scholarly journals The Effects of Potassium Cyanide on the Functional Recovery of Isolated Rat Hearts after Ischemia and Reperfusion: The Role of Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Anica M. Petkovic ◽  
Vladimir Lj. Jakovljevic ◽  
Jovana V. Bradic ◽  
Jovana N. Jeremic ◽  
Nevena S. Jeremic ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Functional Recovery ◽  
Heart Function ◽  
Potassium Cyanide ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Global Ischemia ◽  
Albino Rats ◽  
Rat Hearts ◽  
Isolated Rat

This investigation is aimed at examining the effects of pharmacological PostC with potassium cyanide (KCN) on functional recovery, gene expression, cytochrome c expression, and redox status of isolated rat hearts. Rats were divided into the control and KCN groups. The hearts of male Wistar albino rats were retrogradely perfused according to the Langendorff technique at a constant perfusion pressure of 70 cmH2O. After stabilisation, control hearts were subjected to global ischemia (5 minutes), followed by reperfusion (5 minutes), while experimental hearts underwent global ischemia (5 minutes) followed by 5 minutes of reperfusion with 10 μmol/L KCN. The following parameters of heart function were measured: maximum and minimum rates of pressure development, systolic and diastolic left ventricular pressure, heart rate, and coronary flow. Levels of superoxide anion radical, hydrogen peroxide, nitrites, and index of lipid peroxidation (measured as thiobarbituric acid-reactive substances) were measured in coronary venous effluent, and activity of catalase was determined in heart tissue. Expression of Bax, Bcl-2, SOD-1, SOD-2, and cytochrome c was studied as well. It was shown that expression of Bax, Bcl-2, and SOD-2 genes did not significantly differ between groups, while expression of SOD-1 gene and cytochrome c was lower in the KCN group. Our results demonstrated that KCN improved the recovery of myocardial contractility and systolic and diastolic function, enhanced catalase activity, and diminished generation of prooxidants. However, all possible mechanisms and potential adverse effects of KCN should be further examined in the future.

Effect of Salidroside on Cardiac Functional Recovery

2013 ◽  
Vol 798-799 ◽  
pp. 1030-1032
Author(s):  
Yan Zhang ◽  
Zhong Hua Zheng ◽  
Yue Peng Wang ◽  
Guo Liang Peng ◽  
Liu Hang Wang
Keyword(s):  
Flow Rate ◽  
Functional Recovery ◽  
Rat Heart ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Cardioprotective Effect ◽  
Decrease Rate ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

To investigate the cardioprotective effect of salidroside to rat heart subjected to 8-hour hypothermic storage and 2-hour normothermic reperfusion. Isolated rat hearts were perfused with Langendorff model; after 30 minutes of baseline, the hearts were arrested and stored by St. Thomas solution (STS) without (STS group) or with different concentration salidroside at 4 °C for 8 hours, then reperfused for 2 hours. Compared with STS group, both middle and high dosage in STS greatly improved the recovery of left ventricular developed pressure (LVDP), maximum LVDP increase and decrease rate (±dp/dt), coronary flow rate (CF). Our study demonstrated that the salidroside was beneficial to improving cardiac functional recovery.

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.

scholarly journals The Effects of Diclofenac and Ibuprofen on Heart Function and Oxidative Stress Markers in the Isolated Rat Heart

2014 ◽  
Vol 15 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Maja Jevdjevic ◽  
Ivan Srejovic ◽  
Vladimir Zivkovic ◽  
Nevena Barudzic ◽  
Anica Petkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Flow ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cox Inhibitors ◽  
Stress Markers ◽  
Pressure Development ◽  
And Oxidative Stress ◽  
Isolated Rat

ABSTRACT Eicosanoids lead to the promotion of inflammation, cause fever and pain and have many other eff ects. NSAIDs block the action of cyclooxygenase (COX) during the process of converting arachidonic acid into inflammatory mediators, thus reducing the symptoms of inflammation. Investigations focusing on nonselective COX inhibitors, used in high doses, revealed harmful eff ects on myocardial function. Th e aim of our study was to assess the eff ects of two nonselective NSAIDs, diclofenac and ibuprofen, on cardiodynamic parameters, coronary flow and oxidative stress biomarkers in isolated rat hearts. Th e hearts of male Wistar albino rats were excised and retrogradely perfused according to the Langendorff technique at gradually increased coronary perfusion pressures (40-120 cm H2O). Th e experiments were performed under controlled conditions (Krebs-Henseleit physiological solution). Th e hearts were perfused with 10 μmol/l diclofenac and 10 μmol/l ibuprofen. Th e heart function parameters, including the maximum rate of pressure development (dp/dt max), minimum rate of pressure development (dp/dt min), systolic left ventricular pressure (SLVP), diastolic left ventricular pressure (DLVP), mean perfusion pressure (MBP) and heart rate (HR), were continuously registered. Coronary flow (CF) was measured flowmetrically. Oxidative stress markers, including the index of lipid peroxidation measured as TBARS, nitric oxide measured through nitrites (NO2 -), superoxide anion radical (O2 -), and hydrogen peroxide (H2O2) in the coronary venous effluent, were assessed spectrophotometrically. Our results showed that diclofenac aff ected cardiodynamic parameters more significantly than did ibuprofen. Furthermore, the present data indicate that both estimated COX inhibitors do not promote the production of reactive oxygen species.

Positive staircase effect in the rat heart

1975 ◽  
Vol 228 (2) ◽  
pp. 360-364 ◽  
Author(s):  
PD Henry
Keyword(s):  
Left Ventricular Pressure ◽  
Peak Stress ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Papillary Muscles ◽  
Apparent Lack ◽  
Rat Hearts ◽  
Staircase Effect ◽  
Krebs Buffer ◽  
Isolated Rat

The apparent lack of a positive staircase effect in ray myocardium may reflect inadequate metabolic support. Isolated rat hearts (n equals 10) were perfused at 37 degrees C with Krebs buffer containing 5 mM glucose. In 10 preparations increases in heart rate from 240 to 480/min resulted in twofold increases in left ventricular pressure and dP/dt. Pacing at a rate of 480/min resulted in mechanical deterioration of the preparation and in 50% decreases of myocardial ATP concentration within a 10-min period. Hearts of open-chest rats driven at the same rate for the same period maintained normal ATP stores. In isolated papillary muscles contracting isometrically at a rate of 30/min, peak stress 15g/mm2 (mean plus or minus SE, n equals 8) and was not changed by increasing the concentration of glucose from 5 to 30 mM. When frequency was raised from 30 to 300/min, stress declined to 5.0 plus or minus .15 g/mm2 in the presence of 5mM glucose (P smaller than .001) but increased to 8.8 plus or minus .21 g/mm2 (P smaller than 0.001) in the presence of 30 mM glucose. Thus, rat ventricular myocardium exhibits a positive staircase effect at physiological heart rates when metabolic support is adequate.

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.

Acute inhibition of monoamine oxidase and ischemic preconditioning in isolated rat hearts: interference with postischemic functional recovery but no effect on infarct size reduction

2015 ◽  
Vol 93 (9) ◽  
pp. 819-825 ◽  
Author(s):  
Maria D. Dănilă ◽  
Andreea I. Privistirescu ◽  
Silvia N. Mirica ◽  
Adrian Sturza ◽  
Valentin Ordodi ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Ischemic Preconditioning ◽  
Left Ventricular ◽  
Mao Inhibitors ◽  
Rat Hearts ◽  
System Generation ◽  
Infarct Size Reduction ◽  
Developed Pressure ◽  
Isolated Rat

Monoamine oxidases (MAOs) have recently emerged as important mitochondrial sources of oxidative stress in the cardiovascular system. Generation of reactive oxygen species during the brief episodes of ischemic preconditioning (IPC) is responsible for the cardioprotection at reperfusion. The aim of this study was to assess the effects of two MAO inhibitors (clorgyline and pargyline) on the IPC-related protection in isolated rat hearts. Animals subjected to 30 min global ischemia and 120 min reperfusion were assigned to the following groups: (i) Control, no additional intervention; (ii) IPC, 3 cycles of 5 min ischemia and 5 min reperfusion before the index ischemia; (iii) IPC-clorgyline, IPC protocol bracketed for 5 min with clorgyline (50 μmol/L); (iv) IPC-pargyline, IPC protocol bracketed for 5 min with pargyline (0.5 mmol/L). The postischemic functional recovery was assessed by the left ventricular developed pressure (LVDP) and the indices of contractility (+dLVP/dt max) and relaxation (–dLVP/dt max). Infarct size (IS) was quantified by TTC staining. In both genders, IPC significantly improved functional recovery that was further enhanced in the presence of either clorgyline or pargyline. IS reduction was comparable among all the preconditioned groups, regardless of the presence of MAO inhibitors. In isolated rat hearts, acute inhibition of MAOs potentiates the IPC-induced postischemic functional recovery without interfering with the anti-necrotic protection.

Mechanical workload-myocardial water content relationship in isolated rat hearts

1997 ◽  
Vol 273 (1) ◽  
pp. H271-H278
Author(s):  
E. R. Schertel ◽  
R. M. Daye ◽  
D. E. McClure ◽  
T. Lai ◽  
M. Miyamoto ◽  
...  
Keyword(s):  
Water Content ◽  
Isolated Heart ◽  
Left Ventricular Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Edema Formation ◽  
Perfused Rat Heart ◽  
Rat Hearts ◽  
Heart Preparation ◽  
Isolated Rat

We tested the hypothesis that the mechanical workload of the heart inversely determines the rate of myocardial edema formation in an isolated, perfused rat heart preparation. Heart rate (HR) was varied in three groups by pacing at 125 (HR125), 250 (HR250), or 350 beats/min (HR350). Left ventricular pressure (LVP) was varied in two additional groups by pacing at 250 beats/min and with the addition of either epinephrine (Epi) or propranolol (Pro) to the perfusate. In five otherwise identical groups, variation of coronary vascular resistance was minimized by adenosine. Myocardial water content (MWC) varied significantly and inversely with HR in the HR125, HR250, and HR350 groups. MWC of the HR250 group was significantly less than that of the Pro group but did not differ from the Epi group. However, when adenosine was used, MWC had significant inverse relationships with HR and LVP. We concluded that the mechanical workload of the heart inversely determines the rate and degree of myocardial edema formation in this isolated heart preparation, and both HR and LVP are determinants of this relationship.

Catecholamine–Ouabain Interaction on the Isolated Perfused Rat Heart

1975 ◽  
Vol 53 (1) ◽  
pp. 150-154 ◽  
Author(s):  
G. Tremblay ◽  
G. Porlier ◽  
V. Elharrar ◽  
R. Nadeau ◽  
J. de Champlain ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Inotropic Response ◽  
Perfused Rat Heart ◽  
Rat Hearts ◽  
The Individual ◽  
6 Hydroxydopamine ◽  
Isolated Rat

The effect of catecholamine-depleting pretreatments, reserpine, and 6-hydroxydopamine (6-OH-DA) on left ventricular pressure (LVP) and the inotropic response to graded doses of ouabain (up to 300 μg/0.05 ml) was studied in isolated perfused rat and guinea-pig hearts. In rats, reserpine and 6-OH-DA depleted myocardial catecholamine content (p <0.001), increased initial LVP (p < 0.05), and virtually abolished the inotropic response to ouabain (p < 0.01). The individual maximal inotropic response to ouabain was negatively correlated with the initial LVP (r = −0.47), and this relationship was significant. In guinea pigs, reserpine and 6-OH-DA significantly depleted the cardiac content of catecholamine, but did not increase initial LVP and did not reduce the inotropic response to the highest dose of ouabain. It is concluded that in isolated rat hearts, these catecholamine-depleting pretreatments nearly abolish the inotropic response to ouabain, and this effect appears to be mediated mainly through an increase in initial LVP. The reason why catecholamine depletion failed to increase initial LVP in guinea pigs remains unexplained.

Abstract 1712: The P2Y 12 Antagonist Cangrelor and the GP IIb/IIIa Blocker Abciximab Reduce Platelet-Mediated Myocardial Injury After Ischemia and Reperfusion

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Salvage ◽  
Ischemia And Reperfusion ◽  
Activated Platelets ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Enddiastolic Pressure ◽  
Isolated Rat

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.

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