A simulation study of left ventricular decompression using a double lumen arterial cannula prototype during a veno-arterial extracorporeal membrane oxygenation.

Background: Veno-arterial extracorporeal membrane oxygenation can be vital to support patients in severe or rapidly progressing cardiogenic shock. In cases of left ventricular distension, left ventricular decompression during veno-arterial extracorporeal membrane oxygenation may be a crucial factor influencing the patient outcome. Application of a double lumen arterial cannula for a left ventricular unloading is an alternative, straightforward method for left ventricular decompression during extracorporeal membrane oxygenation in a veno-arterial configuration.

Electrocardiogram-synchronized pulsatile extracorporeal life support preserves left ventricular function and coronary flow in a porcine model of cardiogenic shock.

Introduction: Veno-arterial extracorporeal life support (ECLS) is increasingly being used to treat rapidly progressing or severe cardiogenic shock. However, it has been repeatedly shown that increased afterload associated with ECLS significantly diminishes left ventricular (LV) performance. The objective of the present study was to compare LV function and coronary flow during standard continuous-flow ECLS support and electrocardiogram (ECG)-synchronized pulsatile ECLS flow in a porcine model of cardiogenic shock.

The peripheral cannulas in extracorporeal life support.

Femoral cannulation is a minimally invasive method which is an alternative method for central cannulation. This review focuses on the parameters and features of the available peripheral cannulas. Nowadays there exist many peripheral cannulas in a variety of sizes, configurations and lengths to meet the specific needs of the patients.

Novel porcine model of acute severe cardiogenic shock developed by upper-body hypoxia.

Despite the urgent need for experimental research in the field of acute heart failure and, particularly cardiogenic shock, currently there are only limited options in large animal models enabling research using devices applied to human subjects. The majority of available models are either associated with an unacceptably high rate of acute mortality or are incapable of developing sufficient severity of acute heart failure. The objective of our research was to develop a novel large animal model of acute severe cardiogenic shock.

Ischemic Postconditioning and Nitric Oxide Administration Failed to Confer Protective Effects in a Porcine Model of Extracorporeal Cardiopulmonary Resuscitation.

The protective effects of ischemic postconditioning (IPC) and nitric oxide (NO) administration have been demonstrated in several ischemic scenarios. However, current evidence regarding the effect of IPC and NO in extracorporeal cardiopulmonary resuscitation remains lacking. Fifteen female swine (body weight 45 kg) underwent veno-arterial extracorporeal membrane oxygenation (ECMO) implantation; cardiac arrest-ventricular fibrillation was induced by rapid ventricular pacing.

Increasing venoarterial extracorporeal membrane oxygenation flow negatively affects left ventricular performance in a porcine model of cardiogenic shock.

Background: The aim of this study was to assess the relationship between extracorporeal blood flow (EBF) and left ventricular (LV) performance during venoarterial extracorporeal membrane oxygenation (VA ECMO) therapy.

Methods: Five swine (body weight 45 kg) underwent VA ECMO implantation under general anesthesia and artificial ventilation. Subsequently, acute cardiogenic shock with signs of tissue hypoxia was induced.

[Retroviral reporter systems for the assessment of activity of stress-induced signal transduction pathways controlled by p53, HIF-1 and HSF-1 transcription factors].

The tumor suppressor p53, hypoxia-inducible factor 1 (HIF-1), and heat-shock factor 1 (HSF-1) are the key transcription factors involved in the stress response to damage of the genetic material, hypoxia, or heat shock, respectively. Since these factors play a considerable role in tumor development and progression, modulation of their activities may be used in cancer therapy. To quantitate the transcriptional activities of p53, HIF-1, and HSF-1, reporter constructs were obtained on the basis of retroviral and lentiviral vectors, allowing generation of reporter cultures from almost all cell types.

[Construction of a reporter system for fine quantitative assessment of activity of p53 protein in cultured cells].

Since transcriptional activation of genes downregulating cell proliferation mediates the tumor suppressor activity of p53, induction of p53 targets was assumed to adequately reflect the state of p53-dependent pathways. To estimate the p53 activity in cultured cells, self-inactivating retrovirus constructs pSIP-ConA-GFP and pSIP-ConA-LacZ were obtained to express the GFP or beta-galactosidase reporter gene under the control of a promoter containing p53-responsive elements. The advantages of these constructs were efficient delivery, comparable expression in different cells of a culture, and, consequently, the possibility of quantitating the p53 activity induced by various agents.

[Dominant-negative inactivation of p53: the effect of the proportion between trans-dominant inhibitor and its target].

Dominant-negative mutations of the p53 tumor suppressor gene and oligomerization of the mutant and wild-type p53 are considered responsible for functional inactivation of the p53 tetramer. Although dominant-negative inactivation of p53 is well reproducible in experimental systems, its contribution to processes occurring in tumor cells heterozygous at p53 is still unclear. To study the effect of dominant-negative inhibitor GSE22 on the p53 activity, cultures coexpressing GSE22 and tetracycline-suppressible p53 were derived from p53-negative cell lines.