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Clinical and epidemiological context of COVID-19
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Viswanthram Palanivel, Akanksha Salkar, Radha Yadav, Renuka Bankar, Om Shrivastav, Arup Acharjee
Breathlessness and hypoxemia are considered as primary clinical features in COVID-19 infection. Lungs have a high expression of ACE2. In a disease progression to severity, pro-inflammatory cytokines such as interleukin-6 and interleukin-8 and other signaling molecules like monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and granulocyte colony-stimulating factor (G-CSF) are released, attracting neutrophils and T cells that induce lung injury leading to ARDS. Hence, mechanical oxygen support is essential in COVID-19 management. Non-invasive ventilation (NIV) like continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and hyperbaric oxygen therapy (HBOT) are widely used. Similarly, invasive ventilation such as endotracheal/orotracheal tube and extracorporeal membrane oxygenation (ECMO) is preferred by doctors in critical conditions.
Toxicity of Carbon Monoxide: Hemoglobin vs. Histotoxic Mechanisms
Published in David G. Penney, Carbon Monoxide, 2019
ROS produced from mitochondria after CO hypoxia can be blunted by HBO therapy at 1.5 ATA and enhanced at 2.5 ATA (Piantadosi et al., 1995). This increased ROS production at 2.5 ATA in the CO-exposed brain appears to be related in part to monoamine oxidase (MAO) activity and/or catecholamine release since it can be ameliorated by the MAO inhibitor, par-gyline. MAO (isoforms A and B) located on the outer mitochondrial membrane catalyzes oxidative deamination of catecholamines and produces H2O2 and NH3, and utilizes molecular O2 in the process. The Km for O2 of the enzyme is approximately 100 μM; therefore, high tissue PO2 values can increase its activity. Inhibition of MAO activity with pargyline decreases H2O2 generation in the brain during hyperoxia and protects against CNS O2 toxicity (Zhang and Piantadosi, 1991). This mechanism may be responsible for the increased ROS production after CO hypoxia at the high tissue PO2 values produced by hyperbaric oxygen therapy at 2.5 ATA.
Therapeutic Nanostructures for Improved Wound Healing
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Lalduhsanga Pachuau, Pranab Jyoti Das, Bhaskar Mazumder
Persistent ulcers have been found to be the result of topical malperfusion which causes ischemia or hypoxia, and this condition may be treated efficiently with hyperbaric oxygen therapy. A liposome formulation was applied to encapsulate hemoglobin with high oxygen affinity to accelerate skin wound healing in a mice model (Fukui et al., 2012). To test the wound healing property of the formulation, skin wounds were created on the back of anesthetized mice using a circular skin tome of 6 mm in diameter. The results suggest that liposome-encapsulated hemoglobin may accelerate skin wound healing in BALB/C mice via mechanisms involving reduced inflammation and enhanced metabolism (Fukui et al., 2012). Clodronate liposomes were also shown to reduce the excessive formation of scars in a burn injury wound model in mice by reducing collagen deposition and the expression of TGF-β1 (Lu et al., 2014).
Recent advances in micro-sized oxygen carriers inspired by red blood cells
Published in Science and Technology of Advanced Materials, 2023
Qiming Zhang, Natsuko F. Inagaki, Taichi Ito
Hyperbaric oxygen therapy (HBOT) is the intermittent inhalation of 100% oxygen at a pressure greater than 1 atmosphere. This therapy increases the amount of oxygen dissolved in the blood by 10–20 times compared to the amount of oxygen obtained by breathing under a normal atmospheric pressure. This dissolved oxygen amount is slightly more than sufficient to meet the resting cellular requirements [140,141]. Furthermore, the dissolved oxygen does not transport itself via binding to Hb, so the HBOT can carry oxygen to the body independent of the amount of Hb or its ability to bind. Since Behnke and Shaw succeeded in the treatment of decompression sickness using hyperbaric oxygen in 1937 [142], HBOT has become a useful therapy for treating several diseases such as chronic refractory osteomyelitis, delayed radiation-induced injuries with bone necrosis, cardiac ischemia, air or gas arterial or venous emboli, and severe or symptomatic carbon monoxide poisoning [140,143–147]. However, HBOT typically requires hyperbaric chambers including either mono-place chambers for accommodating a single patient at one time or multi-place chambers for accommodating multiple patients at the same pressure [145]. There is a limitation to the number of hospitals able to provide hyperbaric treatment because of the space required to set up such hyperbaric chambers. In addition, several complications from HBOTs have been described with varying degrees of seriousness [140,141]. The most frequent side effect is hyperbaric-associated middle ear barotrauma [148,149]. Recently, the possibility of using AOCs as an alternative to HBOT was investigated with various animal models. Below, we introduce recent studies using PFOCs.