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Cardiac arrest, stony heart, and cardiopulmonary resuscitation: An updated revisit.
World J Cardiol
March 2024
Department of Anesthesiology, Hamad Medical Corporation, Doha 3050, Qatar.
The post-resuscitation period is recognized as the main predictor of cardiopulmonary resuscitation (CPR) outcomes. The first description of post-resuscitation syndrome and stony heart was published over 50 years ago. Major manifestations may include but are not limited to, persistent precipitating pathology, systemic ischemia/reperfusion response, post-cardiac arrest brain injury, and finally, post-cardiac arrest myocardial dysfunction (PAMD) after successful resuscitation.
View Article and Find Full Text PDFImpact of folic acid supplementation on ischemia‒reperfusion-induced kidney injury in rats: folic acid prophylactic role revisited.
J Physiol Sci
February 2024
Department of Medical Physiology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Folic acid (FA), with its anti-inflammatory and antioxidant properties, may offer protection against ischemia-reperfusion (IR) injury. This study investigated whether FA safeguards rat kidneys from IR by targeting high mobility group box-1 (HMGB1), a key inflammatory mediator. Fifty adult male Wistar rats were randomly allocated into four groups: control, IR, IR + FA pretreatment, and FA alone.
View Article and Find Full Text PDFEffects of hypoxia versus ischaemia on vascular functions of isolated rat thoracic aorta: revisiting the vascular ischaemia/reperfusion model.
Kardiochir Torakochirurgia Pol
September 2023
Department of Medical Pharmacology, Başkent University Faculty of Medicine, Ankara, Turkey.
Introduction: The rat vascular ischaemia and reperfusion model is used to evaluate the molecular and functional effects of potential agents against ischaemia and reperfusion injury of autologous graft veins. However, there is no consensus on whether hypoxia, rather than ischaemia, is sufficient to induce vascular dysfunction.
Aim: To compare the effects of hypoxia and ischaemia, with or without reperfusion, on the vascular functions of isolated thoracic aortic rings of rats.
Revisiting regulatory T cells as modulators of innate immune response and inflammatory diseases.
Front Immunol
November 2023
Regenerative Medicine Institute (REMEDI) at CÚRAM SFI Research Centre for Medical Devices, School of Medicine, College of Medicine, Nursing and Health Sciences, University of Galway, Galway, Ireland.
Regulatory T cells (Treg) are known to be critical for the maintenance of immune homeostasis by suppressing the activation of auto- or allo-reactive effector T cells through a diverse repertoire of molecular mechanisms. Accordingly, therapeutic strategies aimed at enhancing Treg numbers or potency in the setting of autoimmunity and allogeneic transplants have been energetically pursued and are beginning to yield some encouraging outcomes in early phase clinical trials. Less well recognized from a translational perspective, however, has been the mounting body of evidence that Treg directly modulate most aspects of innate immune response under a range of different acute and chronic disease conditions.
View Article and Find Full Text PDFPulmonary reperfusion injury in post-palliative intervention of oligaemic cyanotic CHD: a new catastrophic consequence or just revisiting the same old story?
Cardiol Young
November 2023
Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia.
Pulmonary reperfusion injury is a well-recognised clinical entity in the setting pulmonary artery angioplasty for pulmonary artery stenosis or chronic thromboembolic disease, but not much is known about this complication in post-palliative intervention of oligaemic cyanotic CHD. The pathophysiology of pulmonary reperfusion injury in this population consists of both ischaemic and reperfusion injury, mainly resulting in oxidative stress from reactive oxygen species generation, followed by endothelial dysfunction, and cytokine storm that may induce multiple organ dysfunction. Other mechanisms of pulmonary reperfusion injury are "no-reflow" phenomenon, overcirculation from high pressure in pulmonary artery, and increased left ventricular end-diastolic pressure.
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