Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

2006 ◽  
Vol 101 (4) ◽  
pp. 1091-1096 ◽  
Author(s):  
Xiangshao Fang ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Lei Huang ◽  
Yun-Te Chang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Chronic Myocardial Ischemia

Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

Effects of beta-blockade on regional myocardial flow and function during exercise

1984 ◽  
Vol 247 (1) ◽  
pp. H52-H60 ◽  
Author(s):  
M. Matsuzaki ◽  
J. Patritti ◽  
T. Tajimi ◽  
M. Miller ◽  
W. S. Kemper ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Wall Thickening ◽  
Ischemic Area ◽  
Ischemic Region ◽  
Exercise Induced ◽  
Control Exercise

We examined the effects of a cardioselective beta-blocking drug on exercise-induced regional myocardial ischemia in 10 conscious dogs with chronic coronary artery stenosis. An ameroid constrictor, Doppler flowprobe, and hydraulic cuff were placed around the left circumflex coronary artery, and left ventricular pressure (LVP), systolic wall thickening (% delta WT; by sonomicrometry), and myocardial blood flow (MBF; microspheres) were measured during control standing, control treadmill exercise, and identical exercise after atenolol (1 mg/kg po). Prior to study, in every dog % delta WT and MBF in the ischemic area were normal at rest, indicating collateral development. During control exercise, % delta WT in the ischemic region markedly decreased from 27 to 4%, and transmural ischemia was evident in that region. Heart rate, systolic LVP, and LV (+)dP/dt were significantly lower during exercise after atenolol than during control exercise. % delta WT in the normal area was only 81% of that during control exercise, but dysfunction in the ischemic area was improved (77% increase compared with control exercise). Accompanying the improved function was a significant increase of MBF/beat and relative MBF in the ischemic zone; the endocardial-to-epicardial ratio increased from 0.27 to 0.47. Thus atenolol improved regional MBF distribution, thereby diminishing exercise-induced regional myocardial dysfunction and accelerating its recovery.

Abstract 87: Cyclosporin A does not Prevent Myocardial Dysfunction after Resuscitation from Cardiac Arrest in Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Iyad M Ayoub ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri
Keyword(s):  
Cardiac Arrest ◽  
Cyclosporin A ◽  
Chest Compression ◽  
Rat Model ◽  
Mitochondrial Permeability Transition ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
List Type ◽  
Ischemia And Reperfusion ◽  
Biphasic Waveform

Objective: We have previously reported in a rat model of VF and closed-chest resuscitation that cytochrome c is released into the bloodstream after resuscitation from cardiac arrest attaining plasma levels inversely proportional to survival. Recent evidence indicates that release of cytochrome c during ischemia and reperfusion may be a manifestation of prolonged opening of the mitochondrial permeability transition pore (mPTP). In this study, we investigated whether cyclosporin A (CsA, an inhibitor of mPTP opening) can prevent post-resuscitation (PR) myocardial dysfunction and improve survival. Methods: VF was electrically induced and left untreated for 10 mins. Resuscitation was attempted by 8 mins of chest compression followed by biphasic waveform defibrillation. Rats were randomized to received a bolus CsA (10 mg/kg) five minutes before inducing VF (n=6), immediately before starting chest compression (n=6), or to receive vehicle control before inducing VF (n=3) or before starting chest compression (n=3). CsA-treated (n=12) and vehicle-treated (n=6) rats were pooled for this analysis after noticing no differences between subgroups. Resuscitated rats were monitored for up to 6 hours. Results: All rats were successfully resuscitated. Treatment with CsA did not improve PR myocardial function (Table ). Survival time was comparable between CsA-treated (321±67 mins) and vehicle-treated (331±67 mins) rats. Conclusions: In our rat model of VF and resuscitation, CsA failed to prevent PR myocardial dysfunction and improve survival. These data contrast with numerous studies demonstrating a protective effect in isolated heart models of ischemia and reperfusion. Two possible explanations are the mPTP does not open in this unique setting of cardiac arrest and resuscitation, and the optimal in vivo dose of CsA needs to be determined as the protective effects of CsA are dose dependent. Hemodynamic and Left Ventricular Function

scholarly journals Impact of Arrhythmia on Myocardial Perfusion: A Computational Model-Based Study

Mathematics ◽  
2021 ◽  
Vol 9 (17) ◽  
pp. 2128
Author(s):  
Xinyang Ge ◽  
Sergey Simakov ◽  
Youjun Liu ◽  
Fuyou Liang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Myocardial Ischemia ◽  
Computational Model ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Metabolic Demand ◽  
Severe Coronary Artery ◽  
Artery Disease

(1) Background: Arrhythmia, which is an umbrella term for various types of abnormal rhythms of heartbeat, has a high prevalence in both the general population and patients with coronary artery disease. So far, it remains unclear how different types of arrhythmia would affect myocardial perfusion and the risk/severity of myocardial ischemia. (2) Methods: A computational model of the coronary circulation coupled to the global cardiovascular system was employed to quantify the impacts of arrhythmia and its combination with coronary artery disease on myocardial perfusion. Furthermore, a myocardial supply–demand balance index (MSDBx) was proposed to quantitatively evaluate the severity of myocardial ischemia under various arrhythmic conditions. (3) Results: Tachycardia and severe irregularity of heart rates (HRs) depressed myocardial perfusion and increased the risk of subendocardial ischemia (evaluated by MSDBx), whereas lowering HR improved myocardial perfusion. The presence of a moderate to severe coronary artery stenosis considerably augmented the sensitivity of MSDBx to arrhythmia. Further data analyses revealed that arrhythmia induced myocardial ischemia mainly via reducing the amount of coronary artery blood flow in each individual cardiac cycle rather than increasing the metabolic demand of the myocardium (measured by the left ventricular pressure-volume area). (4) Conclusions: Both tachycardia and irregular heartbeat tend to increase the risk of myocardial ischemia, especially in the subendocardium, and the effects can be further enhanced by concomitant existence of coronary artery disease. In contrast, properly lowering HR using drugs like β-blockers may improve myocardial perfusion, thereby preventing or relieving myocardial ischemia in patients with coronary artery disease.

scholarly journals Neuregulin-1 Promotes Myocardial Angiogenesis in the Rat Model of Diabetic Cardiomyopathy

2018 ◽  
Vol 46 (6) ◽  
pp. 2325-2334 ◽  
Author(s):  
Chun Gui ◽  
Zhi-yu  Zeng ◽  
Qi Chen ◽  
Ya-wei Luo ◽  
Lang Li ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Treatment Group ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Diabetic Cardiomyopathy ◽  
Rat Model ◽  
Capillary Density ◽  
Left Ventricular ◽  
Control Group ◽  
Neuregulin 1

Background/Aims: Microvascular insufficiency takes a critical role in the development of diabetic cardiomyopathy (DCM). So this study was designed to investigate the effects of Neuregulin-1 (NRG-1) treatment on myocardial angiogenesis and the changes of VEGF/Flk1 and Ang-1/Tie-2 signaling in the rat model of DCM. Methods: Diabetic rats were induced by a single intraperitoneal injection of Streptozotocin. 12 weeks after the diabetes induction, the rats with NRG-1 treatment were treated with tail vein injection of NRG-1 at the dose of 10µg/kg/d for consecutive 10 days. Cardiac function was assessed using catheter MPA cardiac function analysis system. Myocardial blood flow (MBF) was assessed with stable-isotope labeled microspheres. Capillary density was measured by CD31 immunohistochemistry. The protein expression and receptors phosphorylation were assessed using western blot. Results: Left ventricular function, capillary density and MBF were significantly reduced in DCM group when compared with those in the control group (P< 0.01, P< 0.01 and P< 0.05 respectively). Left ventricular function and capillary density were significantly increased in NRG-1 treatment group when compared with those in the DCM group (P< 0.05 and P< 0.05 respectively). The expression of VEGF and Ang-1 and the phosphorylation of Flk1 and Tie-1 were significantly decreased in DCM group as compared with those in the control group. However, those in the NRG-1 treatment group were significantly increased as compared with those in the DCM group. In vitro, NRG-1 treatment increased significantly the expression of VEGF and Ang-1 in human coronary artery smooth muscle cells. Conclusions: NRG-1 can increase the myocardial angiogenesis of DCM, probably via the direct effects of NRG-1 and via the increasing expression of VEGF and Ang-1. These findings may contribute to developing a novel approach to reverse the impaired angiogenic responses in diabetes or coronary artery disease.

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.

scholarly journals Case Report: Cardiac arrest due to traumatic coronary artery dissection treated by extracorporeal membrane resuscitation

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1720
Author(s):  
Kumiko Tanaka ◽  
Taka-aki Nakada ◽  
Tadayuki Kadohira ◽  
Shigeto Oda
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Spontaneous Circulation ◽  
Left Ventricular ◽  
Artery Dissection ◽  
Coronary Artery Dissection ◽  
Circumflex Artery ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Left Circumflex Artery

Traumatic coronary artery dissection, which is rare in blunt trauma, has high risk of acute myocardial infarction and cardiac arrest. A 44-year-old man who had a traffic accident was transferred to the emergency department with refractory ventricular fibrillation (VF). After conventional cardiopulmonary resuscitation, we introduced extracorporeal cardiopulmonary resuscitation (ECPR) and obtained return of spontaneous circulation with ST-elevation electrocardiogram at V4-6. Subsequent coronary angiography and intravascular ultrasound supported by extracorporeal membrane oxygenation (ECMO) revealed complete occlusions of left anterior descending and left circumflex artery due to dissections. Drug-eluting stents were placed with restorations of TIMI 2 flows. After ICU admission, his left ventricular function gradually recovered; he was successfully weaned from VA-ECMO on day 9. ECPR may be a valuable option to allow time and stable hemodynamic condition to treat the cause of cardiac arrest.

Abstract 142: Combined Therapy with Polyethylene Glycol-20k and MCC950 Preserves Post-resuscitation Myocardial Mitochondrial Function in a Rat Model of Cardiac Arrest and Cardiopulmonary Resuscitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Lian Liang ◽  
Guozhen Zhang ◽  
Hui Li ◽  
Cheng Cheng ◽  
Tao Jin ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Polyethylene Glycol ◽  
Cardiopulmonary Resuscitation ◽  
Rat Model ◽  
Mitochondrial Function ◽  
Complex I ◽  
Myocardial Dysfunction ◽  
Combined Therapy ◽  
Chain Complex ◽  
Sprague Dawley

Introduction: Mitochondrial dysfunction from global ischemic-reperfusion (I/R) injury is a major contributor to post-resuscitation myocardial dysfunction. Polyethylene Glycol-20k (PEG-20k) shortens the no-flow phenomenon and improves microcirculation while MCC950 selectively inhibits activation of the NLRP3-inflammasome ensuing pyroptosis. We evaluated the effect of combined therapy with PEG-20k and MCC950 on myocardial mitochondrial function as measured by electron transport chain complex respiration in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Methods: 30 Sprague-Dawley rats weighing between 450-550 g were randomized into five groups (n=6): (1) sham (S); (2) control (C); (3) PEG-20k (P); (4) MCC950 (M); (5) combined (P&M). Ventricular fibrillation (VF) was electrically induced and untreated for 6min, followed by 8min CPR. Resuscitation was attempted with a 4J defibrillation. 2mL P was infused over 2 min at the beginning of CPR, while M (10mg/kg) was administered intraperitoneal (IP) immediately after return of spontaneous circulation (ROSC). At ROSC 6hr, 100mg of heart was harvested, transferred directly into ice-cold K medium (1mL), and homogenized to obtain a 10% homogenate. Homogenates (50μL) were transferred to calibrated Oxygraph-2 chambers. Mitochondrial function was measured using high resolution respirometry. Oxygen flux was corrected and expressed by tissue wet weight, pmol/(min*mg). Data were analyzed by one-way analysis of variance (one-way ANOVA) followed by Tukey’s post hoc test for comparisons between multiple groups. Results: Complex I respiration in C was compromised at ROSC 6hr compared to S (564.0±160.0 vs 2729.5±339.5, p<0.001). As expected, P and M restored complex I respiration (1224.4±328.6, p<0.001) and (1804.4±293.1, p<0.01) compared to C. P&M further consolidated Complex I respiration function recovery (2527.6±145.5). Conclusion: Combined Therapy with PEG-20k and MCC950 preserves post-resuscitation myocardial mitochondrial function in a rat model of CA and CPR.

Abstract 211: UAMC-3203 Reduces the Severity of Post-resuscitation Myocardial Dysfunction in a Rat Model of Cardiac Arrest and Cardiopulmonary Resuscitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Tao Jin ◽  
Cheng Cheng ◽  
Hui Li ◽  
Lian Liang ◽  
Guozhen Zhang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Cardiac Function ◽  
Rat Model ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Spontaneous Circulation ◽  
Sprague Dawley

Introduction: Previous studies have demonstrated that ferroptosis, a newly defined iron-dependent cell death, mediates ischemia/reperfusion induced cardiomyopathy. However, it is unclear whether ferroptosis plays a role in post-resuscitation myocardial dysfunction (PRMD). This study investigated the effects of UAMC-3203, a novel analog of ferroptosis specific inhibitors, on myocardial function after cardiopulmonary resuscitation (CPR). Hypothesis: Administration of UAMC-3203 during CPR alleviates PRMD in a rat model of cardiac arrest (CA) and CPR. Methods: 18 male Sprague-Dawley rats weighing between 450-550g were randomized into 3 groups: 1) Sham, 2) Control, and 3) UAMC-3203 (5mg/kg, IP at start of precordial compression). Ventricular fibrillation (VF) was induced and continued for 6min. CPR was then initiated for 8min, after which defibrillation was attempted. Ejection fraction (EF), cardiac output (CO) and myocardial performance index (MPI) were measured by echocardiography at baseline, 15min, 1h, 3h and 6h respectively after return of spontaneous circulation (ROSC). Results: A significant reduction in cardiac function was observed after resuscitation. At 15 minutes after ROSC, ultrasound showed no difference in cardiac function between UAMC and control. However, at 1, 3, and 6 h after ROSC, UAMC significantly improved myocardial function (p<0.05) (Fig. 1). Conclusion: A ferroptosis-specific inhibitor, UAMC-3203, alleviated PRMD significantly in a rat of model of CA and CPR. Further study is needed to determine the benefit of this agent in larger animals and potential safety in humans before it can be tested in clinical resuscitation.

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