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.

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.

Sodium alterations in isolated rat heart during cardioplegic arrest

1996 ◽  
Vol 81 (6) ◽  
pp. 2696-2702 ◽  
Author(s):  
V. D. Schepkin ◽  
I. O. Choy ◽  
T. F. Budinger
Keyword(s):  
Chemical Shift ◽  
Rat Heart ◽  
Shift Reagent ◽  
Isolated Rat Heart ◽  
Rate Pressure Product ◽  
Cardioplegic Arrest ◽  
Enhanced Sensitivity ◽  
Rat Hearts ◽  
Stop Flow ◽  
Isolated Rat

Schepkin, V. D., I. O. Choy, and T. F. Budinger. Sodium alterations in isolated rat heart during cardioplegic arrest. J. Appl. Physiol. 81(6): 2696–2702, 1996.—Triple-quantum-filtered (TQF) Na nuclear magnetic resonance (NMR) without chemical shift reagent is used to investigate Na derangement in isolated crystalloid perfused rat hearts during St. Thomas cardioplegic (CP) arrest. The extracellular Na contribution to the NMR TQF signal of a rat heart is found to be 73 ± 5%, as determined by wash-out experiments at different moments of ischemia and reperfusion. With the use of this contribution factor, the estimated intracellular Na ([Na+]i) TQF signal is 222 ± 13% of preischemic level after 40 min of CP arrest and 30 min of reperfusion, and the heart rate pressure product recovery is 71 ± 8%. These parameters are significantly better than for stop-flow ischemia: 340 ± 20% and 6 ± 3%, respectively. At 37°C, the initial delay of 15 min in [Na+]igrowth occurs during CP arrest along with reduced growth later (∼4.0%/min) in comparison with stop-flow ischemia (∼6.7%/min). The hypothermia (21°C, 40 min) for the stop-flow ischemia and CP dramatically decreases the [Na+]igain with the highest heart recovery for CP (∼100%). These studies confirm the enhanced sensitivity of TQF NMR to [Na+]iand demonstrate the potential of NMR without chemical shift reagent to monitor [Na+]iderangements.

Antiarrhythmic effects of ceruloplasmin during reperfusion in the ischemic isolated rat heart

1995 ◽  
Vol 73 (9) ◽  
pp. 1253-1261 ◽  
Author(s):  
Roxana Atanasiu ◽  
Ramez Chahine ◽  
Réginald Nadeau ◽  
Marie-Josée Dumoulin ◽  
Mircea Alexandra Mateescu
Keyword(s):  
Ventricular Fibrillation ◽  
Rat Heart ◽  
Positive Control ◽  
Isolated Rat Heart ◽  
Dose Effect ◽  
Control Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Rat Hearts ◽  
Isolated Rat

The ability of ceruloplasmin, an important serum antioxidant, to reduce the vulnerability of the isolated rat heart to reperfusion arrhythmias has been investigated. Bovine plasma ceruloplasmin was purified by chromatography on aminoethyl-agarose. Isolated rat hearts were submitted to 15 min of regional ischemia and 10 min of reperfusion. The dose–effect relationship and the role of ceruloplasmin conformational integrity in cardioprotection were established by treatment of ischemic hearts with ceruloplasmin at various concentrations (0.25, 0.5, 1, and 2 μM) and at different degrees of conformational integrity (A610/A280 = 0.02, 0.04, and 0.06), 5 min before reperfusion. Deferoxamine (20–500 μM) was used as a positive control. As negative controls we used chemically inactivated ceruloplasmin (1 μM), heat-denatured ceruloplasmin (1 μM), and albumin (1–4 μM). In the control group during the first 5 min of reperfusion, the incidence of total ventricular fibrillation was 100% and of irreversible ventricular fibrillation was 83%. The incidence of reversible and irreversible ventricular fibrillation was significantly decreased in the cerulopiasmin-treated groups in both a dose and molecular integrity dependent manner. Ceruloplasmin had no effect on the incidence of ventricular tachycardia. Deferoxamine reduced the incidence of ventricular fibrillation to the same degree as ceruloplasmin but at concentrations much higher than those of ceruloplasmin. Chemically inactivated ceruloplasmin, heat-denatured ceruloplasmin, and albumin had no protective effects on reperfusion-induced arrhythmias.Key words: ceruloplasmin, ischemic heart disease, oxygen free radicals, antioxidants, isolated rat heart.

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

Kolaviron and Garcinia kola Seed Extract Protect Against Ischaemia/Reperfusion Injury on Isolated Rat Heart

Drug Research ◽  
2018 ◽  
Vol 68 (05) ◽  
pp. 286-295
Author(s):  
Ademola Oyagbemi ◽  
Dirk Bester ◽  
Johan Esterhuyse ◽  
Ebenezer Farombi
Keyword(s):  
Reperfusion Injury ◽  
Rat Heart ◽  
Caspase 3 ◽  
Isolated Rat Heart ◽  
Seed Extract ◽  
Parp Cleavage ◽  
Control Group ◽  
Ischaemia Reperfusion Injury ◽  
Garcinia Kola ◽  
Isolated Rat

Abstract Background The incidence of cardiovascular diseases and its associated complications have increased greatly in the past three decades. The purpose of this study was to evaluate the acute cardioprotective effects of Garcinia kola (GK) seed extract and Kolaviron (KV) and determine mechanisms of action involving RISK signalling pathways. Methods Male Wistar rats were used in this study. Hearts were excised and mounted on the Langendorff perfusion system. The control, group 1 was perfused with dimethyl sulfoxide (DMSO), group II with KV and group III with GK respectively. Western blot analyses were performed on frozen heart tissues. Results Isolated rat hearts perfused with KV and GK attenuated apoptotic pathways with significant reduction in p38 MAPK protein phosphorylation, as well as reduction in total caspase 3, cleaved caspase 3 (Asp 175) and PARP cleavage. KV and GK also down-regulated p-JNK1 (Tyr 185) and p-JNK 2 (Thr 183) protein expression at the 10 min reperfusion time ponit. Cardioprotection was achieved in part, by enhancement of the reperfusion injury signalling kinase (RISK) pathway; as evidenced by significant increases in protein expresion of Akt/PKB and p-Akt/PKB (Ser 473) in KV and GK respectively. Conclusions KV and GK supplementation led to significant increases in the expressions of survival proteins. It is noteworthy that both KV and GK supplementation offered cardioprotection in ischaemic/reperfusion injury rat heart model. In all, GK showed better cardioprotective effect that KV.

An increase in intracellular [Na+] during Ca2+ depletion is not related to Ca2+ paradox damage in rat hearts

1998 ◽  
Vol 274 (3) ◽  
pp. H846-H852 ◽  
Author(s):  
Maurits A. Jansen ◽  
Cees J. A. Van Echteld ◽  
Tom J. C. Ruigrok
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Creatine Kinase ◽  
Magnetic Resonance ◽  
Rate Pressure Product ◽  
Free Solution ◽  
Rat Hearts ◽  
Significant Change ◽  
Group Recovery ◽  
Isolated Rat ◽  
Nuclear Magnetic

Ca2+paradox damage has been suggested to be determined by Na+ entry during Ca2+ depletion and exchange of Na+ for Ca2+ during Ca2+ repletion. With the use of23Na nuclear magnetic resonance, we previously observed a Ca2+ paradox without a prior Na+ increase. We have now demonstrated a Na+ increase during Ca2+ and Mg2+ depletion without the occurrence of the Ca2+ paradox during Ca2+ repletion. Isolated rat hearts were perfused for 20 min with a Ca2+-free or a Ca2+- and Mg2+-free (Ca2+/Mg2+-free) solution under hypothermic conditions (20 and 25°C). Intracellular Na+ concentration ([Na+]i) increased from 11.9 ± 1.2 to 26.9 ± 5.8 mM ( P < 0.001) during Ca2+/Mg2+-free perfusion at 20°C, whereas no significant change in [Na+]ioccurred during 20 min of Ca2+-free perfusion at 20°C. In addition, we confirmed that [Na+]idid not change significantly during 20 min of normothermic Ca2+-free perfusion. Creatine kinase release during normothermic Ca2+ repletion in the 20°C groups was ∼10% and in the 25°C groups 75% of the release in the normothermia group. Recovery of rate-pressure product was ∼50% in the 20°C groups versus 0% in the normothermia group. In conclusion, hypothermic Ca2+/Mg2+-free perfusion results in a significant increase of [Na+]i, which does not contribute to the extent of the Ca2+ paradox on normothermic Ca2+ repletion.

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.

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.

Effect of diazoxide on flavoprotein oxidation and reactive oxygen species generation during ischemia-reperfusion: a study on Langendorff-perfused rat hearts using optic fibers

2008 ◽  
Vol 294 (5) ◽  
pp. H2088-H2097 ◽  
Author(s):  
Philippe Pasdois ◽  
Bertrand Beauvoit ◽  
Liliane Tariosse ◽  
Béatrice Vinassa ◽  
Simone Bonoron-Adèle ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Optic Fibers ◽  
The One ◽  
Isolated Perfused Rat Hearts

This study analyzed the oxidant generation during ischemia-reperfusion protocols of Langendorff-perfused rat hearts, preconditioned with a mitochondrial ATP-sensitive potassium channel (mitoKATP) opener (i.e., diazoxide). The autofluorescence of mitochondrial flavoproteins, and that of the total NAD(P)H pool on the one hand and the fluorescence of dyes sensitive to H2O2 or O2•− [i.e., the dihydrodichlorofluoroscein (H2DCF) and dihydroethidine (DHE), respectively] on the other, were noninvasively measured at the surface of the left ventricular wall by means of optic fibers. Isolated perfused rat hearts were subjected to an ischemia-reperfusion protocol. Opening mitoKATP with diazoxide (100 μM) 1) improved the recovery of the rate-pressure product after reperfusion (72 ± 2 vs. 16.8 ± 2.5% of baseline value in control group, P < 0.01), and 2) attenuated the oxidant generation during both ischemic (−46 ± 5% H2DCF oxidation and −40 ± 3% DHE oxidation vs. control group, P < 0.01) and reperfusion (−26 ± 2% H2DCF oxidation and −23 ± 2% DHE oxidation vs. control group, P < 0.01) periods. All of these effects were abolished by coperfusion of 5-hydroxydecanoic acid (500 μM), a mitoKATP blocker. During the preconditioning phase, diazoxide induced a transient, reversible, and 5-hydroxydecanoic acid-sensitive flavoprotein and H2DCF (but not DHE) oxidation. In conclusion, the diazoxide-mediated cardioprotection is supported by a moderate H2O2 production during the preconditioning phase and a strong decrease in oxidant generation during the subsequent ischemic and reperfusion phases.

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