Background: Inhalation of hyperbaric oxygen (HBO) has been reported to decrease arterial oxygen tension (PaO(2)) in the early period after exposure. The current investigation aimed at evaluating whether and to what extent arterial blood gases were affected in mechanically ventilated intensive care patients within 6 h after HBO treatment.
Methods: Arterial blood gases were measured in 11 ventilated subjects [nine males, two females, synchronized intermittent mandatory ventilation (SIMV) mode] undergoing HBO therapy for necrotizing soft tissue infection (seven patients), burn injury (two patients), crush injury (one patient) and major abdominal surgery (one patient). Blood gases were obtained with the patients in the supine position under continuous analgesia and sedation before the hyperbaric session (baseline), during isopression, after decompression, after each transport, and 1, 2, 3 and 6 h after exposure. Heart rates and blood pressures were recorded. Intensive care unit (ICU) ventilator settings remained unchanged. Transport and chamber ventilator settings were adjusted to baseline with maintenance of tidal volumes and positive end-expiratory pressure (PEEP) levels. The hyperbaric protocol consisted of 222.9 kPa (2.2 absolute atmospheres) and a 50-min isopression phase. The paired Wilcoxon's test was used.
Results: Major findings (median values, 25%/75% quartiles) as per cent change of baseline: PaO(2) values decreased by 19.7% (7.0/31.7, P < 0.01) after 1 h and were elevated over baseline by 9.3% (1.5/13.7, P < 0.05) after 3 h. SaO(2), alveolar-arterial oxygen tension difference and PaO(2)/FiO(2) ratio behaved concomitantly. Acid-base status and carbon dioxide tension were unaffected.
Conclusion: Arterial oxygen tension declines transiently after HBO and subsequently improves over baseline in intensive care patients on volume-controlled mechanical ventilation. The effectiveness of other ventilation modes or a standardized recruitment manoeuvre has yet to be evaluated.
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http://dx.doi.org/10.1111/j.1399-6576.2006.01197.x | DOI Listing |
ACS Nano
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CAS Key Laboratory of Bio-Inspired Materials and Interfacial Science, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, P. R. China.
Enhancing the wettability of liquid metals (LMs) to address their high surface tensions is crucial for practical applications. However, controlling LMs wetting on various substrates and understanding the underlying mechanisms are challenging. Here, we present a facile dynamic-wetting strategy to modulate eutectic gallium-indium (EGaIn) wettability via chemical surface modification, spontaneously forming a stable and thin (∼18 μm) EGaIn layer.
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Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Friedrich-Schiller-University Jena, Jena, Germany.
Unlabelled: The prevalence of obesity is increasing at an alarming rate in industrialized countries. Obesity is a systemic disease that causes not only macroscopic alterations, but also mitochondrial dysfunction. Laparoscopic sleeve gastrectomy (LSG) poses a potential therapeutic option for patients with severe obesity.
View Article and Find Full Text PDFMicrob Biotechnol
January 2025
Estación Experimental del Zaidín, Consejo Superior de Investigaciones Científicas, Granada, Spain.
The discovery at the end of the 20th century of genes that induce cell death revolutionised the biocontaintment of genetically manipulated bacteria for environmental or agricultural applications. These bacterial 'killer' genes were then assayed for their potential to target and control malignant cells in human cancers. The identification of the bacteriomes in different human organs and tissues, coupled with the observation that bacteria tend to accumulate near tumours, has opened new avenues for anti-cancer strategies.
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View Article and Find Full Text PDFBr J Pharmacol
January 2025
Department of Pharmacology, University of Oxford, Oxford, UK.
Background And Purpose: TMEM16A chloride channels constitute a depolarising mechanism in arterial smooth muscle cells (SMCs) and contractile cerebral pericytes. TMEM16A pharmacology is incompletely defined. We elucidated the mode of action and selectivity of a recently identified positive allosteric modulator of TMEM16A (PAM_16A) and of a range of TMEM16A inhibitors.
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