Pub Date : 2018-08-29DOI: 10.5772/INTECHOPEN.76569
I. Jukić, M. Mišir, M. Mihalj, Z. Mihaljević, S. Unfirer, D. Kibel, Aleksandar Kibel
The mechanisms by which HBO exerts its potentially beneficial effects are not completely clear. Interactions of mechanisms affecting endothelial dysfunction, NO synthesis, EETs and HETE formation, CYP expression changes, oxidative stress and antioxidant defense system changes, and multiple effects on inflammation take place that might be consid ered as mediating factors for the observed positive (or negative) clinical effects in diabe - tes mellitus (for instance in chronic diabetic wounds). Studies on vasculature in diabetic animal models can provide us with more information that can help us understand its effects on blood vessel function. This chapter discusses the most relevant studies that have assessed the potential mechanisms of HBO-induced vascular functional changes in diabetic animal models.
{"title":"Mechanisms of HBO-Induced Vascular Functional Changes in Diabetic Animal Models","authors":"I. Jukić, M. Mišir, M. Mihalj, Z. Mihaljević, S. Unfirer, D. Kibel, Aleksandar Kibel","doi":"10.5772/INTECHOPEN.76569","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.76569","url":null,"abstract":"The mechanisms by which HBO exerts its potentially beneficial effects are not completely clear. Interactions of mechanisms affecting endothelial dysfunction, NO synthesis, EETs and HETE formation, CYP expression changes, oxidative stress and antioxidant defense system changes, and multiple effects on inflammation take place that might be consid ered as mediating factors for the observed positive (or negative) clinical effects in diabe - tes mellitus (for instance in chronic diabetic wounds). Studies on vasculature in diabetic animal models can provide us with more information that can help us understand its effects on blood vessel function. This chapter discusses the most relevant studies that have assessed the potential mechanisms of HBO-induced vascular functional changes in diabetic animal models.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"121 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123151371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-08-29DOI: 10.5772/INTECHOPEN.75025
S. Peković, S. Dacic, D. Krstić, R. Jeremic, M. Djelic, P. Brkić
Traumatic brain injuries (TBI) are among the leading causes of death and chronic disability worldwide. TBI is a complex process encompassing primary injury to the brain tissue and cerebral vasculature induced by the initial impact, secondary injury, including cascade of subsequent neuroinflammatory processes, and regenerative responses with enhanced neurogenesis and angiogenesis. To date, there remains no approved pharmacological therapy that is able to prevent the secondary injury. Therefore, the development of safe and efficacious neuroprotective treatments currently represents the greatest unmet need in the management of TBI. Increasing number of experimental and clinical studies present convincing evidence that hyperbaric oxygen therapy (HBOT), as an adjunctive therapy, may be the suitable neurotherapeutic method for improving neurological outcome after TBI. Irrespective to treatment protocol HBOT appeared to alleviate the detrimental and neurotoxic effects of pathological sequel initiated by TBI and to stimulate endogenous reparative mechanisms. However, the exact mechanisms by which HBOT exerts its beneficial effects on recovery after brain injury are still deficient. In this review we will summarize up to date results of HBOT in experimental and clinical TBI and try to put more light on cellular and molecular mechanisms underlying beneficial effects of HBOT on functional recovery after brain injury.
{"title":"Hyperbaric Oxygen Therapy in Traumatic Brain Injury: Cellular and Molecular Mechanisms","authors":"S. Peković, S. Dacic, D. Krstić, R. Jeremic, M. Djelic, P. Brkić","doi":"10.5772/INTECHOPEN.75025","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.75025","url":null,"abstract":"Traumatic brain injuries (TBI) are among the leading causes of death and chronic disability worldwide. TBI is a complex process encompassing primary injury to the brain tissue and cerebral vasculature induced by the initial impact, secondary injury, including cascade of subsequent neuroinflammatory processes, and regenerative responses with enhanced neurogenesis and angiogenesis. To date, there remains no approved pharmacological therapy that is able to prevent the secondary injury. Therefore, the development of safe and efficacious neuroprotective treatments currently represents the greatest unmet need in the management of TBI. Increasing number of experimental and clinical studies present convincing evidence that hyperbaric oxygen therapy (HBOT), as an adjunctive therapy, may be the suitable neurotherapeutic method for improving neurological outcome after TBI. Irrespective to treatment protocol HBOT appeared to alleviate the detrimental and neurotoxic effects of pathological sequel initiated by TBI and to stimulate endogenous reparative mechanisms. However, the exact mechanisms by which HBOT exerts its beneficial effects on recovery after brain injury are still deficient. In this review we will summarize up to date results of HBOT in experimental and clinical TBI and try to put more light on cellular and molecular mechanisms underlying beneficial effects of HBOT on functional recovery after brain injury.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115052072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-08-29DOI: 10.5772/INTECHOPEN.79866
I. Drenjančević
Hyperbaric oxygen treatment (HBO2) is a widely accepted adjuvant therapy in various health conditions that exhibit impaired tissue blood flow. At high pressures, the delivery of the dissolved oxygen in plasma is enhanced, which contributes to better tissue oxygenation, cellular metabolism and ultimately, healing. However, this is not the only potential mechanism for improved outcome of many diseases treated with HBO2, since oxygen is highly reactive molecule and can induce upregulation of many various enzymatic systems in the cell, at cellular, genetic and molecular level. Particularly, vascular/endothelial function is affected by the HBO2. Our understanding of these mechanisms of the HBO2 effects is still emerging. There have been many controversies related to the HBO2 protocols and indications. It is known that, as well as HBO2 exhibit beneficiary effects on the tissue perfusion, it demonstrates high toxicity at higher pressures, due to increased oxidative stress and barotrauma. On the other hand, there is still a lack of the translation of the knowledge on the mechanisms of action of HBO2 obtained from the experimental research to the clinical practice.
{"title":"Introductory Chapter: Hyperbaric Oxygen Treatment: Old Treatment with New Understanding","authors":"I. Drenjančević","doi":"10.5772/INTECHOPEN.79866","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.79866","url":null,"abstract":"Hyperbaric oxygen treatment (HBO2) is a widely accepted adjuvant therapy in various health conditions that exhibit impaired tissue blood flow. At high pressures, the delivery of the dissolved oxygen in plasma is enhanced, which contributes to better tissue oxygenation, cellular metabolism and ultimately, healing. However, this is not the only potential mechanism for improved outcome of many diseases treated with HBO2, since oxygen is highly reactive molecule and can induce upregulation of many various enzymatic systems in the cell, at cellular, genetic and molecular level. Particularly, vascular/endothelial function is affected by the HBO2. Our understanding of these mechanisms of the HBO2 effects is still emerging. There have been many controversies related to the HBO2 protocols and indications. It is known that, as well as HBO2 exhibit beneficiary effects on the tissue perfusion, it demonstrates high toxicity at higher pressures, due to increased oxidative stress and barotrauma. On the other hand, there is still a lack of the translation of the knowledge on the mechanisms of action of HBO2 obtained from the experimental research to the clinical practice.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"89 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124569456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-08-29DOI: 10.5772/INTECHOPEN.78392
A. Gunes
Hyperbaric oxygen therapy is highly safe in treatments based on internationally accepted treatment tables. However, in some long-term treatments, the internal adjuvant and the patient are exposed to some toxic effects. In the presence of compressed air environment, nitrogen can lead to drunkenness. Another cause of poisoning is oxygen. Oxygen shows toxic effects when inhaled in the high-pressure environment for long periods or above partial pressures on 3 ATA. The excess oxygen has a toxic effect on the lung and central nervous system (CNS). Oxygen poisoning can be seen in long-term oxygen therapy in intensive care, in closed or semi-closed circuit diving, in saturation dives, on decompressions on the surface, in recompression and hyperbaric oxygen therapy. The first goal during convulsion is to prevent trauma prevent the patient from biting his tongue during the seizure. However, in nitrogen narcosis, the first intervention should be to prevent the diver from diving deeper to reduce the effect of anesthesia. The lifeguard must prevent the unconscious movements of the diver, such as removing the regulator from his mouth and holding his breath. He must think that the dive is like a dream.
{"title":"Toxic Effects of Hyperbaric Conditions","authors":"A. Gunes","doi":"10.5772/INTECHOPEN.78392","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.78392","url":null,"abstract":"Hyperbaric oxygen therapy is highly safe in treatments based on internationally accepted treatment tables. However, in some long-term treatments, the internal adjuvant and the patient are exposed to some toxic effects. In the presence of compressed air environment, nitrogen can lead to drunkenness. Another cause of poisoning is oxygen. Oxygen shows toxic effects when inhaled in the high-pressure environment for long periods or above partial pressures on 3 ATA. The excess oxygen has a toxic effect on the lung and central nervous system (CNS). Oxygen poisoning can be seen in long-term oxygen therapy in intensive care, in closed or semi-closed circuit diving, in saturation dives, on decompressions on the surface, in recompression and hyperbaric oxygen therapy. The first goal during convulsion is to prevent trauma prevent the patient from biting his tongue during the seizure. However, in nitrogen narcosis, the first intervention should be to prevent the diver from diving deeper to reduce the effect of anesthesia. The lifeguard must prevent the unconscious movements of the diver, such as removing the regulator from his mouth and holding his breath. He must think that the dive is like a dream.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125120616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-03-28DOI: 10.5772/INTECHOPEN.75609
F. Gul, Ömer Faruk Boran, Reyhan Arslantaş
The microcirculation is anatomical and consists of arterioles, capillaries, and venules that perform metabolic requirements and oxygen distribution to the tissues. During physiological or pathological stress, it balances between the oxygen delivery and the demand. This delicate balance can play an important role in the progression of critical illnesses and has a role in the development of organ dysfunction. Reduced microvascular perfusion is seen in many diseases, and hyperbaric oxygen treatment (HBOT) has potentially beneficial effects on the microcirculatory environment. It has been shown that HBOT improves microcirculation independent from systemic hemodynamic parameters, which is a key therapeutic target in the critically ill patient. HBOT is emerging as an adjunct to traditional surgery and antibiotic therapy for the special kinds of problematic wounds or purpura fulminans, which are caused by meningococcal sepsis. HBOT also can increase oxygen supply to the ischemic tissue to reduce the extent of irreversible tissue damage in ischemic stroke, femoral head necrosis, diabetic foot ulcer, and carbon monoxide intoxication. In this chapter, we aim to describe microcirculation with its monitoring systems and to show the effectiveness of HBOT in different clinical settings, which are related to microcirculatory dysfunction.
{"title":"Microcirculation and Hyperbaric Oxygen Treatment","authors":"F. Gul, Ömer Faruk Boran, Reyhan Arslantaş","doi":"10.5772/INTECHOPEN.75609","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.75609","url":null,"abstract":"The microcirculation is anatomical and consists of arterioles, capillaries, and venules that perform metabolic requirements and oxygen distribution to the tissues. During physiological or pathological stress, it balances between the oxygen delivery and the demand. This delicate balance can play an important role in the progression of critical illnesses and has a role in the development of organ dysfunction. Reduced microvascular perfusion is seen in many diseases, and hyperbaric oxygen treatment (HBOT) has potentially beneficial effects on the microcirculatory environment. It has been shown that HBOT improves microcirculation independent from systemic hemodynamic parameters, which is a key therapeutic target in the critically ill patient. HBOT is emerging as an adjunct to traditional surgery and antibiotic therapy for the special kinds of problematic wounds or purpura fulminans, which are caused by meningococcal sepsis. HBOT also can increase oxygen supply to the ischemic tissue to reduce the extent of irreversible tissue damage in ischemic stroke, femoral head necrosis, diabetic foot ulcer, and carbon monoxide intoxication. In this chapter, we aim to describe microcirculation with its monitoring systems and to show the effectiveness of HBOT in different clinical settings, which are related to microcirculatory dysfunction.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"20 12","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121008820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-03-21DOI: 10.5772/INTECHOPEN.75378
E. Gara
Hyperbaric oxygen therapy (HBOT) is a state-of-the-art medical treatment, which is proved to be beneficial in a number of diseases and promising in new fields as well. HBOT is evidence-based treatment for, among others, severe CO intoxication, decompression disease and chronic wound healing. Recent studies promise beneficial effects of HBOT in multiple sclerosis. In vitro, cellular models of these complex pathological conditions are limited. In this chapter, we aim to mirror in vitro effects of HBOT and other altered oxygen levels on endothelial cells, fibroblast, mesenchymal and pluripotent stem cells. Through these in vitro models, the role of HBOT in angiogenesis, blot clotting, wound healing, cell therapy and tissue engineering will be discussed. To summarize in vitro effects of HBOT, it has beneficial role on proliferation and viability of most cell types. Furthermore, functional characteristics of the investigated cell types, for example, angiogenesis by endothelial cells, are improved in response to HBOT. Standardized preclinical protocols with HBOT help to translate the benefits to clinical trials and clinical use.
{"title":"Cell Culture Effects of Altered Oxygen Levels and Hyperbaric Treatment In Vitro","authors":"E. Gara","doi":"10.5772/INTECHOPEN.75378","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.75378","url":null,"abstract":"Hyperbaric oxygen therapy (HBOT) is a state-of-the-art medical treatment, which is proved to be beneficial in a number of diseases and promising in new fields as well. HBOT is evidence-based treatment for, among others, severe CO intoxication, decompression disease and chronic wound healing. Recent studies promise beneficial effects of HBOT in multiple sclerosis. In vitro, cellular models of these complex pathological conditions are limited. In this chapter, we aim to mirror in vitro effects of HBOT and other altered oxygen levels on endothelial cells, fibroblast, mesenchymal and pluripotent stem cells. Through these in vitro models, the role of HBOT in angiogenesis, blot clotting, wound healing, cell therapy and tissue engineering will be discussed. To summarize in vitro effects of HBOT, it has beneficial role on proliferation and viability of most cell types. Furthermore, functional characteristics of the investigated cell types, for example, angiogenesis by endothelial cells, are improved in response to HBOT. Standardized preclinical protocols with HBOT help to translate the benefits to clinical trials and clinical use.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115817420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-03-16DOI: 10.5772/INTECHOPEN.75026
G. Bosco, Alex Rizzato, G. Vezzani, V. Zanon, E. Camporesi
Femoral head necrosis (FHN) is a disease process resulting from inadequate blood perfu- sion of subchondral bone. While the etiology of this disease is still not fully understood, there are multiple traumatic and atraumatic factors that are associated with the disease. Pathophysiology of the disease is characterized by the death of bone marrow and osteocytes. If left untreated, the disease may progress to joint collapse. While initial stages of the disease are asymptomatic, painful limitation of active and passive motion of the hip is eventually present. The current body of literature cannot identify an optimal treat- ment protocol for FHN. Postcollapse cases require surgical intervention, core decompression, or total hip arthroplasty. However, current strides in conservative management are being made. One of the possible conservative modalities that may effectively delay hip arthroplasty or even prevent the need for a surgical approach is hyperbaric oxygen (HBO 2 ) therapy. HBO 2 increases extracellular oxygen concentration and reduces cellular ischemia and edema by inducing vasoconstriction. Studies have reported radiographic improvement, reduction in pain, and increases in range of motion for early stages of the disease. Hyperbaric oxygen therapy has also been shown to stimulate angiogenesis and enhance osteoclast and osteoblast function for remodeling and repair.
{"title":"Therapeutic Mechanisms of Action for Hyperbaric Oxygen on Femoral Head Necrosis","authors":"G. Bosco, Alex Rizzato, G. Vezzani, V. Zanon, E. Camporesi","doi":"10.5772/INTECHOPEN.75026","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.75026","url":null,"abstract":"Femoral head necrosis (FHN) is a disease process resulting from inadequate blood perfu- sion of subchondral bone. While the etiology of this disease is still not fully understood, there are multiple traumatic and atraumatic factors that are associated with the disease. Pathophysiology of the disease is characterized by the death of bone marrow and osteocytes. If left untreated, the disease may progress to joint collapse. While initial stages of the disease are asymptomatic, painful limitation of active and passive motion of the hip is eventually present. The current body of literature cannot identify an optimal treat- ment protocol for FHN. Postcollapse cases require surgical intervention, core decompression, or total hip arthroplasty. However, current strides in conservative management are being made. One of the possible conservative modalities that may effectively delay hip arthroplasty or even prevent the need for a surgical approach is hyperbaric oxygen (HBO 2 ) therapy. HBO 2 increases extracellular oxygen concentration and reduces cellular ischemia and edema by inducing vasoconstriction. Studies have reported radiographic improvement, reduction in pain, and increases in range of motion for early stages of the disease. Hyperbaric oxygen therapy has also been shown to stimulate angiogenesis and enhance osteoclast and osteoblast function for remodeling and repair.","PeriodicalId":106208,"journal":{"name":"Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus","volume":"65 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127094094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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