Necrosulfonamide improves post-resuscitation myocardial dysfunction via inhibiting pyroptosis and necroptosis in a rat model of cardiac arrest.

The systemic inflammatory response following global myocardial ischemia/reperfusion (I/R) injury is a critical driver of poor outcomes. Both pyroptosis and necroptosis are involved in the systemic inflammatory response and contribute to regional myocardial I/R injury. This study aimed to explore the effect of necrosulfonamide (NSA) on post-resuscitation myocardial dysfunction in a rat model of cardiac arrest.

The Selective NLRP3-inflammasome inhibitor MCC950 Mitigates Post-resuscitation Myocardial Dysfunction and Improves Survival in a Rat Model of Cardiac Arrest and Resuscitation.

Purpose: To investigate the effects of the selective NLRP3 inflammasome inhibitor MCC950 on post-resuscitation myocardial function and survival in a rat model of cardiopulmonary resuscitation (CPR).

Methods: Thirty-six Sprague Dawley rats were randomized into three groups: (1) MCC950, (2) control, and (3) sham. Each group consisted of a 6 h non-survival subgroup (n = 6) and a 48 h survival subgroup (n = 6).

Effects of NLRP3 inflammasome blockade on postresuscitation cerebral function in a rat model of cardiopulmonary resuscitation.

Cardiac arrest (CA) remains a major public health issue. Inflammatory responses with overproduction of interleukin-1β regulated by NLRP3 inflammasome activation play a crucial role in cerebral ischemia/reperfusion injury. We investigated the effects of the selective NLRP3-inflammasome inhibitor MCC950 on post-resuscitation cerebral function and neurologic outcome in a rat model of cardiac arrest.

Cerebral and myocardial mitochondrial injury differ in a rat model of cardiac arrest and cardiopulmonary resuscitation.

Brain mitochondria are more sensitive to global ischemia compared to heart mitochondria. Complex I in the electron transport chain (ETC) is sensitive to ischemic injury and is a major control point of the rate of ADP stimulated oxygen consumption. The purpose of this study was to explore whether changes in cerebral and myocardial mitochondria differ after cardiac arrest.

PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation.

The dysregulated expression of microRNAs (miRs) has been associated with pathological and physiological processes of atherosclerosis (AS). In addition, PR domain-containing 16 (PRDM16), a transcriptional mediator of brown fat cell identity and smooth muscle cell activities, may be involved in the hypercholesterolemia during development of AS. The bioinformatic analysis identified a regulatory miR-448 of PRDM16.

Effects of Polyethylene Glycol-20k on Coronary Perfusion Pressure and Postresuscitation Myocardial and Cerebral Function in a Rat Model of Cardiac Arrest.

Background Epinephrine increases the rate of return of spontaneous circulation. However, it increases severity of postresuscitation myocardial and cerebral dysfunction and reduces duration of survival. We investigated the effects of aortic infused polyethylene glycol, 20 000 molecular weight (PEG-20k) during cardiopulmonary resuscitation on coronary perfusion pressure, postresuscitation myocardial and cerebral function, and duration of survival in a rat model of cardiac arrest.

Adenoviral.βARKct Cardiac Gene Therapy Ameliorates Cardiac Function Following Cardiopulmonary Bypass in A Swine Model.

Objective: This study is to evaluate the effects of the Adenoviral βARKct (Adv. βARKct) myocardial gene transfection following cardioplegic arrest on cardiopulmonary bypass (CPB) in a swine model.

Methods: Swine models of cardioplegic arrest on CPB were established after 5 days of myocardial injection of Adv.

Adenoviral βARKct Cardiac Gene Transfer Ameliorates Postresuscitation Myocardial Injury in a Porcine Model of Cardiac Arrest.

Objective: The aim of the study was to determine whether the inhibition of the G-protein-coupled receptor kinase 2 by adenoviral βARKct cardiac gene transfer can ameliorate postresuscitation myocardial injury in pigs with cardiac arrest (CA) and explore the mechanism of myocardial protection.

Methods: Male landrace domestic pigs were randomized into the sham group (anesthetized and instrumented, but ventricular fibrillation was not induced) (n = 4), control group (ventricular fibrillation 8 min, n = 8), and βARKct group (ventricular fibrillation 8 min, n = 8). Hemodynamic parameters were monitored continuously.

Protective effects of nicorandil against cerebral injury in a swine cardiac arrest model.

The present study investigated the effects of nicorandil on cerebral injury following cardiopulmonary resuscitation (CPR) in a swine model of cardiac arrest. CPR was performed on swine following 4 min induced ventricular fibrillation. Surviving animals were randomly divided into 3 groups: A nicorandil group (n=8), a control group (n=8) and a sham group (n=4).

[Effects of mild hypothermia on β-adrenergic signaling pathway in a cardiac arrest swine model].

Objective: To observe the effect of mild hypothermia on myocardial β-adrenergic receptor (β-AR) signal pathway after cardiopulmonary resuscitation (CPR) in pigs with cardiac arrest (CA) and explore the mechanism of myocardial protection.

Methods: Healthy male Landraces were collected for reproducing the CA-CPR model (after 8-minute untreated ventricular fibrillation, CPR was implemented). The animals were divided into two groups according to random number table (n = 8).

Cardioprotective effect of nicorandil against myocardial injury following cardiac arrest in swine.

Introduction: Nicorandil, a vasodilatory drug used to treat angina, was reported to protect against myocardial ischemia-reperfusion injury in various animal models. However, its cardioprotective action following cardiac arrest is unknown. We examined the cardioprotective effects of nicorandil in a porcine model of cardiac arrest and resuscitation.

Sodium Ferulate Protects against Angiotensin II-Induced Cardiac Hypertrophy in Mice by Regulating the MAPK/ERK and JNK Pathways.

. It has been reported that sodium ferulate (SF) has hematopoietic function against anemia and immune regulation, inflammatory reaction inhibition, inhibition of tumor cell proliferation, cardiovascular and cerebrovascular protection, and other functions. Thus, this study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways.

Association of Genetic Polymorphisms on VEGFA and VEGFR2 With Risk of Coronary Heart Disease.

Coronary heart disease (CHD) is a cardiovascular disease which is contributed by abnormal neovascularization. VEGFA (vascular endothelial growth factor A) and VEGFR2 (vascular endothelial growth factor receptor 2) have been revealed to be involved in the pathological angiogenesis. This study was intended to confirm whether single nucleotide polymorphisms (SNPs) of VEGFA and VEGFR2 were associated with CHD in a Chinese population, considering pathological features and living habits of CHD patients.

Complete mitochondrial genome sequence of the heart failure model of cardiomyopathic Syrian hamster (Mesocricetus auratus).

In this study we sequenced the complete mitochondrial genome sequencing of a heart failure model of cardiomyopathic Syrian hamster (Mesocricetus auratus) for the first time. The total length of the mitogenome was 16,267 bp. It harbored 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes and 1 non-coding control region.

Shen-Fu injection reduces impaired myocardial β-adrenergic receptor signaling after cardiopulmonary resuscitation.

Background: Post-resuscitation myocardial dysfunction has been implicated as a major cause of fatal outcome in patients who survive initially successful cardiopulmonary resuscitation (CPR). In our previous study, we found that impaired myocardial β-adrenergic receptor (AR) signaling is a key mechanism in post-resuscitation myocardial dysfunction and Shen-Fu injection (SFI) can attenuate post-resuscitation myocardial dysfunction. However, whether SFI can prevent impaired post-resuscitation myocardial β-AR signaling is not yet known.

Evaluation of respiratory dysfunction in a pig model of severe acute dichlorvos poisoning.

Background: Respiratory failure is the main cause of death in acute organophosphorus pesticide poisoning. In this study, a pulse-induced contour cardiac output monitor was used to evaluate the respiratory status in a pig model of acute dichlorvos poisoning.

Methods: Twenty female pigs were randomly allocated to dichlorvos (n = 7), atropine (n = 7), and control (n = 6) groups.

Shen-fu injection attenuates postresuscitation lung injury in a porcine model of cardiac arrest.

Objective: To investigate the effects of Shen-Fu injection (SFI) on postresuscitation lung injury in a porcine model of cardiac arrest.

Methods: Twenty-four anaesthetised male Landrace pigs were subjected to 4 min of untreated ventricular fibrillation (VF), followed by standard cardiopulmonary resuscitation. Sixteen successfully resuscitated pigs were randomised into two groups (eight pigs per group); one group received an SFI infusion and the other group received a normal saline infusion, at an infusion rate of 0.

Impaired β-adrenergic receptor signalling in post-resuscitation myocardial dysfunction.

Objective: Post-resuscitation myocardial dysfunction is a major cause of fatality in patients receiving successful cardiopulmonary resuscitation. The mechanism of post-resuscitation myocardial dysfunction is largely unknown, although is generally considered related to ischaemia occurring during cardiac arrest and resuscitation and/or reperfusion injury after restoration of circulation. A key mechanism responsible for reduced contractile reserves in chronic heart failure is impaired β-adrenergic receptor signalling.

Investigation of myocardial stunning after cardiopulmonary resuscitation in pigs.

Objective: To investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.

Methods: After 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.

Shen-fu injection attenuates postresuscitation myocardial dysfunction in a porcine model of cardiac arrest.

To investigate the effect of Shen-Fu injection (SFI) for the management of postresuscitation myocardial dysfunction in a porcine model of cardiac arrest. Ventricular fibrillation was induced electrically in anesthetized domestic swine. After 4 min of untreated ventricular fibrillation, cardiopulmonary resuscitation was initiated.

Effect of continuous compressions and 30:2 cardiopulmonary resuscitation on global ventilation/perfusion values during resuscitation in a porcine model.

Objective: Rescue ventilations during bystander resuscitation, although previously considered essential, interrupt the continuity of chest compressions and might have deleterious effects in basic life support. This study was undertaken to analyze the global ventilation/perfusion values of continuous compressions and 30:2 cardiopulmonary resuscitation to determine the effectiveness for each approach in a porcine model of prolonged bystander cardiopulmonary resuscitation for ventricular fibrillation.

Design: Prospective, randomized animal study.

Comparison of the efficacy of nifekalant and amiodarone in a porcine model of cardiac arrest.

Objective: To compare the efficacy of nifekalant and amiodarone in the treatment of cardiac arrest in a porcine model.

Methods: After 4min of untreated ventricular fibrillation, animals were randomly treated with nifekalant (2mgkg(-1)), amiodarone (5mgkg(-1)) or saline placebo (n=12 pigs per group). Precordial compression and ventilation were initiated after drug administration and defibrillation was attempted 2min later.