Hyperbaric oxygenation improves redox control and reduces mortality in the acute phase of myocardial infarction in a rat model

Abstract

among the mechanisms of action of hyperbaric oxygenation (HBo), the chance of reducing injury by interfering with the mechanisms of redox homeostasis in the heart leads to the possibility of extending the period of viability of the myocardium at risk. This would benefit late interventions for reperfusion to the ischemic area. The objective of the present study was to investigate the changes in the redox system associated with HBO therapy maintained during the first hour after coronary occlusion in an acute myocardial infarction (Mi) rat model. Surviving male rats (n=105) were randomly assigned to one of three groups: Sham (SH=26), myocardial infarction (Mi=45) and infarction+hyperbaric therapy (HBo=34, 1 h at 2.5 atm). after 90 min of coronary occlusion, a sample of the heart was collected for western blot analysis of total protein levels of superoxide dismutase, catalase, peroxiredoxin and 3-nitrotyrosine. Glutathione was measured by enzyme-linked immunosorbent assay (eliSa). The detection of the superoxide radical anion was carried out by oxidation of dihydroethidium analyzed with confocal microscopy. The mortality rate of the MI group was significantly higher than that of the HBO group. no difference was noted in the myocardial infarction size. The oxidized/reduced glutathione ratio and peroxiredoxin were significantly higher in the SH and MI when compared to the HBo group. Superoxide dismutase enzymes and catalase were significantly higher in the HBO group compared to the MI and SH groups. 3-nitrotyrosine and the superoxide radical were significantly lower in the HBO group compared to these in the Mi and SH groups. These data demonstrated that hyperbaric oxygenation therapy decreased mortality by improving redox control in the hearts of rats in the acute phase of myocardial infarction.

Redox-related biomarkers in human cardiovascular disease - classical footprints and beyond

“… [ 243 ] 3-NT Animal study + Dot blot method analysis of rat hearts Increased 3-NT after MI in rats. [ 244 ] HNE Clinical trial (23 patients with dilated cardiomyopathy, 13 CTR) ++ Immunohistochemical analysis of endomyocardial biopsies 5-fold increased HNE in cardiomyopathy patients. Treatment with carvedilol reduces HNE by 40%.…”

Effects of Hyperbaric Oxygen Preconditioning on Doxorubicin Cardiorespiratory Toxicity

“…Increasing evidence supports the use of HBO as an effective therapy to maintain muscle redox balance, prevent mitochondrial dysfunction and preserve muscle function [ 10 , 40 ]. While limited information exists regarding the effects of HBO treatment in combination with DOX chemotherapy, preclinical investigation reveals potential benefits to tumor growth reduction [ 41 ] and accelerated healing of extravasation injury [ 26 ].…”

“…Increased ROS production following HBO triggers activation of the oxidative stress-sensitive transcription factor Nrf2 to upregulate antioxidant enzyme gene expression and preserve redox homeostasis [ 47 , 48 ]. These antioxidant genes include SOD1, SOD2, catalase and GPX1, all of which are established targets of Nrf2 and are demonstrated to increase following HBO therapy [ 5 , 6 , 9 , 40 , 49 ]. Our data also show an HBO-specific antioxidant response with catalase protein expression increased in the diaphragm muscle and both SOD2 and catalase increased in the heart ( Figure 6 ).…”

Protective Effect of Hyperbaric Oxygen Treatment on Axon Degeneration after Acute Motor Axonal Neuropathy

“…e HBO therapy increases GSH indicating a very efficient antioxidant mechanism to protect against oxidative stress [7]. GSH represents an essential cellular redox buffer and plays an important role in the detoxification of not only MDA but also NO and other ROS-induced fat peroxidation products, such as 4-hydroxyinonenal (4-HNE) [8].…”