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PURPOSE: This study examined the effects of normobaric oxygen in patients diagnosed with either a Central Retinal Vein Occlusion (CRVO) or Branched Retinal Vein Occlusion (BRVO) who had previously undergone treatment via Anti-VEGF or PRP treatment. The investigation looked into the changes in Macular Thickness (MT) and Visual Acuity (VA). METHODS: This pilot study analyzed patient data from Beth Israel Deaconess Medical Center (Boston, MA) that had been diagnosed with Retinal Vein Occlusions. The patients were brought in and given 3 hours of normobaric oxygen via an oxygen concentrator with imaging and vision checked both before and after the therapy. RESULTS: Eighty-eight percent of our patients in this pilot study saw a decrease in macular thickness after 3-hour oxygen therapy. The mean change in Maximal Macular Thickness was a decrease of 7.1% which was statistically significant when compared to healthy eyes (p<0.001). Additionally, 44% of patients saw an increase in visual acuity, the primary measure of vision. Visual acuity showed a statistically significant change when compared to changes in healthy eyes (p=0.015). No statistical significance was found in the testing of contrast sensitivity nor intraocular pressure. CONCLUSION: Our study showed improvement in central macular thickness and quality of life for individuals using noninvasive normobaric hyperoxia as a treatment for retinal vein occlusions. However, further research is needed to improve the impact of the study and a full randomized control trial should be implemented to further understand the potential impacts of a noninvasive normobaric hyperoxia treatment as a means to alleviate symptoms in retinal vein occlusions. In addition, in the future oxygen supplementation in conjunction with periodic injections of Anti- VEGF could be investigated as a treatment regimen with potential benefits beyond individual therapy. / 2020-06-17T00:00:00Z

PURPOSE: Age-related macular degeneration (AMD) is a complex, progressive ocular disorder that results in outer retinal ischemia and severe vision loss. Dry AMD, the most common form of AMD, is characterized by the build-up of extracellular drusen deposits, dysfunction of the outer retinal layers and degeneration of photoreceptors. This study aimed to examine the anatomic and physiologic effects of short-term normobaric hyperoxia in patients at different stages of dry AMD. METHODS: Twenty-two eyes from 16 patients diagnosed with dry AMD (11 females, 5 males) were used in this study. Eyes were categorized as having either small drusen or drusenoid pigment epithelial detachments (DPEDs) through optical coherence tomography (OCT) imaging. Eyes associated with small drusen received 3-hours of 40% fraction of inspired oxygen (FiO2) normobaric hyperoxia (NBH), whereas eyes associated with DPEDs received either 3-hour NBH or 3-hours of 20% FiO2 normobaric normoxia (NBN). Visual acuity and OCT images of the macula were taken before and after oxygen treatment. Anatomic outcomes consisted of foveal thickness, foveal volume, macular volume and maximum drusen height; visual acuity was the functional outcome. The relationship between maximum drusen height and visual acuity was then examined to determine if these outcomes were associated. RESULTS: Eyes associated with DPED treated with 3-hour NBH had the largest decreases in foveal thickness, foveal volume, macular volume and maximum drusen height. The macular layers were then divided into inner and outer layers. The outer layers, comprised of Bruch’s membrane, drusen and the retinal pigment epithelium, had significant decreases in anatomic outcomes, whereas the inner layers showed no changes. DPED patients treated with 3-hour NBH also had the largest increase in visual acuity following treatment. There was a significant negative correlation between baseline drusen height and baseline visual acuity. For patients with small drusen treated with 3-hour NBH, there were no significant changes to anatomic or functional outcomes. CONCLUSION: The current study demonstrates the efficacy of short-term administration of normobaric hyperoxia in high-risk dry AMD patients with associated DPEDs. Normobaric hyperoxia appears to be a novel and promising treatment that requires further investigation.

PURPOSE: Diabetes Mellitus (DM) is one of the most prevalent metabolic diseases worldwide and can lead to ocular complications such as diabetic retinopathy (DR). As chronic hyperglycemia leads to endothelial pathologies in the retina, diabetic macular edema (DME) develops and worsens visual acuity. Current treatment methods include laser photocoagulation, intravitreal anti-vascular endothelial growth factor (anti-VEGF) injections, and surgical interventions. This case report explores the effects of nocturnal normobaric hyperoxia (NNBH) treatment in a patient with DME. METHODS: A 64-year-old pseudophakic man with bilateral DME regularly treated with anti-VEGF injections was instructed to self-administer 40% fraction of inspired oxygen (FiO2) at 5 liters per minute (LPM) for 6 to 8 hours per day during sleep. Retrospective data of visual acuity (VA), optical coherence tomography (OCT) imaging, and number of injections during a one-year time frame prior to starting NNBH was compared with newly collected data of a one-year time frame while on NNBH. RESULTS: The patient was treated with a total of 12 anti-VEGF injections in the year prior to starting NNBH treatment. After one year of supplemental oxygen, subject’s VA stabilized to 20/20 in both eyes. When comparing average values of OCT data prior to NNBH and during NNBH, all measurements including central macular thickness (CMT), maximum macular thickness (MMT), foveal volume (FV), and total macular volume (TMV) decreased anywhere from 5.4% to 20.3%, reflecting a stabilization of the retina bilaterally. Subject did not require any intravitreal injections during NNBH treatment. After one month of planned cessation of NNBH, DME recurred. CONCLUSION: This model case demonstrates NNBH may be a novel treatment approach in reducing DME and improving VA in patients with DR. NNBH can be a cost-effective, convenient, and accessible therapy for patients with complications from diabetic retinopathy.

Carbon monoxide (CO) is an odorless, colorless, tasteless gas that binds to hemoglobin with high affinity. This property underlies the use of low doses of CO to determine hemoglobin mass (MHb) in the fields of clinical and sports medicine. However, hemoglobin bound to CO is unable to transport oxygen and exposure to high CO concentrations is a significant environmental and occupational health concern. These contrasting aspects of CO—clinically useful in low doses but potentially lethal in higher doses—mandates a need for a quantitative understanding of the temporal profiles of the uptake and distribution of CO in the human body. In this dissertation I have (i) used a mathematical model to analyze CO-rebreathing techniques used to estimate total hemoglobin mass and proposed a CO-rebreathing procedure to estimate hemoglobin mass with low errors, (ii) enhanced and validated a multicompartment model to estimate O2, CO and CO2 tensions, bicarbonate levels, pH levels, blood carboxyhemoglobin (HbCO) levels, and carboxymyoglobin (MbCO) levels in all the vascular (arterial, mixed venous and vascular subcompartments of the tissues) and tissue (brain, heart and skeletal muscle) compartments of the model in normoxia, hypoxia, CO hypoxia, hyperoxia, isocapnic hyperoxia and hyperbaric oxygen, and (iii) used this developed mathematical model to propose a treatment to improve O2 delivery and CO removal by comparing O2 and CO levels during different treatment protocols administered for otherwise-healthy CO-poisoned subjects.

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Recently, they are examined various means for activating the endogenous signalling pathways leading to increased resistance of the myocardium from ischemic/reperfusion (I/R) injury. One of them is the adaptation to chronic hypoxia, which has been shown to reduce the incidence and severity of ventricular arrhythmias, improves the recovery of postischemic contractile function of the heart and particularly reduces the extent of myocardial infarction. Since the function of the heart depends on the maintenance of membrane integrity of cardiomyocytes there are very important phospholipase A2 (PLA2) which are involved in the repair of cellular membranes. Also they are an important component of the protective signalling pathways because they cleave membrane phospholipids to produce lipid signalling molecules. Elucidate the role of PLA2 and the precise mechanism of action of signalling pathways leading to cardioprotection could be important for the prevention and treatment of cardiovascular diseases. Therefore, in this thesis we examined the influence of continuous normobaric hypoxia (CNH) to the relative representation of cardiac PLA2 (secretory - sPLA2IIA, calcium-independent - iPLA2, cytosolic - cPLA2α and its phosphorylated form - p-cPLA2α), and proteins involved in the activation and phosphorylation of...

Adaptation to chronic hypoxia provides cardioprotective effects. Molecular mechanism of this phenomenon is not yet completely understood, but it is known that cardiac mitochondria play an essential role in induction of protective effects. The purpose of this diploma thesis is to study effects of continuous normobaric hypoxia (CNH; 10 % O2, 21 days) on spontaneously hypertensive rats (SHR) and conplastic strain that is derived from SHR. These animals have nuclear genome of SHR strain and mitochondrial genome of Brown Norway (BN) strain. Cardiac homogenate was used to measure enzymatic activity of malate dehydrogenase (MDH), citrate synthase (CS), NADH-cytochrome c oxidoreductase, succinate-cytochrome c oxidoreductase and cytochrome oxidase (COX). Using Western blot procedure the protein amount of antioxidant enzymes was measured - manganese superoxide dismutase and copper-zinc superoxide dismutase (MnSOD, Cu/ZnSOD), catalase and chosen subunits of oxidative phosphorylation complexes (Ndufa9, Sdha, Uqcrc2, COX-4, MTCO1, Atp5a1). Under normoxic conditions the conplastic strain has lower amount of complex IV subunit MTCO1 in comparison with SHR. This subunit is encoded by mitochondrial DNA and it is one of the seven protein-coding genes in conplastic strain that differ from SHR. Adaptation to hypoxia causes an...