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.

Isoflurane and Halothane Increase Adenosine Triphosphate Preservation, but Do Not Provide Additive Recovery of Function after Ischemia, in Preconditioned Rat Hearts

1997 ◽  
Vol 86 (1) ◽  
pp. 109-117 ◽  
Author(s):  
Ashraf Boutros ◽  
Jun Wang ◽  
Christine Capuano
Keyword(s):  
Adenosine Triphosphate ◽  
Coronary Flow ◽  
Recovery Of Function ◽  
Left Ventricular ◽  
Untreated Group ◽  
Control Group ◽  
Time Control ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

Background Brief ischemic periods render the myocardium resistant to infarction from subsequent ischemic insults by a process called ischemic preconditioning. Volatile anesthetics have also been shown to be cardioprotective if administered before ischemia. The effect of preconditioning alone and combined with halothane or isoflurane on hemodynamic recovery and preservation of adenosine triphosphate content in isolated rat hearts was evaluated. Methods Seven groups of isolated rat hearts (n = 6 each) were perfused in a retrograde manner at constant temperature and pressure. A latex balloon was placed in the left ventricle to obtain isovolumetric contraction. Heart rhythm, coronary flow, left ventricular pressure and its derivative dP/dt (positive and negative), and developed pressure were monitored. The hearts were paced at 300 beats per minute. Each heart was randomly allocated to (1) a time-control group that received no ischemia, (2) an untreated group that received 25 min of normothermic ischemia only. (3 and 4) an isoflurane group and a halothane group that received 40 min of anesthetic (2.2% and 1.5%, respectively) before ischemia; (5) a preconditioning group that received two 5-min periods of ischemia separated by 10 min of reperfusion before ischemia; or (6 and 7) a isoflurane+preconditioning group and a halothane+preconditioning group that received anesthetic for 10 min at concentrations of 2.2% or 1.5%, respectively, before two 5-min periods of ischemia separated by 10 min of reperfusion. All treated groups received 25 min of normothermic ischemia followed by 30 min of reperfusion. Results The time-control group remained hemodynamically stable for the entire experiment, and the adenosine triphosphate content was 18.3 +/- 1.7 (SEM) microM/g at the end of 115 min. The untreated group had depressed recovery after 25 min of normothermic ischemia, and the developed pressure was significantly depressed and recovered only 30 +/- 9% (P < 0.001) of its preischemic value. There was also a significant increase in the incidence of ventricular fibrillation (P < 0.001). Adenosine triphosphate content was significantly lower in this group than in all other groups. Five minutes of ischemia in the preconditioning group had little effect on hemodynamics and decreased developed pressure only 6.4%. Halothane depressed developed pressure by 16 +/- 5% (P < 0.001), and isoflurane increased coronary flow by 145 +/- 9% (P < 0.001) but had no significant hemodynamic effect. The treated groups had significantly better recovery of postischemic function than did the untreated group. In the preconditioning group, developed pressure recovered to 85% of control and dP/dt+ to 87% of control. The addition of halothane or isoflurane to preconditioning did not provide additional functional recovery but did increase the level of adenosine triphosphate preservation (13.1 +/- 1.1 and 12.4 +/- 1.1 microM/g, respectively). Conclusions The results indicate that preconditioning, halothane, and isoflurane provide significant protection against ischemia. The combination of preconditioning and halothane or isoflurane did not improve hemodynamic recovery but did increase preservation of adenosine triphosphate.

Contribution of adenosine to changes in coronary flow in metabolically stimulated rat heart

1988 ◽  
Vol 66 (2) ◽  
pp. 171-173 ◽  
Author(s):  
John Headrick ◽  
Roger J. Willis
Keyword(s):  
Adenosine Deaminase ◽  
Rat Heart ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Extracellular Adenosine ◽  
Mediated Action ◽  
Adenosine Receptor Antagonist ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Metabolic Stimulation

The extent to which endogenous, extracellular adenosine mediates increased coronary flow in crystalloid-perfused, isovolumic rat hearts stimulated with either norepinephrine or isoproterenol was examined. When infused into the coronary circulation, norepinephrine (1 × 10−7 M) rapidly increased left ventricular developed pressure (LVDP) from 81 ± 6 to 235 ± 13 mmHg (1 mmHg = 133.3 Pa) and coronary flow from 12.7 ± 0.8 to 18.4 ± 0.7 mL∙mn−1∙g−1. The presence of either adenosine deaminase (2 U∙mL−1) or the adenosine receptor antagonist, 8-phenyltheophylline (5 × 10−6 M) in the perfusate of norepinephrine-stimulated hearts augmented the increase in LVDP and ±dP/dtmax by 10–20% but reduced the increase in coronary flow by 34%. Doubling the rate of adenosine deaminase infusion, or infusing the enzyme and 8-phenyltheophylline together did not alter their inhibitory effectiveness. Similar results were observed with hearts stimulated with isoproterenol (5 × 10−8 M). These data show that about a third of the vasodilation that results from the metabolic stimulation of rat heart by catecholamines is due to the receptor-mediated action of extracellular adenosine.

Effect of preconditioning on ryanodine-sensitive Ca2+ release from sarcoplasmic reticulum of rat heart

1996 ◽  
Vol 271 (3) ◽  
pp. H876-H881 ◽  
Author(s):  
M. Tani ◽  
Y. Asakura ◽  
H. Hasegawa ◽  
K. Shinmura ◽  
Y. Ebihara ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Function ◽  
Rat Heart ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Ventricular Tachyarrhythmias ◽  
Beneficial Effects ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

The effect of varying the number of preconditioning (PC) episodes on the recovery of cardiac function and on the function of the sarcoplasmic reticulum (SR) was investigated to determine the correlation between the effect of PC and SR function. Isolated rat hearts were subjected to zero to three 5-min episodes of global ischemia with intermittent perfusion (PC0-PC3) followed by 25 min of ischemia (I) and 30 min of reperfusion. The left ventricular (LV) pressure and SR 45Ca2+ uptake in the absence or presence of ryanodine were then measured. The increase in LV end-diastolic pressure and the incidence and duration of ventricular tachyarrhythmias during reperfusion decreased. The recovery of LV developed pressure, LV dP/dtmax and dP/dtmin, increased as the number of episodes of PC increased. The rates of SR 45Ca2+ uptake after PC and after reperfusion were lower in PC3 than in PC0. Conversely, the rate of 45Ca2+ uptake after I did not differ between PC0 and PC3. The ryanodine-sensitive Ca2+ release increased after I, and additional increases were observed during reperfusion in PC0, whereas the release after I and reperfusion decreased progressively in PC3. These observations show that the beneficial effects of PC are associated with a decrease in ryanodine-sensitive SR Ca2+ release.

Protective Effect of Danshen During Myocaredial Ischemia and Reperfusion: An Isolated Rat Heart Study

1990 ◽  
Vol 18 (01n02) ◽  
pp. 19-24 ◽  
Author(s):  
W. Zhou ◽  
T.J.C. Ruigrok
Keyword(s):  
Flow Rate ◽  
Coronary Flow ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Mechanical Activity ◽  
Ischemia And Reperfusion ◽  
Radix Salviae Miltiorrhizae ◽  
Developed Pressure ◽  
Isolated Rat

The effect of Danshen (Radix salviae miltiorrhizae) on mechanical activity and coronary flow rate if isolated rat hearts was examined to assess the ability of Danshen to protect the myocardium against the effects of ischemia and reperfusion. After 20 min of control perfusion, in the presence or absence of Danshen, the hearts were made totally ischemic for 30 min and then reperfused for 30 min. Danshen had a negative inotropic effect and caused an increase of coronary flow rate. During post-ischemic reperfusion recovery of left ventricular developed pressure in the pressure in the Danshen-treated hearts was significantly better and contracture was significantly less than in the untreated hearts. The results indicate that Danshen protects the heart against some of the deleterious effects of ischemia abd 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.

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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