Cardio- and Vasoprotective Effects of Quinacrine in an In Vivo Rat Model of Myocardial Ischemia/Reperfusion Injury.

This study aimed to investigate the cardioprotective effect of quinacrine in an in vivo model of myocardial ischemia/reperfusion injury. A 30-min regional myocardial ischemia followed by a 2-h reperfusion was modeled in anesthetized Wistar rats. Starting at the last minute of ischemia and during the first 9 min of reperfusion the rats in the control (n=8) and experimental (n=9) groups were injected with 0.

Advanced technique of myocardial no-reflow quantification using indocyanine green.

The post-ischemic no-reflow phenomenon after primary percutaneous coronary intervention (PCI) is observed in more than half of subjects and is defined as the absence or marked slowing of distal coronary blood flow despite removal of the arterial occlusion. To visualize no-reflow in experimental studies, the fluorescent dye thioflavin S (ThS) is often used, which allows for the estimation of the size of microvascular obstruction by staining the endothelial lining of vessels. Based on the ability of indocyanine green (ICG) to be retained in tissues with increased vascular permeability, we proposed the possibility of using it to assess not only the severity of microvascular obstruction but also the degree of vascular permeability in the zone of myocardial infarction.

Influenza A(H1N1)pdm09 Virus Aggravates Pathology of Blood Vessels in Wistar Rats with Premorbid Acute Cardiomyopathy.

Influenza virus can infect the vascular endothelium and cause endothelial dysfunction. Persons at higher risk for severe influenza are patients with acute and chronic cardiovascular disorders; however, the mechanism of influenza-induced cardiovascular system alteration remains not fully understood. The aim of the study was to assess the functional activity of mesenteric blood vessels of Wistar rats with premorbid acute cardiomyopathy infected with Influenza A(H1N1)pdm09 virus.

Acute Effect of Selective Chemical Inactivation of Sympathetic or Parasympathetic Atrial Ganglionated Plexus Structures on Atrial Fibrillation Inducibility in Pigs.

We studied the role of both parts of the autonomic intracardiac nervous system in the pathogenesis of atrial fibrillation (AF). In 12 pigs weighing 39±3 kg, AF was induced by burst stimulation. Chemical inactivation of intrinsic cardiac neurons within the right atria was performed by transendocardial injections of liposomal neuromodulators into the dorsal part of the right atrial wall.

Biocomposite films based on chitosan and cerium oxide nanoparticles with promising regenerative potential.

Polymeric nanocomposite materials have great potential in the development of tissue-engineered scaffolds because they affect the structure and properties of polymeric materials and regulate cell proliferation and differentiation. In this work, cerium oxide nanoparticles (CeONPs) were incorporated into a chitosan (CS) film to improve the proliferation of multipotent mesenchymal stem cells (MSCs). The citrate-stabilized CeONPs with a negative ζ-potential (-25.