S-Nitroso Human Serum Albumin Enhances Left Ventricle Hemodynamic Performance and Reduces Myocardial Damage after Local Ischemia-Reperfusion Injury.
Daniele LinardiSeth HallströmGiovanni Battista LucianiAlessio RungatscherPublished in: Biomedicines (2024)
Endothelial nitric oxide (NO) production is crucial in maintaining vascular homeostasis. However, in the context of ischemia-reperfusion (I/R) injury, uncoupled endothelial nitric oxide synthase (eNOS) can exacerbate reactive oxygen species (ROS) generation. Supplementation with S-nitroso human serum albumin (S-NO-HSA) offers a potential solution by mitigating eNOS uncoupling, thereby enhancing NO bioavailability. In a study conducted at the University of Verona, male rats underwent thoracotomy followed by 30 min left anterior descendant coronary (LAD) occlusion and subsequent reperfusion. Hemodynamic parameters were meticulously assessed using a conductance catheter inserted via the carotid artery. The rats were stratified into two main groups based on reperfusion duration and the timing of drug infusion, with the effects of S-NO-HSA evaluated after 2 or 24 h. Remarkably, intravenous administration of S-NO-HSA, initiated before or during ischemia, exhibited notable benefits. It significantly improved left ventricular function, safeguarded energetic substrates such as phosphocreatine and ATP, and sustained glutathione levels akin to basal conditions, indicative of diminished oxidative stress. The data from this study strongly suggest a protective role for S-NO-HSA in mitigating I/R injury induced by LAD artery occlusion, a phenomenon observed at both 2 and 24 h post-reperfusion. These findings underscore the promising therapeutic potential of NO supplementation in alleviating myocardial damage subsequent to ischemic insult.
Keyphrases
- nitric oxide synthase
- human serum albumin
- nitric oxide
- oxidative stress
- left ventricular
- ischemia reperfusion injury
- cerebral ischemia
- acute myocardial infarction
- reactive oxygen species
- dna damage
- endothelial cells
- acute ischemic stroke
- subarachnoid hemorrhage
- hydrogen peroxide
- aortic stenosis
- blood brain barrier
- mitral valve
- heart failure
- coronary artery disease
- cardiac resynchronization therapy
- coronary artery
- brain injury
- induced apoptosis
- pulmonary hypertension
- cell death
- high dose
- diabetic rats
- percutaneous coronary intervention
- electronic health record
- low dose
- emergency department
- ultrasound guided
- acute coronary syndrome
- risk assessment
- big data
- heat shock
- signaling pathway
- deep learning
- endoplasmic reticulum stress
- solid state