Changes In Tissue Oxygen Tension Research Articles

Мониторинг изменения содержания кислорода в тканях по кинетике замедленной флуоресценции экзогенных красителей

The dynamics of oxygen consumption during photodynamic processes and its subsequent restoration in malignant tumors and healthy tissues of mice were studied in vitro by kinetics of long-term luminescence of xanthene dyes. It was shown that to estimate changes in tissue oxygen tension, specific type of delayed fluorescence can be used which caused by singlet-triplet annihilation of singlet oxygen and a sensitizer in triplet state. In tumors under pulse excitation of sensitizers, reversible quenching of delayed fluorescence was observed, which is associated with a decrease in the tissue oxygen tension during photodynamic processes. Method for visualizing the restoration of the initial oxygen level in tissues after photodynamic action is proposed.

Changes in tissue oxygen tension, venous saturation, and Fick-based assessments of cardiac output during hyperoxia.

Hyperoxemia (arterial oxygen tension >100mmHg) may occur in critically ill patients and have effects on mixed venous saturation (SvO2 ) and on Fick-based estimates of cardiac output (CO). We investigated the effect of hyperoxemia on SvO2 and on assessments of CO using the Fick equation. Yorkshire swine (n=14) were anesthetized, intubated, and paralyzed for instrumentation. SvO2 (co-oximetry) and tissue oxygen tension (tPO2 , implantable electrodes) in brain and myocardium were measured during systematic manipulation of arterial oxygen tension (PaO2 ) using graded hyperoxia (fraction of inspired oxygen 0.21 → 0.8). Secondarily, oxygen- and carbon dioxide-based estimates of CO (FickO2 and FickCO2 , respectively) were compared with measurements from a flow probe placed on the aortic root. Independent of changes in measured oxygen delivery, cerebral and myocardial tPO2 increased in proportion to PaO2 , as did SvO2 (P<0.001 for all). Based on mixed model analysis, each 100mmHg increase in PaO2 resulted in a 4.8±0.9% increase in SvO2 under the conditions tested. Because neither measured oxygen consumption, arterial oxyhemoglobin saturation or cardiac output varied significantly during hyperoxia, changes in SvO2 resulted in successively increasing errors in FickO2 during hyperoxia (34% during normoxia, 72% during FiO2 0.8). FickCO2 lacked the progressively worsening errors present in FickO2 , but correlated poorly with CO. SvO2 acutely changes following changes in PaO2 even absent changes in measured DO2 . This may lead to errors in FickO2 estimates of CI. Further work is necessary to understand the impact of this phenomenon in disease states.

Hypoxia Imaging of Tumor and Spatiotemporal Analysis during Oxygen Inhalation

SUMMARYTumor hypoxia is considered a potential therapeutic problem because it reduces the effects of radiation therapy. Clinical experience has shown that long‐term tumor oxygenation cannot be achieved with oxygen inhalation, but the mechanisms behind this phenomenon remain unknown. In this study, we designed an optical system for evaluating spatiotemporal changes in tissue oxygen tension (pO2) by phosphorescence quenching. The system can measure continuous changes in pO2 at a fixed point and can also perform two‐dimensional mapping of pO2 in any part of the tumor tissue. We implanted tumor tissue in a dorsal skinfold chamber (DSC) of C57BL/6 mice and observed tumor growth. The mice received oxygen inhalation and pO2 was measured. Tumor pO2 increased after inhalation but the oxygen level was not maintained despite continuous inhalation of pure oxygen; the tumor returned to a hypoxic state. These results mimic the clinical experience of oxygen inhalation treatment in radiation therapy. Our system reproduces the repeat hypoxic phenomenon in a murine tumor model and can be used to determine the mechanisms of oxygen metabolism in tumors.

Measurement of brain oxygenation changes using dynamic T1-weighted imaging

Magnetic resonance imaging (MRI) has proven useful in evaluating oxygenation in several types of tissue and blood. This study evaluates brain tissue oxygenation changes between normoxia and hyperoxia in healthy subjects using dynamic T1 and T2*-weighted imaging sequences. The change in FiO2 induced by hyperoxia caused a significant decrease in T1. A model to determine changes in tissue oxygen tension from the T1-weighted MRI signal is presented based on previous findings that T1 is sensitive to oxygen tension whereas T2* is sensitive to blood saturation. The two sequences produce results with different regional and temporal dynamics. These differences combined with results from simulations of the T1 signal intensities, indicate an increase in extravascular oxygen tension during hyperoxia. This study concludes that T1 and T2* responses to FiO2 serve as independent biomarkers of oxygen physiology in the brain with a potential to provide quantitative information on tissue oxygenation.

Hypoxia Imaging of Tumor and Spatiotemporal Analysis during Oxygen Inhalation

SUMMARY Tumor hypoxia is considered a potential therapeutic problem because it reduces the effects of radiation therapy. Clinical experience has shown that long-term tumor oxygenation cannot be achieved with oxygen inhalation, but the mechanisms behind this phenomenon remain unknown. In this study, we designed an optical system for evaluating spatiotemporal changes in tissue oxygen tension (pO2) by phosphorescence quenching. The system can measure continuous changes in pO2 at a fixed point and can also perform two-dimensional mapping of pO2 in any part of the tumor tissue. We implanted tumor tissue in a dorsal skinfold chamber (DSC) of C57BL/6 mice and observed tumor growth. The mice received oxygen inhalation and pO2 was measured. Tumor pO2 increased after inhalation but the oxygen level was not maintained despite continuous inhalation of pure oxygen; the tumor returned to a hypoxic state. These results mimic the clinical experience of oxygen inhalation treatment in radiation therapy. Our system reproduces the repeat hypoxic phenomenon in a murine tumor model and can be used to determine the mechanisms of oxygen metabolism in tumors.

Dynamics of Airway Blood Vessels and Lymphatics: Lessons from Development and Inflammation

Blood vessels and lymphatic vessels in the respiratory tract play key roles in inflammation. By undergoing adaptive remodeling and growth, blood vessels undergo changes that enable the extravasation of plasma and leukocytes into inflamed tissues, and lymphatic vessels adjust to the increased fluid clearance and cell traffic involved in immune responses. Blood vessels and lymphatics in adult airways are strikingly different from those of late-stage embryos. Before birth, blood vessels in mouse airways make up a primitive plexus similar to that of the yolk sac. This plexus undergoes rapid and extensive remodeling at birth. In the early neonatal period, parts of the plexus regress. Capillaries then rapidly regrow, and with arterioles and venules form the characteristic adult vascular pattern. Lymphatic vessels of the airways also undergo rapid changes around birth, when lymphatic endothelial cells develop button-like intercellular junctions specialized for efficient fluid uptake. Among the mechanisms that underlie the onset of rapid vascular remodeling at birth, changes in tissue oxygen tension and mechanical forces associated with breathing are likely to be involved, along with growth factors that promote the growth and maturation of blood vessels and lymphatics. Whatever the mechanisms, the dynamic nature of airway blood vessels and lymphatics during perinatal development foretells the extraordinary vascular plasticity found in many diseases.

Unilateral Stellate Ganglion Block Produces Bidirectional Changes in Tissue Oxygen Tension of the Mental Nerve in Rabbits

The purpose of this study was to investigate changes in the tissue oxygen tension (PO(2)) of the mental nerve bilaterally before and after unilateral stellate ganglion block (SGB). Nine male Japan white rabbits were used. Anesthesia was maintained by a continuous infusion of propofol under mechanical ventilation with room air. For the SGB, the tip of a 26-gauge needle was placed on the left transverse process of the cervical vertebra; 0.2 mL of 1% lidocaine solution was injected. Data were recorded immediately before SGB and when the maximal change in PO(2) after SGB was observed. Observed variables were heart rate, blood pressure, common carotid arterial blood flow, tongue mucosal blood flow, left PO(2), and right PO(2). PO(2) showed maximal changes 7.9 ± 2.0 minutes after SGB. No changes were observed in heart rate and blood pressure after SGB. Common carotid arterial blood flow, tongue mucosal blood flow, and left PO(2) were increased by 106.4% ± 39.8%, 36.2% ± 35.2%, and 38.7% ± 19.8%, respectively, after SGB. In contrast, right PO(2) was decreased by 29.8% ± 7.4% after SGB. These results suggest that unilateral SGB produces bidirectional changes in the PO(2) of the mental nerve and that SGB decreases the PO(2) of the mental nerve on the contralateral side.

Hypoxic downregulation of cellular proliferation and loss of phenotype stability in human osteoblasts is mediated by HIF-1α

Both, skeletal development and fracture healing depend on an orchestrated sequence of cellular growth and differentiation processes. Regional changes in tissue oxygen tension were proposed as key regulators of osteoblast proliferation and phenotype. Hypoxia results in the stabilization of hypoxia-inducible factor-1α (HIF-1α), thus influencing expression of a multitude of genes required for cellular adaptation. In the present study we dissected the effects of HIF-1α on cellular proliferation and gene expression of primary human osteoblasts. Primary human osteoblasts were studied by transfecting siRNA and plasmids coding for human HIF-1α. Gene expression was analyzed by western blot and quantitative PCR. Functional assays were performed to study HIF-1α function, i.e. proliferation and cell cycle analysis. As previously reported exposure to hypoxia led to a stabilization of HIF-1α on protein level and resulted in reduced rates of proliferation and osteocalcin expression. Furthermore, the expression of the proproliferative gene survivin was significantly reduced (p < 0.01). Knock down of HIF-1α attenuated hypoxic downregulation of proliferation (p < 0.05), and osteocalcin (p < 0.05) as well as survivin (p < 0.05) expression significantly. Importantly, the isolated overexpression of HIF-1α impaired proliferative activity and led to significantly reduced rates of expression of osteocalcin (p < 0.05) and survivin (p < 0.01). The present study shows that HIF-1α might reduce proliferation and survivin expression in primary human osteoblasts independently from cellular hypoxia. Furthermore, HIF-1α promoted the loss of the characteristic osteoblastic marker, osteocalcin in vitro. These findings underline the important role of HIF-1α in bone physiology and pathophysiology. Modulating HIF-1α function in hypoxic environments could be of value for future therapeutic approaches.

Oxygen sensing and conducted vasomotor responses in mouse cremaster arterioles in situ

This study examines mechanisms by which changes in tissue oxygen tension elicit vasomotor responses and whether localized changes in oxygen tension initiates conducted vasomotor responses in mouse cremaster arterioles. Intravital microscopy was used to visualize the mouse cremaster microcirculation. The cremaster was superfused with Krebs' solution with different oxygen tensions, and a gas exchange chamber was used to induce localized changes in oxygen tension. In arterioles where red blood cells were removed by buffer perfusion, arterioles responded with same magnitudes of vasodilatation (DeltaD = 16.0 +/- 4.9 microm) when changing from high (PO(2) = 242.5 +/- 13.3 mm Hg) to low (PO(2) = 22.5 +/- 4.8 mm Hg) oxygen tension as seen in the intact cremaster circulation (DeltaD = 18.7 +/- 1.0 microm). Blockade of NO synthases by L: -NAME and adenosine receptors by DPCPX had no effects on vasomotor responses to low or high oxygen. Induction of localized low (PO(2) = 23.3 +/- 5.7 mmHg) or high (PO(2) = 300.0 +/- 25.7 mm Hg) oxygen tension caused vasodilatation or -constriction locally and at a site 1,000 microm upstream (distantly). Glibenclamide blocker of ATP-sensitive K(+) channels inhibited vasodilatation and -constriction to low (PO(2) = 16.0 +/- 6.4 mm Hg) and high (PO(2) = 337.4 +/- 12.8 mm Hg) oxygen tension. 1) ATP-sensitive K(+) channels seem to mediate, at least in part, vasodilatation and vasoconstriction to low and high oxygen tension; 2) Red blood cells are not necessary for inducing vasodilatation and vasoconstriction to low or high oxygen tension; 3) localized changes in the oxygen tension cause vasomotor responses, which are conducted upstream along arterioles in mouse cremaster microcirculation.

Cerebral oxygen delivery and consumption during evoked neural activity

Increases in neural activity evoke increases in the delivery and consumption of oxygen. Beyond observations of cerebral tissue and blood oxygen, the role and properties of cerebral oxygen delivery and consumption during changes in brain function are not well understood. This work overviews the current knowledge of functional oxygen delivery and consumption and introduces recent and preliminary findings to explore the mechanisms by which oxygen is delivered to tissue as well as the temporal dynamics of oxygen metabolism. Vascular oxygen tension measurements have shown that a relatively large amount of oxygen exits pial arterioles prior to capillaries. Additionally, increases in cerebral blood flow (CBF) induced by evoked neural activation are accompanied by arterial vasodilation and also by increases in arteriolar oxygenation. This increase contributes not only to the down-stream delivery of oxygen to tissue, but also to delivery of additional oxygen to extra-vascular spaces surrounding the arterioles. On the other hand, the changes in tissue oxygen tension due to functional increases in oxygen consumption have been investigated using a method to suppress the evoked CBF response. The functional decreases in tissue oxygen tension induced by increases in oxygen consumption are slow to evoked changes in CBF under control conditions. Preliminary findings obtained using flavoprotein autofluorescence imaging suggest cellular oxidative metabolism changes at a faster rate than the average changes in tissue oxygen. These issues are important in the determination of the dynamic changes in tissue oxygen metabolism from hemoglobin-based imaging techniques such as blood oxygenation-level dependent functional magnetic resonance imaging (fMRI).

Possible mechanisms of peritoneal tissue-oxygen tension changes during CO2-pneumoperitoneum: the role of design, methodology and animal models: Editorial commentary on the articles 'Peritoneal tissue-oxygen tension during a carbon dioxide pneumoperitoneum in a mouse laparoscopic model with controlled respiratory support' by Bourdel et al. (2007) and 'Effects of supplemental perioperative oxygen on post-operative abdominal wound adhesions in a mouse laparotomy model

Possible mechanisms of peritoneal tissue-oxygen tension changes during CO2-pneumoperitoneum: the role of design, methodology and animal models: Editorial commentary on the articles 'Peritoneal tissue-oxygen tension during a carbon dioxide pneumoperitoneum in a mouse laparoscopic model with controlled respiratory support' by Bourdel et al. (2007) and 'Effects of supplemental perioperative oxygen on post-operative abdominal wound adhesions in a mouse laparotomy model

Relationship between Oral Tissue Blood Flow and Oxygen Tension in Rabbit

Several studies have reported tissue blood flow and tissue oxygen tension during anesthesia, whereas there are few reports that discuss the relationship between tissue blood flow and tissue oxygen tension. The goal of this study was to investigate the relationship between these two variables before and after stellate ganglion block (SGB). We utilized 8 male Japan White rabbits. Anesthesia was maintained with propofol. For SGB, 0.2 ml of 1% lidocaine was injected and changes in mandibular bone marrow blood flow (BBF) and mandibular bone marrow oxygen tension (PbO(2)) were observed (Group B). After the observed variables completely recovered, 0.2 ml of 1% lidocaine was again injected and changes in masseter muscle blood flow (MBF) and masseter muscle oxygen tension (PmO(2)) were observed (Group M). The observed variables were hemodynamic parameters, common carotid artery blood flow, L (left side)-BBF, R (right side)-BBF, L-PbO(2), R-PbO(2), L-MBF, R-MBF, L-PmO(2) and R-PmO(2). In both groups, positive correlations (r=0.99; y=0.68x - 3.49 in Group B and r=0.99; y=0.62x + 0.47 in Group M) were observed when tissue blood flow was set at the X-axis and tissue oxygen tension at the Y-axis. In contrast, when tissue blood flow was set at the Y-axis and tissue oxygen tension at the X-axis, two regression lines almost overlapped (y=1.47x + 5.12 in Group B and y=1.59x - 0.28 in Group M). Therefore, it is estimated that tissue blood flow increases by approximately 15 ml/min/100g when tissue oxygen tension increases by 10 mmHg. In conclusion, there is a positive correlation between tissue blood flow and tissue oxygen tension. Changes in tissue oxygen tension should reflect the increase or decrease in tissue blood flow.

The Role of the Kidney in Blood Volume Regulation: The Kidney as a Regulator of the Hematocrit

The kidney plays a pivotal role in the regulation of blood volume by controlling the plasma volume and red blood cell (RBC) mass. Further, it is proposed that the kidney coordinates the relative volumes of these 2 blood components and in so doing regulates the hematocrit. This novel function as proposed is a functional concept whereby the kidney does not simply produce erythropoietin, but that the kidney regulates the hematocrit is termed the critmeter function. The kidney is unique in that it can indirectly report on blood volume as a tissue oxygen signal. It is proposed that the kidneys detect small changes in tissue oxygen tension for erythropoietin production at the critmeter, a functional unit of marginal oxygen tension within the kidneys. As the production of erythropoietin is modulated by angiotensin II, the renin-angiotensin system entrains the production of erythropoietin as part of the effector signals of the feedback loop of blood volume regulation. Collectively, the consideration of these points generates a paradigm shift in our understanding of blood volume regulation in that the role of the kidney may be expanded from simply "producing" erythropoietin to regulating the hematocrit. Further, this concept broadens the scope of the traditionally identified effector mechanisms of plasma volume regulation to include the modulation of erythropoietin production and hence RBC mass. The inclusion of both plasma volume and RBC mass as factors targeted by the effector signals recapitulates that whole blood volume is sensed and reported in the afferent signals. In summary, distinct sensing and effector mechanisms for regulating the volume of the two components of whole blood (plasma and red cell mass) are recognized. The coupling of the regulation of these 2 components of blood volume is highlighted.

Novel 1H NMR approach to quantitative tissue oximetry using hexamethyldisiloxane

19F NMR spin-lattice relaxometry of hexafluorobenzene (HFB) has been shown to be a highly sensitive indicator of tumor oxygenation. In this study hexamethyldisiloxane (HMDSO) was identified as a proton NMR analog, and its potential as a probe for investigating dynamic changes in tissue oxygen tension (pO2) was evaluated. HMDSO has a single proton resonance (delta= -0.3 ppm) and the spin-lattice relaxation rate, Rl (= 1/T1) exhibits a linear dependence on pO2: R1 (s(-1)) = 0.1126 + 0.0013* pO2 (torr) at 37 degrees C. To demonstrate application in vivo, HMDSO was administered into healthy rat thigh muscle (100 microl) and tumors (50 microl). Local pO2 was determined by using pulse-burst saturation recovery (PBSR) 1H NMR spectroscopy to assess R1. Water and fat signals were effectively suppressed by frequency-selective excitation of the HMDSO resonance. Rat thigh muscle had a mean baseline pO2 of 35 +/- 11 torr, with a typical stability of +/-3 torr over 20 min, when the rats breathed air. Altering the inhaled gas to oxygen produced a significant increase in pO2 to 100-200 torr. In tumors, altering the inspired gas also produced significant (albeit generally smaller) changes. This new pO2 reporter molecule offers a potentially valuable new tool for investigating pO2 in vivo.

Diel `tuning' of coral metabolism: physiological responses to light cues

Hermatypic-zooxanthellate corals track the diel patterns of the main environmental parameters - temperature, UV and visible light - by acclimation processes that include biochemical responses. The diel course of solar radiation is followed by photosynthesis rates and thereby elicits simultaneous changes in tissue oxygen tension due to the shift in photosynthesis/respiration balance. The recurrent patterns of sunlight are reflected in fluorescence yields, photosynthetic pigment content and activity of the two protective enzymes superoxide dismutase (SOD) and catalase (CAT), enzymes that are among the universal defenses against free radical damage in living tissue. All of these were investigated in three scleractinian corals: Favia favus, Plerogyra sinuosa and Goniopora lobata. The activity of SOD and CAT in the animal host followed the course of solar radiation, increased with the rates of photosynthetic oxygen production and was correlated with a decrease in the maximum quantum yield of photochemistry in Photosystem II (PSII) (DeltaF'/F(m)'). SOD and CAT activity in the symbiotic algae also exhibited a light intensity correlated pattern, albeit a less pronounced one. The observed rise of the free-radical-scavenger enzymes, with a time scale of minutes to several hours, is an important protective mechanism for the existence and remarkable success of the unique cnidarian-dinoflagellate associations, in which photosynthetic oxygen production takes place within animal cells. This represents a facet of the precarious act of balancing the photosynthetic production of oxygen by the algal symbionts with their destructive action on all living cells, especially those of the animal host.

Temporal Variation In Tissue Oxygen Tension And Perfusion Response To Hypoxia And Ischaemia: The Importance Of Local Control Of The Microcirculation

Introduction: The relationship between tissue oxygenation and perfusion is important since hypoxia remains a core component of many acute and chronic diseases, particularly those leading to admission to the intensive care unit. We hypothesised that skeletal muscle perfusion and oxygenation would behave similarly regardless of whether tissue hypoxia was caused by reducing blood flow or arterial oxygen content. Methods: We performed a prospective laboratory study in 18 Sprague-Dawley rats. We measured (simultaneously) tissue oxygen tension and perfusion in hind limb skeletal muscle. Rats were allocated to three groups: control (n=6), ischaemia-anoxia (n=6) and anoxia-ischaemia (n=6). Ischaemia was induced by aortic occlusion for 30 minutes and anoxia by reducing the inspired oxygen concentration to zero for 90 seconds. Results: Tissue perfusion and PtO2 changed according to an exponential mathematical model during ischaemia, anoxia, reperfusion and reoxygenation. Irrespective of whether ischaemia was the initial or subsequent insult, both LDF and PtO2 decreased. This was followed by a hyperaemic LDF response with partial recovery of PtO2. In contrast, LDF increased when anoxia was the first intervention but not when it was preceded by ischaemia; this combination resulted in reduced perfusion. Following reoxygenation, PtO2 and LDF generally recovered to baseline values. Conclusions: We conclude that changes in tissue oxygen tension and perfusion during ischaemia and anoxia depend on the order in which the insults occur, and that they may be described by an exponential model. These data also confirm the presence of exhaustible local hypoxic control mechanisms in the microcirculation.

Evaluation of Subcutaneous Tissue Gases and pH during Induction of Acidosis and Alkalosis

Peripheral tissue oxygen utilization was studied during hypoxic-induced acidosis and sodium bicarbonate-induced alkalosis in 8 domestic pigs by measurements of subcutaneous oxygen tension (P_scO₂), carbon dioxide tension (P_scCO₂) and pH (pH_sc) in relation to central hemodynamic parameters and oxygenation. Hypoxic-induced acidosis resulted in a decrease in P_scCO₂ and arterial oxygen tension (P_aO₂) to one third of baseline values (p < 0.05), an increase in P_scCO₂ and arterial carbon dioxide tension (P_aCO₂) from 41 to 55 and 34 to 39 mm Hg, respectively (p < 0.05), and a decrease in pH_sc from 7.47 to 7.30 (p < 0.05). P_scO₂ and P_aO₂ increased during reversal of hypoxia and infusion of bicarbonate (p < 0.05), without reaching baseline values. In parallel P_scCO₂ decreased and pH_sc increased but changes lagged behind changes in blood gases. Alkalosis established by further infusion of bicarbonate resulted in a decrease in P_aO₂ to 62 mm Hg whereas P_scO₂ remained below baseline values (p < 0.05). Correction of oxygen utilization in the subcutaneous tissue as measured by the markers P_scCO₂ and pH_sc is slower than indicated by changes in tissue oxygen tension, blood gases and pH. Overcompensation of acidosis with bicarbonate resulting in alkalosis impairs oxygenation.

Is Tissue Oxygen Tension during Esophagectomy a Predictor of Esophagogastric Anastomotic Healing?

Purpose: The genesis of anastomotic leakage and late stenosis of esophagogastrostomy is still unknown, although minimal blood flow and tissue hypoxia of the gastric tube are discussed as main reasons. However, the changes in tissue oxygen tension (PtO2) on esophagogastric anastomoses have not yet been evaluated in the perioperative course. Methods: Submucosal tissue oxygen tension (PtO2) was measured in 33 patients with cervical esophagogastrostomy during resection of esophageal carcinoma and reconstruction by a gastric tube. Measurements were taken close to the projected resection line and latter anastomosis using a Clark-type oxygen electrode. Results: Mean baseline PtO2was 55.1 ± 10.4 mmHg. Following the ligature of the vasa gastricae brevis and the left gastroepiploic artery (46.1 ± 9.7 mmHg), the left gastric artery (34.8 ± 9.8 mmHg), and the pull up of the gastric tube, PtO2decreased to 25.8 ± 9.4 mmHg. Anastomotic leakage occurred in 6 patients and late stenosis in 10 patients. During the operation there was no significant evidence of decreased PtO2levels in these two groups. Postoperative PtO2levels showed a significant increase in patients with anastomotic leakage. Conclusion: A disorder in oxygen consumption may cause a significant increase of PtO2in anastomotic tissue, which is associated with anastomotic leakage.

Changes in tissue oxygen tension caused by contrast media injected into the femoral artery of the dog

Changes in tissue oxygen tension caused by contrast media injected into the femoral artery of the dog

Ischemic tissue oxygen capacitance after hyperbaric oxygen therapy: a new physiologic concept.

In an effort to better understand the effects of hyperbaric oxygen therapy on ischemic tissue, we monitored the real-time changes in subcutaneous tissue oxygen tension before, during, and after exposure to hyperbaric oxygen treatments. We identified an elevation of the tissue oxygen partial pressure to over 300 mmHg during the treatment period (up from a baseline mean of 24 mmHg) in a sustained ischemia rabbit ear model (n = 22 rabbits). There was no sustained change in tissue oxygen tension beyond the period of treatment. This manner of response is consistent with several current theories used to explain the mechanism of action of hyperbaric oxygen therapy. It is also consonant with our opinion that molecular oxygen, when delivered at high pressure, can function both as a respiratory metabolite and as a signal transducer. We also studied the impact of nontherapeutic 100% oxygen at 1 atm on tissue. The sustained peak tissue oxygen tension during such challenges increased in direct proportion to the number of hyperbaric oxygen treatments given. The clinical relevance and extension of these findings are discussed.