67,945 research outputs found

    Oxygenation inhibits the physiological tissue-protecting mechanism and thereby exacerbates acute inflammatory lung injury

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    Acute respiratory distress syndrome (ARDS) usually requires symptomatic supportive therapy by intubation and mechanical ventilation with the supplemental use of high oxygen concentrations. Although oxygen therapy represents a life-saving measure, the recent discovery of a critical tissue-protecting mechanism predicts that administration of oxygen to ARDS patients with uncontrolled pulmonary inflammation also may have dangerous side effects. Oxygenation may weaken the local tissue hypoxia-driven and adenosine A2A receptor (A2AR)-mediated anti-inflammatory mechanism and thereby further exacerbate lung injury. Here we report experiments with wild-type and adenosine A2AR-deficient mice that confirm the predicted effects of oxygen. These results also suggest the possibility of iatrogenic exacerbation of acute lung injury upon oxygen administration due to the oxygenation-associated elimination of A2AR-mediated lung tissue-protecting pathway. We show that this potential complication of clinically widely used oxygenation procedures could be completely prevented by intratracheal injection of a selective A2AR agonist to compensate for the oxygenation-related loss of the lung tissue-protecting endogenous adenosine. The identification of a major iatrogenic complication of oxygen therapy in conditions of acute lung inflammation attracts attention to the need for clinical and epidemiological studies of ARDS patients who require oxygen therapy. It is proposed that oxygen therapy in patients with ARDS and other causes of lung inflammation should be combined with anti-inflammatory measures, e.g., with inhalative application of A2AR agonists. The reported observations may also answer the long-standing question as to why the lungs are the most susceptible to inflammatory injury and why lung failure usually precedes multiple organ failure

    Alkalinization during re-oxygenation prevents functional damage by hyperglycaemic hypoxia

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    HYPERGLYCAEMIA impairs recovery from transient cerebral ischaemia: the importance of tissue acidification for this phenomenon has not been clarified in detail. We investigated this issue in a less complex in vitro preparation of isolated rat dorsal spinal roots exposed for 30 min to hyperglycaemic hypoxia. Peak height of compound action potentials recovered minimally in 5 mM bicarbonate. However, recovery was greatly improved by addition of the weak base trimethylamine during re-oxygenation. Addition of the weak acid propionate had no such effect. Cytoplasmic alkalinization improved recovery in a brief time window only: application of trimethylamine after 15 min of re-oxygenation was without beneficial effect. These data emphasize the importance of cytoplasmic acidification for neurophysiological recovery from hyper-glycaemic hypoxia during the initial period of re-oxygenation

    How bold is blood oxygenation level dependent (BOLD) magnetic resonance imaging of the kidney? Opportunities, challenges and future directions

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    Renal tissue hypoperfusion and hypoxia are key elements in the pathophysiology of acute kidney injury and its progression to chronic kidney disease. Yet, in vivo assessment of renal haemodynamics and tissue oxygenation remains a challenge. Many of the established approaches are invasive, hence not applicable in humans. Blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI) offers an alternative. BOLD-MRI is non-invasive and indicative of renal tissue oxygenation. Nonetheless recent (pre-)clinical studies revived the question as to how bold renal BOLD-MRI really is. This review aims to deliver some answers. It is designed to inspire the renal physiology, nephrology, and imaging communities to foster explorations into the assessment of renal oxygenation and haemodynamics by exploiting the powers of MRI. For this purpose the specifics of renal oxygenation and perfusion are outlined. The fundamentals of BOLD-MRI are summarized. The link between tissue oxygenation and the oxygenation sensitive MR biomarker T2 * is outlined. The merits and limitations of renal BOLD-MRI in animal and human studies are surveyed together with their clinical implications. Explorations into detailing the relation between renal T2 * and renal tissue partial pressure of oxygen (pO2 ) are discussed with a focus on factors confounding the T2 * versus tissue pO2 relation. Multi-modality in vivo approaches suitable for detailing the role of the confounding factors that govern T2 * are considered. A schematic approach describing the link between renal perfusion, oxygenation, tissue compartments and renal T2 * is proposed. Future directions of MRI assessment of renal oxygenation and perfusion are explored

    Three dimensional optical imaging of blood volume and oxygenation in the neonatal brain

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    Optical methods provide a means of monitoring cerebral oxygenation in newborn infants at risk of brain injury. A 32-channel optical imaging system has been developed with the aim of reconstructing three-dimensional images of regional blood volume and oxygenation. Full image data sets were acquired from 14 out of 24 infants studied; successful images have been reconstructed in 8 of these infants. Regional variations in cerebral blood volume and tissue oxygen saturation are present in healthy preterm infants. In an infant with a large unilateral intraventricular haemorrhage, a corresponding region of low oxygen saturation was detected. These results suggest that optical tomography may provide an appropriate technique for investigating regional cerebral haemodynamics and oxygenation at the cotside. (c) 2006 Elsevier Inc. All rights reserved

    Cerebral and Peripheral Tissue Oxygenation in Children Supported on ECMO for Cardio-Respiratory Failure

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    Extracorporeal membrane oxygenation (ECMO) is a rescue therapy for patients with cardio-respiratory failure. Establishing, maintaining and weaning from ECMO may increase the risk for intracranial injury. We used a dual channel near infrared system to monitor cerebral and peripheral tissue oxygenation in 3 venoarterial (VA) and 1 venovenous (VV) ECMO patients undergoing manipulations in the ECMO circuit flows. Spectral analysis was performed on the oxyhaemoglobin data collected from these patients with the aim of comparing oscillations at range of frequencies appearing in the two measurement sites

    Measuring tissue oxygenation

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    Methods and systems for calculating tissue oxygenation, e.g., oxygen saturation, in a target tissue are disclosed. In some embodiments, the methods include: (a) directing incident radiation to a target tissue and determining reflectance spectra of the target tissue by measuring intensities of reflected radiation from the target tissue at a plurality of radiation wavelengths; (b) correcting the measured intensities of the reflectance spectra to reduce contributions thereto from skin and fat layers through which the incident radiation propagates; (c) determining oxygen saturation in the target tissue based on the corrected reflectance spectra; and (d) outputting the determined value of oxygen saturation

    Utilizing real-time pressure and tissue oxygenation monitoring to assess the adequacy of hinge craniotomy

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    AbstractHinge craniotomy has been described as a feasible option for certain patients in need of decompression as a result of a mass lesion. The technique of hinging the bone flap alleviates the need to return to the operating room for cranioplasty as is the case with a traditional decompressive craniectomy. Intracranial pressure and brain tissue oxygenation monitoring can be utilized for intraoperative guidance to assess adequacy of hinge craniotomy. We report a case where intraoperative monitoring helped guide surgical decision making for a 23year old male patient with a left traumatic subdural hematoma. The patient had a Licox monitor placed in the right frontal region, showing elevated intracranial pressure and decreased brain tissue oxygenation. The patient underwent hinge craniotomy, which initially lowered his intracranial pressure from 54 to 11cmH2O and allowed his brain tissue oxygenation to rise to a normal value of 20.5mmHg. However, upon closure of the skin, the patient's intracranial pressure increased to 24cmH2O and brain tissue oxygenation decreased to 7.8mmHg. As a result, the patient underwent decompressive craniectomy and the intracranial pressure and brain tissue oxygenation values normalized postoperatively. Intracranial pressure and brain tissue oxygenation can be helpful intraoperative guides in determining whether hinge craniotomy is adequate

    Different patterns of cerebral and muscular tissue oxygenation 10 years after coarctation repair

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    The purpose of this study was to assess whether the lower exercise tolerance in children after coarctation repair is associated with alterations in peripheral tissue oxygenation during exercise. A total of 16 children after coarctation repair and 20 healthy control subjects performed an incremental ramp exercise test to exhaustion. Cerebral and locomotor muscle oxygenation were measured by means of near infrared spectroscopy. The responses of cerebral and muscle tissue oxygenation index (cTOI, mTOI), oxygenated (O(2)Hb), and deoxygenated hemoglobin (HHb) as a function of work rate were compared. Correlations between residual continuous wave Doppler gradients at rest, arm-leg blood pressure difference and local oxygenation responses were evaluated. Age, length, and weight was similar in both groups. Patients with aortic coarctation had lower peak power output (Ppeak) (72.3 +/- 20.2% vs. 106 +/- 18.7%, P < 0.001), VO(2)peak/kg (37.3 +/- 9.1 vs. 44.2 +/- 7.6 ml/kg, P = 0.019) and %VO(2)peak/kg (85.7 +/- 21.9% vs. 112.1 +/- 15.5%, P < 0.001). Cerebral O(2)Hb and HHb had a lower increase in patients vs. controls during exercise, with significant differences from 60 to 90% Ppeak (O(2)Hb) and 70% to 100% Ppeak (HHb). Muscle TOI was significantly lower in patients from 10 to 70% Ppeak and muscle HHb was significantly higher in patients vs. controls from 20 to 80% Ppeak. Muscle O(2)Hb was not different between both groups. There was a significant correlation between residual resting blood pressure gradient and Delta muscle HHb/Delta P at 10-20W and 20-30W (r = 0.40, P = 0.039 and r = 0.43, P = 0.034). Children after coarctation repair have different oxygenation responses at muscular and cerebral level. This reflects a different balance between O-2 supply to O-2 demand which might contribute to the reduced exercise tolerance in this patient population
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