Relationship ◽  
Isolated Rat

Protein kinase C (PKC) plays an important role in mediating ischemic preconditioning (PC). However, the relationship between PKC isoforms and PC is still uncertain. We analyzed subcellular localization of PKC isoforms by Western blot analysis in isolated rat heart and demonstrate that PKC-α, -δ, and -ε were translocated to the membrane fraction associated with the improvement of cardiac function. Translocation of PKC-δ and -ε persisted after a 30-min period following PC, but the translocation of PKC-α was transient. Under low Ca2+ perfusion (0.2 mmol/l), PC improved the cardiac function associated with the translocation of PKC-δ. Chelerythrine (1.0 μmol/l) suppressed the translocation of all PKC isoforms associated with the loss of improvement of the cardiac function. On the other hand, bisindolylmaleimide (0.1 μmol/l) did not inhibit the improvement of cardiac function induced by PC, which was associated with the translocation of PKC-ε. These results indicate that the effect of PC on cardiac function is mediated by the translocation of either PKC-δ or -ε independently in rat hearts.

Ischemia-induced and reperfusion-induced arrhythmias: importance of heart rate

1989 ◽  
Vol 256 (1) ◽  
pp. H21-H31 ◽  
Author(s):  
M. Bernier ◽  
M. J. Curtis ◽  
D. J. Hearse
Keyword(s):  
Heart Rate ◽  
Coronary Occlusion ◽  
Ischemia And Reperfusion ◽  
Rate Of Development ◽  
Rate Dependent ◽  
Rat Hearts ◽  
Wide Range ◽  
The Right ◽  
The Relationship ◽  
Isolated Rat

The relationship between heart rate and ischemia-induced and reperfusion-induced arrhythmias was studied using 573 isolated rat hearts. Hearts (12/group), subjected to 7 min of coronary occlusion and 10 min reperfusion, were paced at 300, 330, 360, 390, 420, 480, or 540 beats/min. Pacing either throughout the experiment or during ischemia alone led to a rate-dependent increase in the incidence of reperfusion-induced ventricular fibrillation (VF) from 25% in the unpaced hearts to greater than 90% when the rate was 420 beats/min or higher. However, pacing during reperfusion alone did not increase the incidence of reperfusion-induced VF. In separate hearts, the right atrium was removed to permit examination of both low and high rates (167 +/- 2, 240, 336 +/- 3, or 480 beats/min throughout the experiment) over a wide range of durations of occlusion (3, 5, 7, 10, 15, 20, or 40 min). Ischemia-induced VF incidence was critically dependent on heart rate, low rates being protective. During reperfusion, the incidence of VF was also highly rate dependent if reperfusion was initiated within 10 min of the onset of ischemia (ranging from 8% when rate was 167 +/- 2 beats/min to 100% when rate was 480 beats/min) but was unrelated to heart rate when reperfusion occurred at later times (ranging from 33 to 50% when ischemia duration was 40 min). Heart rate can therefore influence susceptibility to ischemia- and reperfusion-induced arrhythmias, probably as a result of an effect on the rate of development of ischemic injury.

Detection of Cardiac Variability in the Isolated Rat Heart

2006 ◽  
Vol 8 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Autumn M. Schumacher ◽  
Joseph P. Zbilut ◽  
Charles L. Webber ◽  
Dorie W. Schwertz ◽  
Mariann R. Piano
Keyword(s):  
Rat Heart ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Rat Hearts ◽  
Before And After ◽  
Quantification Analysis ◽  
Physical Attributes ◽  
Cardiac Variability ◽  
Isolated Rat

Cardiac variability can be assessed from two perspectives: beat-to-beat performance and continuous performance during the cardiac cycle. Linear analysis techniques assess cardiac variability by measuring the physical attributes of a signal, whereas nonlinear techniques evaluate signal dynamics. This study sought to determine if recurrence quantification analysis (RQA), a nonlinear technique, could detect pharmacologically induced autonomic changes in the continuous left ventricular pressure (LVP) and electrographic (EC) signals from an isolated rat heart—a model that theoretically contains no inherent variability. LVP and EC signal data were acquired simultaneously during Langendorff perfusion of isolated rat hearts before and after the addition of acetylcholine (n = 11), norepinephrine (n = 12), or no drug (n = 12). Two-minute segments of the continuous LVP and EC signal data were analyzed by RQA. Findings showed that%recurrence,%determinism, entropy, maxline, and trend from the continuous LVP signal significantly increased in the presence of both acetylcholine and norepinephrine, although systolic LVP significantly increased only with norepinephrine. In the continuous EC signal, the RQA trend variable significantly increased in the presence of norepinephrine. These results suggest that when either the sympathetic or parasympathetic division of the autonomic nervous system overwhelms the other, the dynamics underlying cardiac variability become stationary. This study also shows that information concerning inherent variability in the isolated rat heart can be gained via RQA of the continuous cardiac signal. Although speculative, RQA may be a tool for detecting alterations in cardiac variability and evaluating signal dynamics as a nonlinear indicator of cardiac pathology.

Lipid Emulsion Reverses Bupivacaine-induced Asystole in Isolated Rat Hearts

2010 ◽  
Vol 113 (6) ◽  
pp. 1320-1325 ◽  
Author(s):  
Ying Chen ◽  
Yun Xia ◽  
Le Liu ◽  
Tong Shi ◽  
Kejian Shi ◽  
...  
Keyword(s):  
Recovery Phase ◽  
Isolated Rat Heart ◽  
Time Response ◽  
Rate Pressure Product ◽  
Control Group ◽  
Myocardial Tissue ◽  
Langendorff Preparation ◽  
Dependent Relationship ◽  
Rat Hearts ◽  
Isolated Rat

Background The concentration-response and time-response relationships of lipid emulsions used to reverse bupivacaine-induced asystole are poorly defined. Methods Concentration response across a range of lipid concentrations (0-16%) to reverse bupivacaine-induced asystole were observed using isolated rat heart Langendorff preparation. Cardiac function parameters were recorded during infusion. Concentrations of bupivacaine in myocardial tissue were measured by liquid chromatography and tandem mass spectrometry at the end of the experiment. Results Although all lipid-treated hearts recovered (cardiac recovery was defined as a rate-pressure product more than 10% baseline), no nonlipid-treated hearts (control group) did so. The ratio of the maximum rate pressure product during recovery to baseline value demonstrated a concentration-dependent relationship among lipid groups, with 0.25, 0.5, 1, 2, 4, 8, and 16%. Mean ± SD values for each corresponding group were 22 ± 4, 24 ± 5, 29 ± 6, 52 ± 11, 73 ± 18, 119 ± 22, and 112 ± 10%, respectively (n = 6, P < 0.01). Rate-pressure product in lipid groups with 4-16% concentrations was lower at 15-40 min than at 1 min, showing a decreasing tendency during recovery phase (P < 0.01). The concentration of myocardial bupivacaine in all lipid-treated groups was significantly lower than in the control group (P < 0.01). It was also lower in lipid groups with 2-16% concentrations than in those with concentrations at 0.25-1% (P < 0.05), with the 16% group lower than groups with 2-8% concentrations (P < 0.001). Conclusion Lipid application in bupivacaine-induced asystole displays a concentration-dependent and time-response relationship in isolated rat hearts.

scholarly journals Investigation of cardiotoxic effect of A-1 apo + D actinomycin complex on isolated rat heart

2016 ◽  
Vol 20 (4) ◽  
pp. 88
Author(s):  
R. A. Knyazev ◽  
N. V. Trifonova ◽  
A. R. Kolpakov ◽  
L. M. Polyakov
Keyword(s):  
Anticancer Drug ◽  
Conflict Of Interest ◽  
Rat Heart ◽  
Actinomycin D ◽  
Isolated Rat Heart ◽  
Protein Component ◽  
Solution Temperature ◽  
Apolipoprotein A ◽  
Rat Hearts ◽  
Isolated Rat

<p><strong>Aim.</strong> Chemotherapy is one of the main methods of treating malformations. However, this technique causes a great deal of side effects, among which are complications related to cardiac toxicity. Development of new anticancer drugs is directly related to a decrease in the general toxic effect on the organism and the cardiovascular system in particular. The aim of the study was to investigate the capability of apolipoprotein A-1 together with an anticancer drug, actinomycin D, to induce functional disturbances in the performance of an isolated rat heart and to compare the effect with that of pure actinomycin D. <br /><strong>Methods.</strong> For experiments use was made of Wistar male rats weighing 220-250 g. A modified Krebbs-Henseleit buffer saturated with carbogene (95 % O2 and 5 % CO2, solution temperature 37.5 °C) was used as perfusate. Experiments were conducted on isolated rat hearts. The isolated rat hearts were perfused retrogradely by a standard procedure, with isovolumic pressure registered in the left ventricle. Apolipoprotein A-I was isolated of human high-density lipoprotein by delipidating followed by separation of the proteins mix by means of column chromatography. In the experiment, apolipoprotein A-I- was mixed with actinomycin D, with concentration of the anticancer drug in the complex being 0.1 µg/ml.<br /><strong>Results</strong>. Actinomycin D with concentration 1 µg/ml aggravates the functional indicators of the heart and enhances energy load on the myocardium. Decreasing the concentration of cytostatic down to 0.1 µg/ml of perfusate brings the indicators to the baseline values. Apolipoprotein A-I combined with actinomycin D offsets the changes introduced by the cytostatic without a carrier. The complex improves hemodynamics, which can be interpreted by the presence of a protein component.<br /><strong>Conclusion.</strong> An isolated rat heart model shows that apolipoprotein A-I in combination with 0.1 µg/ml actinomycin D does not cause cardio toxicity. The complex improves myocardial efficiency through the use of the protein component as a carrier of the anticancer drug.</p><p>Received 15 November 2016. Accepted 30 November 2016.</p><p><strong>Funding:</strong> The research was supported by the federal budget project implemented by Research Institute of Biochemistry, Reg. R-085.<br /><strong>Conflict of interest:</strong> The authors declare no conflict of interest.<br /><strong>Author contributions</strong><br />Conceptualization and study design: Kolpakov AR. <br />Сбор и обработка материала: Knyazev R.A., Trifonova N.V.<br />Statistical data processing: Knyazev R.A.<br />Article writing: Knyazev R.A.<br />Review &amp; editing: Polyakov L.M.</p>

Transient hypothermic reperfusion and postischemic recovery in isolated rat heart

1990 ◽  
Vol 259 (3) ◽  
pp. H879-H888
Author(s):  
R. D. Kempsford ◽  
T. Murashita ◽  
D. J. Hearse
Keyword(s):  
Creatine Kinase ◽  
Cardiac Output ◽  
Potential Benefit ◽  
Recovery Of Function ◽  
Isolated Rat Heart ◽  
Ischemia And Reperfusion ◽  
Cardioplegic Solution ◽  
Rat Hearts ◽  
Postischemic Recovery ◽  
Isolated Rat

The potential benefit of transient hypothermic reperfusion of the ischemic myocardium was investigated in isolated working rat hearts (n = 6/group) subjected to 25 min of global ischemia at 37 degrees C. Hearts were reperfused in the Langendorff mode at 5, 10, 20, 30, or 37 degrees C for 10 min plus 5 min at 37 degrees C before assessment of functional recovery (working mode). Compared with normothermic reperfusion (recovery of cardiac output = 42.3 +/- 6.1%), transient hypothermia failed to improve the recovery of cardiac output, which was 47.9 +/- 12.7 (P = NS), 54.3 +/- 11.5 (P = NS), 25.3 +/- 2.7 (P = NS), and 6.4 +/- 3.8% (P less than 0.05) in the 30, 20, 10, and 5 degrees C groups, respectively. Reduced recovery in the 5 degrees C group was reflected in increased creatine kinase leakage from 0.26 +/- 0.04 IU.ml-1.g dry wt-1 (37 degrees C reperfusion) to 0.62 +/- 0.12 IU. ml-1.g dry wt-1 (5 degrees C reperfusion; P less than 0.05). Brief periods (3 x 1 min) of hypothermic (5 degrees C) perfusion during normothermic Langendorff reperfusion (15 min) also reduced recovery of cardiac output to 12.1 +/- 7.2% (P less than 0.01). In additional studies, hearts were subjected to a 2-min preischemic infusion with the St. Thomas' Hospital cardioplegic solution before either 25 or 35 min of normothermic ischemia and reperfusion with transient hypothermia at 5, 10, 20, or 30 degrees C. Once again hypothermic reperfusion failed to improve recovery but detrimental effects were not observed in the 5 degrees C group. These results indicate no beneficial effect of transient hypothermic reperfusion on recovery of function measured following global normothermic ischemia.

Promotion of copper excretion from the isolated rat heart attenuates postischemic cardiac oxidative injury

1999 ◽  
Vol 277 (3) ◽  
pp. H956-H962 ◽  
Author(s):  
Saul R. Powell ◽  
Ellen M. Gurzenda ◽  
Mark A. Wingertzahn ◽  
Raul A. Wapnir
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Oxidative Injury ◽  
Isolated Rat Heart ◽  
Protein Carbonyls ◽  
Rate Pressure Product ◽  
Beneficial Effects ◽  
Rat Hearts ◽  
Postischemic Period ◽  
Isolated Rat

This study examined the role of Cu as a mediator of cardiac postischemic oxidative injury. Isolated rat hearts were subjected to 20 min of normothermic global ischemia, followed by 30 min of reperfusion; after 20 min of preischemic loading with Krebs-Henseleit buffer ± 20 or 30 μM zinc-bis-histidinate (Zn-His2), 0.5 mM deferoxamine (DEF) or 42 μM neocuproine (NEO). Postischemic developed systolic pressure and rate-pressure product were highest and postischemic end-diastolic pressure was lowest in hearts treated with 20 or 30 μM Zn-His2 and 0.5 mM DEF. Cu efflux was significantly increased by 225 and 290% (end of preischemic loading), and 325 and 375% (immediate postischemic period) of control basal rates in hearts treated with 30 μM Zn-His2 and 0.5 mM DEF, respectively. NEO did not effect any of these parameters. By the end of ischemia, protein carbonyls were lowest in Zn-His2-treated hearts and highest in DEF-treated hearts when compared with control hearts. The results of this study suggest that removal of redox-active Cu before ischemia has beneficial effects, indicating a mediatory role in postischemic cardiac oxidative injury.

Ischemic preconditioning attenuates acidosis and postischemic dysfunction in isolated rat heart

1992 ◽  
Vol 263 (3) ◽  
pp. H887-H894 ◽  
Author(s):  
G. K. Asimakis ◽  
K. Inners-McBride ◽  
G. Medellin ◽  
V. R. Conti
Keyword(s):  
Rat Heart ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Isolated Rat Heart ◽  
Rate Pressure Product ◽  
Anaerobic Glycolysis ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Tissue Acidosis ◽  
Isolated Rat

The hypothesis that brief ischemia (preconditioning) protects the isolated heart from prolonged global ischemia was tested. Isovolumic rat hearts were preconditioned with either 5 min of ischemia followed by 5 min of perfusion (P1) or two 5-min episodes of ischemia separated by 5 min of perfusion (P2). Control hearts received no preconditioning. All hearts received 40 min of sustained ischemia and 30 min of reperfusion. Preconditioning (P1 or P2) significantly (P less than 0.0005) improved recovery of the rate-pressure product; percentage recoveries were 17.8 +/- 3.2 (n = 14), 59.9 +/- 5.5 (n = 6), and 46.4 +/- 4.7 (n = 8) for control, P1, and P2, respectively. Improved functional recovery of preconditioned hearts was associated with reduced end-diastolic pressure and improved myocardial perfusion. During the 40-min ischemic period, myocardial pH decreased from approximately 7.4 to 6.3 +/- 0.1 (n = 7) in the control hearts and to 6.7 +/- 0.1 (n = 7) in the preconditioned hearts (P less than 0.01). Also during the 40-min ischemic period, myocardial lactate (expressed as nmol/mg protein) increased to 146 +/- 11 (n = 7) and 101 +/- 12 (n = 8) in control and preconditioned hearts, respectively (P less than 0.02). The results demonstrate that a brief episode of ischemia can protect the isolated rat heart from a prolonged period of ischemia. This protection is associated with decreased tissue acidosis and anaerobic glycolysis during the sustained ischemic period.

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