Abstract 253: Complete Reversal of Xylazine-induced Bradycardia With Intralipid in Female Mice

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Negar Motayagheni ◽  
Mansoureh Eghbali
Keyword(s):  
Heart Rate ◽  
Cardiac Arrest ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Control Group ◽  
Heart Rates ◽  
Female Mice

Sudden cardiac arrest accounts for 300 000 to 400 000 deaths annually in united states both in men and women. Cardiac arrest could be due to abnormally slow heart rate known as bradycardia. Bradycardia is a catastrophic event which is associated with significant mortality and morbidity. We have previously shown that Intralipid, an emulsion of soy bean oil, egg yolk phospholipids and glycerol, protects the heart against ischemia/reperfusion injury as well as Bupivacaine induced cardiotoxicity. Here we examined whether intralipid can protects the heart against bradycardia. Wild type female mice C57/Bl6 (2-4 month old) were anesthetized by isoflurane after heparinization. The heart was removed immediately and placed in cold Krebs-Henseleit buffer. The aorta was cannulated and the isolated heart (Langendorff) was perfused with Krebs-Henseleit at 37°C for 15 min for stabilization. Xylazine (100-300 mg) was directly applied to the heart surface for 1-2 min until bradycardia was achieved. The heart was then perfused with either Krebs-Henseleit (KH) solution (control group), or 1% ILP (intralipid group). Hemodynamic parameters and heart rates were recorded with a catheter directly inserted into left ventricle (n=5-8 per group). The heart rates at the baseline before inducing bradycardia was 224±7 beats/min and the left ventricular pressures was 64±4 mmHg. Administration of Xylazine decreased the heart rate significantly to 81±9 beats/min and left ventricular pressure to 5±2 mmHg (p<0.001). Perfusion of the heart with intralipid rapidly restored the heart rate to 209±30 and left ventricular pressure to 59±4 which were not significantly different than their values before inducing bradycardia at the baseline. In the hearts that received Krebs-Henseleit after bradycardia, the heart rate (81±10 beats/min) and left ventricular pressure (20±8 mmHg) were significantly lower than intralipid group. In conclusion Intralipid has the ability to rapidly reverse bradycardia in female mice.

Inhibition of vascular peroxidase alleviates cardiac dysfunction and apoptosis induced by ischemia–reperfusion

2012 ◽  
Vol 90 (7) ◽  
pp. 851-862 ◽  
Author(s):  
Ting-Ting Li ◽  
Yi-Shuai Zhang ◽  
Lan He ◽  
Bin Liu ◽  
Rui-Zheng Shi ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Clinical Value ◽  
Pharmacologic Inhibition

Myeloperoxidase (MPO) is involved in myocardial ischemia–reperfusion (IR) injury and vascular peroxidase (VPO) is a newly identified isoform of MPO. This study was conducted to explore whether VPO is involved in IR-induced cardiac dysfunction and apoptosis. In a rat Langendorff model of myocardial IR, the cardiac function parameters (left ventricular pressure and the maximum derivatives of left ventricular pressure and coronary flow), creatine kinase (CK) activity, apoptosis, VPO1 activity were measured. In a cell (rat-heart-derived H9c2 cells) model of hypoxia–reoxygenation (HR), apoptosis, VPO activity, and VPO1 mRNA expression were examined. In isolated heart, IR caused a marked decrease in cardiac function and a significant increase in apoptosis, CK, and VPO activity. These effects were attenuated by pharmacologic inhibition of VPO. In vitro, pharmacologic inhibition of VPO activity or silencing of VPO1 expression significantly suppressed HR-induced cellular apoptosis. Our results suggest that increased VPO activity contributes to IR-induced cardiac dysfunction and inhibition of VPO activity may have the potential clinical value in protecting the myocardium against IR injury.

scholarly journals Shenxian-Shengmai Oral Liquid Reduces Myocardial Oxidative Stress and Protects Myocardium from Ischemia-Reperfusion Injury

2018 ◽  
Vol 48 (6) ◽  
pp. 2503-2516 ◽  
Author(s):  
Yixiu Zhao ◽  
Xin Zhang ◽  
Jing Luan ◽  
Buchang Zhao ◽  
Na An ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Ventricular Pressure ◽  
Control Group ◽  
Maximal Increase ◽  
Rat Cardiomyocytes ◽  
Increase Rate ◽  
Oral Liquid

Background/Aims: Shenxian-shengmai (SXSM) oral liquid, a Chinese patent compound medicine, has been used to treat sinus bradyarrhythmias induced by mild sick sinus syndrome in clinical practice. Myocardial ischemia, in particular in serious or right coronary-related heart diseases, can cause bradyarrhythmias and cardiac dysfunction. Moreover, reperfusion of ischemic myocardium is associated with additional myocardial damage known as myocardial ischemia-reperfusion (I/R) injury. This study was designed to evaluate the effects of SXSM on bradyarrhythmias and cardiac dysfunction induced by myocardial I/R injury, and to explore the underlying mechanisms. Methods: Administration of SXSM to adult male Sprague Dawley (SD) rats was achieved orally by gavage and control rats were given equivalent deionized water every day for 14 days. After the last administration, the heart was connected with the Langendorff perfusion apparatus and both groups were subjected to ischemia for 20 min followed by reperfusion for 40 min to induce myocardial I/R injury. Heart rate (HR), left ventricular developed pressure (LVDP), the maximal increase rate of left ventricular pressure (+dp/dtmax) and the maximal decrease rate of left ventricular pressure (-dp/dtmax) were recorded by a physiological signal acquisition system. The heart treated with ischemic preconditioning (IPC) for 3 times at a range of 5 min/time before ischemia served as a positive control group. The hearts without I/R injury served as control group. After reperfusion, superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH-Px) activities in the myocardium were determined by appropriate assay kits. Myocardial SOD1 and glutamate cysteine ligase catalytic subunit (GCLC) expression were assessed by western blot analysis. For the in vitro study, SXSM serum was prepared according to the serum pharmacological method and neonatal rat cardiomyocytes were isolated from the heart of new born SD rats. Neonatal rat cardiomyocytes were pretreated with SXSM serum and subjected to H2O2 or anoxia/ reoxygenation (A/R) treatment to induce oxidative damage. Cell viability was evaluated using a Cell Counting Kit-8 (CCK8) assay. Levels of reactive oxygen species (ROS), SOD, GSH and GSH-Px in cardiomyocytes were determined by appropriate assay kits. SOD1 and GCLC expression were assessed by western blot analysis. Buthionine-[S, R]-sulfoximine (BSO), a GCLC inhibitor, and SOD1 siRNA were also used for identifying the cardiac protective targets of SXSM. Results: SXSM and ischemic preconditioning (IPC) significantly increased heart rate during myocardial reperfusion and protected cardiac function against myocardial I/R injury, including an increase in left ventricular diastolic pressure (LVDP), the maximal increase rate of left ventricular pressure (+dp/dtmax) and the maximal decrease rate of left ventricular pressure (-dp/dtmax). We also found that SXSM and IPC improved the expansion of myocardial interstitium, the structural abnormality and morphological changes of cardiomyocytes induced by I/R injury. Meanwhile, SXSM protected cardiomyocytes against the oxidative damage induced by H2O2 and A/R injury through reducing intracellular ROS levels. Moreover, SXSM increased SOD activity through enhancing SOD1 expression and increased GSH content through promoting GCLC expression as well as GSH-Px activity. BSO and SOD1 siRNA counteracted anti-arrhythmic and cardiac protective effect of SXSM, suggesting that the therapeutic targets of SXSM might be SOD1 and GCLC. Conclusion: SXSM is effective in protecting the myocardium from I/R injury, with myocardial SOD1 and GCLC being the potential therapeutic targets.

Bainbridge reflex in conscious, unrestrained, and tranquilized baboons

1981 ◽  
Vol 240 (2) ◽  
pp. H164-H167 ◽  
Author(s):  
S. F. Vatner ◽  
M. Zimpfer
Keyword(s):  
Heart Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Increase Heart Rate ◽  
Cardiac Rate ◽  
Volume Loading ◽  
Heart Rates ◽  
Cholinergic Blockade ◽  
Bilateral Vagotomy

The effects of volume loading were examined in conscious, unrestrained, and tranquilized baboons (20-25 kg) 1-3 mo after instrumentation with miniature left ventricular pressure and diameter gauges. The response to volume loading was accompanied by significant increases (P less than 0.01) in cardiac rate (32 +/- 4 beats/min) in tranquilized baboons. When rapid saline infusion was accomplished in conscious unrestrained baboons by means of activating a remote-controlled interrogator, heart rate also rose significantly (41 +/- 8 beats/min, P less than 0.01). After cholinergic blockade with atropine, ganglionic blockade with hexamethonium, bilateral vagotomy, or combined cholinergic and beta-adrenergic blockades, volume loading failed to increase heart rate. In two smaller (12-14 kg) intact conscious baboons with relatively high spontaneous heart rates, volume loading did not alter heart rate. These experiments suggest that the Bainbridge reflex exists in larger primates with relatively low spontaneous heart rates.

scholarly journals Synthesis and Biological Activity of a Bis-steroid-methanocyclobutanaphthalene- dione Derivative against Ischemia/Reperfusion Injury via Calcium Channel Activation

2020 ◽  
Vol 19 (4) ◽  
pp. 393-412
Author(s):  
Figueroa-Valverde Lauro ◽  
Diaz-Cedillo Francisco ◽  
Rosas-Nexticapa Marcela ◽  
Mateu-Armand Virginia ◽  
Garcimarero-Espino E. Alejandra ◽  
...  
Keyword(s):  
Biological Activity ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Bay K 8644 ◽  
Ventricular Pressure ◽  
Dione Derivative

Background: There is some experimental data on the effect exerted by some steroid derivatives against ischemia/reperfusion injury; however, the molecular mechanism is very confusing, perhaps this phenomenon could be due to the protocols used and/or differences in the chemical structure of each one of the steroid derivatives. Objective: The aim of this study was to synthesize a new bis-steroid-methanocyclobutanaphthalene- dione derivative using some tools chemical. Methodology: The biological activity exerted by the bis-steroid-methanocyclobutanaphthalene- dione derivative against ischemia/reperfusion injury was evaluated in an isolated heart model using noradrenaline, milrinone, dobutamine, levosimendan, and Bay-K- 8644 as controls. In addition, other alternative experiments were carried out to evaluate the biological activity induced by the bis-steroid-methanocyclobuta-naphthalene-dione derivative against left ventricular pressure in the absence or presence of nifedipine. Results: The results showed that 1) the bis-steroid-methanocyclobuta-naphthalene-dione derivative significantly decreases the ischemia-reperfusion injury translated as a decrease in the the infarct area in a similar manner to levosimendan drug; 2) both bis-steroidmethanocyclobuta- naphthalene-dione and Bay-K-8644 increase the left ventricular pressure and 3) the biological activity exerted by bis-steroid-methanocyclobuta-naphthalenedione derivative against left ventricular pressure is inhibited by nifedipine. Conclusion: In conclusion, the bis-steroid-methanocyclobuta-naphthalene-dione derivative decreases the area of infarction and increases left ventricle pressure via calcium channels activation; this phenomenon could constitute a new therapy for ischemia/reperfusion injury.

scholarly journals Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

2014 ◽  
Vol 307 (5) ◽  
pp. H722-H731 ◽  
Author(s):  
Kentaro Yamakawa ◽  
Eileen L. So ◽  
Pradeep S. Rajendran ◽  
Jonathan D. Hoang ◽  
Nupur Makkar ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Regional Differences ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Pressure ◽  
Electrophysiological Effects

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial ( n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial ( n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/d tmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/d tmax showed the strongest correlation with ventricular ARI effects ( R2 = 0.81, P < 0.0001) than either heart rate ( R2 = 0.58, P < 0.01) or left ventricular pressure ( R2 = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

Intramyocardial blood volume change in first moments of cardiac arrest in anesthetized goats

1987 ◽  
Vol 253 (2) ◽  
pp. H307-H316 ◽  
Author(s):  
I. Vergroesen ◽  
M. I. Noble ◽  
J. A. Spaan
Keyword(s):  
Cardiac Arrest ◽  
Blood Volume ◽  
Volume Change ◽  
Venous Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beating Heart ◽  
Ventricular Pressure ◽  
The Mean ◽  
Change In Mean

The effect of cardiac relaxation on the intramyocardial blood volume was studied by measuring the integrated difference between arterial inflow and great cardiac venous outflow. In nine anesthetized goats, the left main coronary artery was perfused under constant pressure. The great cardiac vein was drained under pressure control. The venous flow signal was amplified so that the integrated intramyocardial blood volume was constant in the beating heart. With normal vasomotor tone, the mean change in vascular volume was 3.01 +/- 0.18 (SE) ml/100 g left ventricle (LV); 67% of the volume change was achieved in 1.60 +/- 0.09 s. For the fully dilated bed (adenosine infusion), the values were 4.13 +/- 0.33 ml/100 g and 0.96 +/- 0.06 s, respectively. The volume change could be correlated with the venous pressure during cardiac arrest (Pvd) and the change in mean left ventricular pressure after cardiac arrest (r = 0.95). The correlation improved when data were selected for Pvd less than 6 mmHg to r = 0.98. We assumed that the change in vascular transmural pressure can be approximated as half the mean left ventricular pressure change. The intramyocardial vascular compliance was then estimated as 0.104 +/- 0.012 and 0.146 +/- 0.028 ml X mmHg-1 X 100 g-1 for control and adenosine conditions, respectively. The long time constants excluded the large epicardial veins as the site of volume change; they were much longer than the duration of diastole in the beating heart. We conclude that the intramyocardial vascular compartment is capable of volume expansion on the order of 20% of its normal volume when myocardial compression by ventricular systole is suspended.

scholarly journals Merit of Anisodamine Combined with Opioidδ-Receptor Activation in the Protection against Myocardial Injury during Cardiopulmonary Bypass

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Xuan Hong ◽  
Huimin Fan ◽  
Rong Lu ◽  
Paul Chan ◽  
Zhongmin Liu
Keyword(s):  
Cardiopulmonary Bypass ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Combined Treatment ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Control Group ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia/reperfusion (MIR) injury easily occurrs during cardiopulmonary bypass surgery in elderly patients. In an attempt to develop an effective strategy, we employed a pig model of MIR injury to investigate the maximum rate of change of left ventricular pressure, left ventricular enddiastolic pressure, and left intraventricular pressure. Coronary sinus cardiac troponin T (TnT) and adenosine-triphosphate (ATP) content in myocardium were measured. The ultrastructures for MIR injury were visualized by transmission electron microscopy (TEM). The role ofδ-opioid receptor activation using D-Ala2, D-Leu5-enkephalin (DADLE) in both early (D1) and late (D2) phases of cardioprotection was identified. Also, the merit of cardioprotection by DADLE in combination with anisodamine, the muscarinic receptor antagonist (D+M), was evaluated. Glibenclamide was employed at the dose sufficient to block ATP-sensitive potassium channels. Significant higher cardiac indicators, reduced TnT and increased ATP contents, were observed in D1, D2, and D+M groups compared with the control group. DADLE induced protection was better in later phase of ischemia that was attenuated by glibenclamide. DADLE after the ischemia showed no benefit, but combined treatment with anisodamine showed a marked postischemic cardioprotection. Thus, anisodamine is helpful in combination with DADLE for postischemic cardioprotection.

scholarly journals Changes of left ventricular pressure-diameter-velocity relations by alterations of heart rate in conscious dogs.

1984 ◽  
Vol 48 (12) ◽  
pp. 1312-1321 ◽  
Author(s):  
MASUAKI FUJIYAMA ◽  
YOH-ICHIRO FURUTA ◽  
JUN MATSUMURA ◽  
AKIHIRO TANABE ◽  
JUN OHBAYASHI ◽  
...  
Keyword(s):  
Heart Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Pressure

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

1963 ◽  
Vol 205 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Andrew G. Wallace ◽  
N. Sheldon Skinner ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Complex Function ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Pressure Development ◽  
Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

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