The Effects of Hyperbaric Oxygen on Human Physiological and Metabolic Functions
Table of Contents
Introduction
Hyperbaric oxygen therapy can significantly alter the body’s uptake and utilization of oxygen, increasing both the partial pressure of oxygen in the blood and the oxygen content in the blood, thereby inducing a series of physiological changes in the central nervous, circulatory, respiratory, hematological, endocrine, and immune systems. The extent of these changes depends on pressure, oxygen concentration, and duration of oxygen exposure. The greater the pressure, the higher the oxygen concentration, and the longer the duration of oxygen exposure, the more pronounced the changes become. Most of these changes are beneficial, while a few may have adverse effects on the body; however, these effects are typically transient and reversible. To maximize the benefits and minimize the drawbacks, it is essential to study and elucidate the patterns and mechanisms by which hyperbaric oxygen affects human physiological functions.
1. Effects of Hyperbaric Oxygen on the Nervous System
1.1 Central Nervous System Activity
The effects of hyperbaric oxygen on higher central nervous system activity manifest as two consecutive phases: enhancement and inhibition. Enhancement Phase: Higher central nervous system activity is enhanced, manifested by heightened tactile sensitivity, improved memory, heightened perception, the ability to sustain complex mental work, and increased coordination and flexibility in physical movement. Inhibition phase: Approximately 30–45 minutes after exposure to hyperbaric oxygen, higher central nervous system activity gradually transitions from the enhancement phase to a phase of cortical inhibition. This is manifested by reduced coordination of physical movements, relatively scattered attention, slowed reading and writing speeds, and a decrease in alpha waves on the electroencephalogram (EEG), along with increased amplitudes of the 0-wave and 8-wave components. The effect of hyperbaric oxygen on the functional activity of the normal nonspecific central nervous system transmission system is the primary cause of these phasic changes.
1.2 Increased Permeability of the Blood-Brain Barrier
Hyperbaric oxygen therapy can increase the permeability of the blood-brain barrier; this increase in permeability is reversible. Therefore, hyperbaric oxygen therapy can be utilized to facilitate the passage of drugs from the bloodstream across the blood-brain barrier, enabling effective pharmacological treatment of conditions such as cerebral infections or malignant brain tumors.
1.3 Increased Partial Pressure of Oxygen in Brain Tissue and Cerebrospinal Fluid
Under hyperbaric oxygen conditions, normal cerebral blood flow decreases slightly, but the partial pressure of oxygen in brain tissue and cerebrospinal fluid increases. The partial pressure of oxygen in cerebrospinal fluid is typically equal to that in arterial blood. Under hyperbaric oxygen conditions, the partial pressure of oxygen in both brain tissue and cerebrospinal fluid rises (Table 1-8-1-1); consequently, this can be used to resolve or alleviate cerebral hypoxia, thereby restoring or improving brain function.
Table 1-8-1-1: Relationship Between Hyperbaric Oxygen Therapy and Cerebral Blood Flow, Intracranial Pressure, and Partial Pressure of Oxygen in Brain Tissue and Cerebrospinal Fluid
|
Pressure |
Air |
Rate
of Decrease in Cerebral Blood Flow /% |
Rate
of Decrease in Intracranial Pressure /% |
Brain
tissue PO2 |
Cerebrospinal
fluid PO2 |
|||
|
/kPa |
/mmHg |
/kPa |
/mmHg |
/kPa |
/mmHg |
|||
|
13.3 |
100 |
Normal
air |
|
|
4.5 |
34 |
4.4 |
33 |
|
13.3 |
100 |
O2 |
10~12 |
15 |
12 |
90 |
11 |
83 |
|
26.7 |
200 |
O2 |
21 |
36 |
32.5 |
244 |
36.9 |
277 |
|
26.7 |
300 |
O2 |
25 |
40 |
60.3 |
452 |
64 |
480 |
|
53.3 |
400 |
O2 |
25 |
40~50 |
85.7 |
643 |
93.2 |
699 |
2. Effects of Hyperbaric Oxygen on the Circulatory System
2.1 Decrease in Heart Rate
Hyperbaric oxygen therapy can cause a decrease in heart rate. When inhaling pure oxygen at atmospheric pressure, the heart rate decreases by 5% to 16%; under an oxygen pressure of 1,500 to 3,000 mmHg (200 to 400 kPa), the heart rate may decrease by 14% to 33% (Table 1-8-1-2). It is generally accepted that at a standard therapeutic pressure of 1,500 mmHg (200 kPa), the heart rate slows by an average of approximately 10 beats per minute. This deceleration is directly related to the oxygen pressure and the duration of oxygen administration. It is commonly believed that the bradycardia results from reflex stimulation of the vagus nerve (due to reduced afferent impulses from the carotid and aortic bodies) in response to high partial pressure of oxygen. Vagal nerve section prevents the heart rate deceleration observed under hyperbaric oxygenation, and the administration of 0.1–0.2 mg of atropine can also inhibit this deceleration. Another cause of the heart rate deceleration is the marked change in systemic hemodynamics resulting from increased blood oxygen partial pressure: vasoconstriction and elevated blood pressure can also lead to a slower heart rate. Under normal conditions, even with complete elimination of sympathetic nervous system influence, the heart rate decreases by only 20%; however, under hyperbaric oxygen conditions, it can decrease by up to 33%. Therefore, it is hypothesized that other factors are at play. Examples include the direct effects of high partial pressure of oxygen on the myocardium and the regulatory role of peripheral blood vessels on cardiac pumping function.
2.2 Decreased Myocardial Contractility and Cardiac Output
At an oxygen pressure of 2250 mmHg (300 kPa), cardiac output decreases by an average of 19% (Table 1-8-1-2), and the myocardial contractility index decreases by 14%. Concurrently, the durations of isometric and isotonic contractions are prolonged by 14%. The reduction in myocardial contractility may be due to increased oxygen content in the coronary circulation, which lowers myocardial metabolic rate and consequently leads to impaired cardiac function.
2.3 Elevated Blood Pressure
Under hyperbaric oxygen conditions, vasoconstriction occurs and peripheral resistance increases, leading to elevated arterial blood pressure. In healthy individuals at an oxygen pressure of 2,250 mmHg (300 kPa), total vascular resistance increases by more than 50%. However, due to a slowed heart rate and reduced myocardial contractility, the effective circulating blood volume decreases (typically by no more than 10%). If the reduction in cardiac output is not significant, systolic blood pressure will rise slightly, while diastolic blood pressure will rise more markedly, and the pulse pressure will decrease. Due to the blood-pressure-raising effect of hyperbaric oxygen therapy, patients with concomitant hypertension should have their blood pressure controlled below 160 mmHg (21.3 kPa) for systolic pressure and 100 mmHg (13.3 kPa) for diastolic pressure before being permitted to enter the chamber for treatment. Blood pressure should be measured repeatedly before and after treatment; if blood pressure rises significantly, hyperbaric oxygen therapy should be temporarily suspended.
Vasoconstriction under hyperbaric oxygen conditions can counteract the dilation of the capillary bed caused by histamine released from mast cells during hypoxia, thereby raising blood pressure, increasing tissue blood flow, improving microcirculation, and correcting shock. Therefore, hyperbaric oxygen therapy can be used for the emergency treatment of shock caused by various etiologies.
Table 1-8-1-2 Effects of Hyperbaric Oxygen on Heart Rate and Cardiac Output
|
Oxygen
pressure |
Heart
Rate Decrease Rate /% |
Percentage
Reduction in Cardiac Output /% |
|
|
/kPa |
/mmHg |
/% |
/% |
|
200 |
1500 |
14 |
11 |
|
300 |
2250 |
20 |
19 |
|
400 |
3000 |
33 |
13~15 |
2.4 Hemodynamic Changes
Under hyperbaric oxygen conditions, the characteristic hemodynamic changes are: blood vessels in most major organs and peripheral blood vessels undergo varying degrees of constriction.
There are currently two main theories regarding the mechanisms of vascular responses under hyperbaric oxygen conditions. The humoral autoregulation theory posits that during hypoxia, tissues release large amounts of metabolic byproducts (such as histamine) that have vasodilatory effects, causing small arteries to dilate. Under hyperbaric oxygen conditions, increased blood oxygen content corrects the hypoxic state, thereby inhibiting the production of metabolic byproducts in tissues, increasing vascular wall tension, and narrowing the lumen. The oxygen-response autoregulation theory, on the other hand, posits that the primary factor causing the vascular response is the partial pressure of oxygen in the blood, while metabolic byproducts play a secondary role. Oxygen deficiency can cause paralysis of vascular smooth muscle, leading to vasodilation; when the partial pressure of oxygen increases, vascular smooth muscle contracts, causing vasospasm. This difference in vascular response results from competition for oxygen between endothelial cells and smooth muscle cells. If endothelial cells consume a large amount of oxygen, the smooth muscle becomes paralyzed due to hypoxia, leading to vasodilation. Under hyperbaric oxygen conditions, with adequate blood oxygen levels, the smooth muscle receives sufficient oxygen, causing the blood vessels to constrict.
The aforementioned theories of humoral autoregulation and oxygen-response autoregulation cannot fully explain the complex and diverse vascular responses under hyperbaric oxygen conditions; for example, they cannot account for the differing vascular responses in the systemic and pulmonary circulations. When free pulmonary arteries are perfused under hyperbaric oxygen, their resistance increases, just as in other blood vessels; however, in living organisms, hyperbaric oxygen actually reduces resistance in the pulmonary circulation.
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(1) Cerebral Blood Flow
Hyperbaric oxygen has the greatest effect on cerebral blood vessels. When oxygen is inhaled at atmospheric pressure, cerebral blood flow decreases by 10% to 12% (Table 1-8-1-1). As a local regulatory mechanism, the response of cerebral blood vessels to hyperbaric oxygen varies depending on the pressure-time profile, brain region, pathological state of the brain, and the specific blood vessels involved: blood flow increases in damaged, ischemic areas. This is caused by local vasodilation resulting from tissue hypoxia, CO₂ retention, and the accumulation of certain metabolic byproducts.
The reduction in cerebral blood flow helps alleviate cerebral edema and lower intracranial pressure. Under hyperbaric oxygen conditions, although cerebral blood flow decreases, the increased oxygen content in the blood is sufficient to improve cerebral hypoxia, thereby breaking the vicious cycle between cerebral hypoxia and cerebral edema. This makes hyperbaric oxygen therapy highly effective for the emergency treatment of patients with cerebral hypoxia and cerebral edema, as well as for the treatment of various cerebrovascular diseases.
Under hyperbaric oxygen conditions, carotid blood flow decreases while vertebral artery blood flow increases. Consequently, blood supply to the reticular activating system of the brainstem and the brainstem itself increases, and the partial pressure of oxygen rises accordingly. This enhances the excitability of the ascending reticular activating system, facilitating the recovery of consciousness in comatose patients and supporting vital functions. Therefore, hyperbaric oxygen therapy can be used to treat patients in a coma caused by various etiologies.
(2) Coronary Blood Flow
In recent years, as hyperbaric oxygen therapy has been routinely used to treat angina pectoris and myocardial infarction, research on its effects on coronary blood flow has begun to receive increased attention. Coronary blood flow decreases under hyperbaric oxygen conditions; however, because blood oxygen content increases, the myocardium can still receive an adequate oxygen supply. The reduction in coronary blood flow is closely related to the duration of oxygen administration. After 30 minutes of oxygen administration at a pressure of 1,500 mmHg (200 kPa), coronary blood flow decreases by 26%; after 180 minutes, it decreases by 60%. After hyperbaric oxygen therapy is discontinued, coronary blood flow returns to normal more slowly than in other organs. Following exposure to an oxygen pressure of 750 mmHg (100 kPa), coronary blood flow does not return to 80% of its baseline value until 30 minutes after oxygen administration is stopped; at an oxygen pressure of 1,500 mmHg (200 kPa), it takes more than 1 hour to return to baseline levels.
If 2% carbon dioxide is added to the oxygen, coronary blood flow increases. Therefore, when using hyperbaric oxygen therapy to treat coronary heart disease, vasodilators should routinely be administered or a mixture of oxygen and carbon dioxide inhaled prior to treatment to counteract the coronary vasoconstrictive effects of hyperbaric oxygen, ensuring that the heart receives an adequate blood and oxygen supply.
(3) Hepatic Blood Flow
HBO increases hepatic blood flow, which enhances the metabolic and detoxification functions of hepatocytes. Consequently, HBO can protect hepatocytes from damage caused by various toxins and is used to treat severe hepatitis.
(4) Renal Blood Flow
HBO has a vasoconstrictive effect on renal vessels, reducing renal blood flow. At an oxygen pressure of 750 mmHg (100 kPa), renal blood flow decreases by 17%; at 1,500 mmHg (200 kPa), it decreases by 33%; and at 3,000 mmHg (400 kPa), it decreases by 57%. Despite the reduction in renal blood flow, the partial pressure of oxygen in the renal vein increases, and renal diuresis increases nearly threefold, with increased excretion of sodium, chloride, magnesium, creatine, and other substances. Therefore, hyperbaric oxygen therapy provides a certain degree of protection to ischemic kidneys.
(5) Skeletal Muscle Blood Flow
At an oxygen pressure of 750 mmHg (100 kPa), blood flow in the upper limbs decreases by 11.2%; at 1,500 mmHg (200 kPa), it decreases by 18.9%. However, in affected limbs, blood flow remains unchanged under hyperbaric oxygen conditions, resulting in an increase in available oxygen. Consequently, hyperbaric oxygen therapy can be used to treat peripheral vascular diseases, such as arterial occlusive diseases and thromboangiitis obliterans.
After hyperbaric oxygen therapy is discontinued, the recovery of muscle blood flow is slow, taking at least 1 hour to return to baseline levels. Therefore, strenuous exercise should be avoided for a period following hyperbaric oxygen therapy. For example, athletes should not compete within 2 hours after hyperbaric oxygen therapy to avoid compromising their performance.
(6) Retinal Blood Flow
Retinal blood vessels lack intrinsic sympathetic innervation but possess the ability to constrict and dilate. Their response to hyperoxia is similar to that of cerebral blood vessels; however, when inhaling pure oxygen, the reduction in retinal blood flow is several times greater than that of cerebral blood flow. Oxygen levels in retinal tissue increase significantly under hyperbaric oxygen conditions; therefore, hyperbaric oxygen therapy can be used to treat ischemic diseases of the fundus, such as central retinal artery occlusion and retinal vein thrombosis. However, since excessive oxygen can cause significant constriction of retinal blood vessels, vasodilators should be routinely administered prior to treatment.
2.5 Effects on Microcirculation
Hyperbaric oxygen therapy improves microcirculation, primarily through the following mechanisms: (1) enhancing red blood cell deformability; (2) inhibiting the blood coagulation system. At an oxygen pressure of 2,025–3,000 mmHg (270–400 kPa), blood clotting time is prolonged by 34%, the prothrombin index decreases by 2.4%, and plasma thrombogenic activity is reduced. At the same time, under hyperbaric oxygen conditions, phagocytic cell function is enhanced, fibrinolysin activity increases, and blood clots are dissolved. Therefore, the use of hyperbaric oxygen therapy must be carefully considered for patients with coagulation disorders. (3) Reducing blood viscosity. (4) Improving microcirculatory regulatory function.
3. Effects of Hyperbaric Oxygen on the Respiratory System
Under hyperbaric oxygen conditions, changes occur in respiratory function. These changes are related to the respiratory center’s response to increased partial pressure of oxygen in the blood, as well as the physical effects of compressed gas on the respiratory process.
3.1 Decreased Respiratory Rate
Generally, at an oxygen pressure of 1,500–2,250 mmHg (200–300 kPa), approximately 90% of patients experience a decrease in respiratory rate. This is due to the increased partial pressure of oxygen in the blood, which reflexively inhibits the respiratory center via chemoreceptors such as the carotid bodies. If the corresponding afferent nerves are severed, the body’s respiratory rate remains unchanged under hyperbaric oxygen conditions. However, if the partial pressure of oxygen is too high or oxygen administration is prolonged, carbon dioxide retention in the blood and tissues, coupled with an increase in hydrogen ion concentration, stimulates the respiratory center, causing the respiratory rate to accelerate instead.
3.2 Increased Vital Capacity
Under hyperbaric oxygen conditions, gas in the gastrointestinal tract is compressed, causing the diaphragm to descend by 1.5–2.0 cm and the vertical diameter of the thoracic cavity to expand, thereby increasing lung volume and, consequently, vital capacity. At oxygen pressures of 1,500–2,250 mmHg (200–300 kPa), functional residual capacity typically remains unchanged, while vital capacity increases by an average of approximately 7%.
3.3 Increased Respiratory Work
Respiratory work = pressure × volume. Under hyperbaric oxygen conditions, the density of the inhaled gas increases, leading to greater inelastic resistance; simultaneously, the thoracic cavity expands and lung volume increases, resulting in a significant increase in respiratory work.
Most hyperbaric oxygen therapy sessions are conducted at an oxygen pressure of 1,500–1,875 mmHg (200–250 kPa), with each session lasting no longer than 2.5 hours. Within these limits, hyperbaric oxygen generally has no adverse effects on lung function, or only very mild adverse effects occur. Mild adverse effects generally resolve within 24 hours. However, for patients with respiratory insufficiency, airway stenosis, or respiratory muscle dystrophy, the treatment pressure should be reduced or the treatment duration shortened.
4. Effects of Hyperbaric Oxygen Therapy on the Hematological System
The primary factor stimulating erythropoiesis is erythropoietin. Between 90% and 95% of this substance is produced by the kidneys and then enters the bloodstream. Tissue oxygenation is the fundamental regulatory factor for erythropoietin; any factor that reduces tissue oxygen supply can increase the release of erythropoietin, thereby accelerating the rate of erythropoiesis. Conversely, an increase in blood oxygen partial pressure inhibits erythropoiesis. Unless a patient remains in a hyperbaric oxygen environment for an extended period, clinical hyperbaric oxygen therapy does not inhibit erythropoiesis. Increased blood oxygen levels can also reduce the body’s demand for erythrocytes to transport oxygen, with some erythrocytes being stored in the liver and spleen. After 4 hours at an oxygen pressure of 1,500 mmHg (200 kPa), hemoglobin levels and erythrocyte counts in peripheral blood decrease, while white blood cell counts increase. A bone marrow aspiration reveals a marked decrease in erythroblasts, along with an increase in neutrophils, polymorphonuclear leukocytes, reticulocytes, and plasma cells. After discontinuing hyperbaric oxygen therapy, these blood cell changes typically return to normal within a short period. Following hyperbaric oxygen therapy, the deformability of red blood cells increases, their ability to pass through capillaries improves, and blood flow accelerates. Prolonged hyperbaric oxygen therapy can induce an increase in free radicals within the body; excessive free radicals trigger lipid peroxidation reactions in red blood cell membranes, damaging lipids, leading to increased red blood cell fragility, and may cause hemolysis, resulting in a decrease in hematocrit.
5. Effects of Hyperbaric Oxygen Therapy on the Digestive System
5.1 Effects on Gastric Juice Secretion
Under hyperbaric oxygen conditions, the secretion of gastric acid and pepsin is significantly reduced, which may be due to decreased enzyme activity in parietal cells and chief cells.
5.2 Promotion of Intestinal Gas Absorption
Hyperbaric oxygen therapy can significantly promote the absorption of gas in the intestines and is therefore used to treat paralytic ileus and intestinal gas cysts.
5.3 Protective Effects on the Liver
Hyperbaric oxygen increases blood flow and oxygen supply to the liver, enhancing the detoxification function of hepatocytes. This may be the mechanism by which hyperbaric oxygen protects hepatocytes from damage caused by various toxins and ischemia.
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6. Effects of Hyperbaric Oxygen on the Endocrine System
Under hyperbaric oxygen conditions, the production of pituitary and adrenal cortical hormones increases, stimulating the body’s defense systems and hormonal regulatory mechanisms (the pituitary-adrenal axis) as well as neural regulatory mechanisms (the sympathetic-adrenal medulla system). Changes also occur in other endocrine organs, placing the body in a state of stress to some degree.
6.1 Pituitary-Adrenal Axis
Hyperbaric oxygen stimulation increases the secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland, leading to elevated levels of adrenal corticosteroids. The mechanism by which hyperbaric oxygen stimulates the pituitary-adrenal axis remains unclear; however, this response is nonspecific and is thought to occur through excitation of the reticular formation, which in turn stimulates the hypothalamus and pituitary gland.
In addition to their anti-inflammatory and immunosuppressive effects, corticosteroids also increase vascular sensitivity to catecholamines, promote gluconeogenesis, raise blood glucose levels, and stabilize lysosomal membranes to prevent the leakage of lysosomal enzymes that could damage cells. Therefore, the increase in corticosteroids under hyperbaric oxygen conditions can be used to treat inflammation, shock, and prevent organ transplant rejection. It is particularly beneficial for managing certain conditions that require hormone therapy, such as multiple sclerosis, myasthenia gravis, and bronchial asthma.
6.2 Sympathetic-Adrenal Medulla System
The sympathetic-adrenal medulla system serves as another line of defense for the body. Stimulation of the adrenal medulla leads to the release of epinephrine. Adrenaline plays an active role in both specific and nonspecific responses of the central nervous system. Adrenaline in the brainstem can induce a cortical arousal response and stimulate the connections between the reticular formation and the spinal cord. Additionally, adrenaline can stimulate the secretion of adrenocorticotropic hormone (ACTH), which serves as a regulatory factor in the neurohormonal mechanisms promoted by hyperbaric oxygenation.
6.3 Thyroid
Hyperbaric oxygen has no effect on thyroxine levels in healthy individuals, but it can restore thyroxine levels to normal in patients with hyperthyroidism. The mechanism remains unclear, but it may be related to hyperbaric oxygen promoting the normalization of the pituitary-thyroid axis regulatory function.
6.4 Prostaglandins
As oxygen pressure increases, renal blood flow gradually decreases, and the secretion of renal prostaglandin E2 also decreases in tandem with the reduction in blood flow. Although plasma antidiuretic hormone (ADH) levels remain unchanged, hyperbaric oxygen therapy exerts an antidiuretic effect. This is thought to result from reduced renal vascular blood flow, which increases the medullary osmotic gradient, or from a reduction in the normal antagonistic interaction between prostaglandin E2 and antidiuretic hormone, leading to an enhanced effect of endogenous antidiuretic hormone.
6.5 Testosterone
Under hyperbaric oxygen conditions, testicular blood flow decreases, and plasma testosterone concentrations decline.
In summary, endocrine factors have a significant impact on the efficacy of hyperbaric oxygen therapy, particularly the pituitary-adrenal axis and the sympathetic-adrenal medulla system, which enhance the body’s stress response to help it survive the critical period. However, it is essential to closely monitor patients’ individual responses and emotional changes under hyperbaric oxygen conditions. Particular attention should be paid to the adverse effects caused by stress dysregulation in patients being treated for bronchial asthma, trauma, infections, and those recovering from surgery.
7. Effects of Hyperbaric Oxygen Therapy on the Immune System
Numerous studies indicate that hyperbaric oxygen therapy has an immunosuppressive effect and may have potential applications in organ transplantation.
7.1 Humoral Immunity
Hyperbaric oxygen therapy reduces serum immunoglobulin levels; these levels generally return to normal within 1 to 3 months after treatment ends. Since immunoglobulins are part of the humoral immune system, hyperbaric oxygen therapy has an immunosuppressive effect on humoral immunity.
7.2 Cellular Immunity
Hyperbaric oxygen therapy reduces the number of white blood cells and lymphocytes. These changes gradually return to normal levels 24 hours after discontinuation of therapy. However, following five consecutive days of hyperbaric oxygen therapy (once daily), the reduction in white blood cells and lymphocytes tends to stabilize and does not readily return to normal levels.
The mechanism by which hyperbaric oxygen suppresses immune function may be as follows: hyperbaric oxygen increases intracellular oxygen concentration, causing the endogenous antioxidant system to become overwhelmed. As a result, peroxide concentrations rise above physiological levels, leading to increased ionic permeability of lymphocyte membranes and an imbalance in the ionic composition of the cytoplasm and organelles, which in turn causes metabolic disorders and mitotic abnormalities.
In summary, hyperbaric oxygen therapy does indeed have a marked immunosuppressive effect and can therefore be applied in organ transplantation and the treatment of certain immune-related diseases, such as bronchial asthma, myasthenia gravis, and multiple sclerosis. However, for patients with pre-existing immunodeficiency or those whose immune function is temporarily compromised but who are otherwise candidates for hyperbaric oxygen therapy, such treatment should be used with caution. Alternatively, measures to enhance immune function should be implemented concurrently with hyperbaric oxygen therapy to prevent further suppression of the patient’s immune function.
8. Effects of Hyperbaric Oxygen on Enzyme Activity
Under hyperbaric oxygen conditions, the body’s metabolism undergoes significant changes, affecting the activity of various enzymes. Hyperbaric oxygen can enhance the activity of lactate dehydrogenase, isocitrate dehydrogenase, succinate dehydrogenase, cytochrome oxidase, and mitochondrial ATP synthase in brain tissue. Increased lactate dehydrogenase activity indicates enhanced aerobic glycolysis, which can generate more energy. Isocitrate dehydrogenase, located in the mitochondrial matrix, is the rate-limiting enzyme of the tricarboxylic acid cycle, and succinate dehydrogenase is also a key enzyme in this cycle. Under hyperbaric oxygen conditions, the increased activity of isocitrate dehydrogenase and succinate dehydrogenase accelerates the citric acid cycle, thereby increasing ATP production. Cytochrome oxidase activity serves as an indicator of cellular aerobic metabolism. Under hyperbaric oxygen conditions, enhanced cytochrome oxidase activity accelerates the electron transport chain, leading to increased ATP production. Mitochondrial ATPase is a hydrolase that hydrolyzes the substrate ATP to release energy. Hyperbaric oxygen therapy increases the activity of this enzyme, enhances aerobic oxidation, leads to increased ATP production, and alleviates tissue damage. Therefore, hyperbaric oxygen therapy can be used for the treatment of acute cerebral hypoxia.
Under hyperbaric oxygen conditions, the activity of alkaline phosphatase (AKP), lactate dehydrogenase (LDH), glucose-6-phosphatase (G-6-PD), and acetylcholinesterase (AchE) in cardiac muscle increases, while the activity of monoamine oxidase and peroxidase decreases.
Generally speaking, under hyperbaric oxygen conditions, enzymes in the body associated with aerobic metabolism—such as ATPase, succinate dehydrogenase, cytochrome oxidase, and lactate dehydrogenase—are activated; whereas enzymes associated with anaerobic metabolism are inhibited, such as a decrease in epoxidase activity. It is worth noting that excessively high pressure [such as an oxygen pressure of 3,750 mmHg (500 kPa)] can cause damage to the enzyme system.
9. Effects of Hyperbaric Oxygen Therapy on Metabolic Functions
9.1 Brain Tissue Metabolism
The most significant effect of hyperbaric oxygen on human metabolism occurs in brain tissue. Under hyperbaric oxygen conditions, the rate of glucose metabolism increases, leading to greater energy production, which promotes the repair of damaged brain tissue. Gamma-aminobutyric acid (GABA) has been shown to play a crucial role in brain physiological activity; GABA is involved in the regulation and transmission of nerve impulses in the central nervous system and is also an important intermediate product of brain metabolism. A decrease in GABA levels under hyperbaric oxygen conditions may represent the mechanism by which oxygen toxicity induces seizures. Concentrations of ammonia, glutamate, and glutamine in brain tissue rise under hyperbaric oxygen conditions; this is due to the diffusion of blood ammonia across the blood-brain barrier into brain tissue. After 60 minutes of exposure to an oxygen pressure of 2,250 mmHg (300 kPa), the concentration of ammonia in brain tissue decreases. This is due to the activation of glutamate dehydrogenase in the mitochondria of brain cells, which increases the conversion of α-ketoglutarate to glutamate; ammonia then combines with glutamate to form glutamine, which is subsequently excreted from the brain into the bloodstream via capillaries. The mechanism by which hyperbaric oxygen therapy treats severe hepatitis and hepatic encephalopathy may be related to this process.
9.2 Myocardial Metabolism
The metabolic rate of the myocardium decreases under hyperbaric oxygen conditions. However, when hyperbaric oxygen therapy is administered during myocardial infarction, it can increase the myocardial metabolic rate. It is currently believed that the reduction in myocardial metabolic rate under hyperbaric oxygen conditions is coordinated with a decrease in coronary blood flow, while the partial pressure of oxygen in the myocardium is the most important factor in maintaining both myocardial metabolism and coronary blood flow at normal levels.
