Introduction: It is recognized that epithelial ion transport depends on oxygen supply, but this dependence has not been characterized in the human colon in vitro despite its surgical and clinical implications.
Purposes: The aim of this study is to measure the oxygen consumption of colonic epithelium under conditions which preserve vectorial ion transport and to assess the sensitivity of the human colonic epithelium short-circuit current (I (sc)) to acute hypoxia induced in vitro.
Methods: Isolated mucosa preparations from human sigmoid colon were placed in a modified Ussing chamber which allows simultaneous measurement of short-circuit current (I (sc)) and oxygen consumption (QO(2)). In separate experiments, the sensitivity to acute hypoxia induced in a conventional Ussing chamber was assessed.
Results: Basal mean ± SEM values (n = 8) were I (sc) = 3.3 ± 0.5 μEq h(-1) cm(-2) and QO(2) = 8.09 ± 0.55 μmol h(-1) cm(-2). The contribution of the serosal side to the oxygen supply was higher than that of the mucosal side (p = 0.0023). Ouabain reduced I (sc) by 70% (P < 0.0001) and QO(2) by 26% (n = 8; P = 0.0009), suggesting that a large fraction of QO(2) is needed to support ouabain-sensitive electrogenic transport. Induction of hypoxia at both sides of the Ussing chamber caused a rapid decrease in I (sc) after 2 min. I (sc) was also significantly depressed when hypoxia was induced by 5 min in the serosal side (n = 6, P < 0.0001), but was unaffected by hypoxia induced in the mucosal side.
Conclusion: The present results allow a better understanding of the clinical consequences of acute hypoxia on intestinal ion transport.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00384-011-1215-7 | DOI Listing |
Cell Death Dis
January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
View Article and Find Full Text PDFIschemic stroke can cause damage to neurons, resulting in neurological dysfunction. The main treatments in the acute phase include intravenous thrombolysis, endovascular stent-assisted vascular thrombectomy and antiplatelet therapy. Due to the limitations of the time window and the risk of early intracranial hemorrhage, finding active treatment plans is crucial for improving therapy.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Pontypridd, UK.
To what extent sildenafil, a selective inhibitor of the type-5 phosphodiesterase modulates systemic redox status and cerebrovascular function during acute exposure to hypoxia remains unknown. To address this, 12 healthy males (aged 24 ± 3 y) participated in a randomized, placebo-controlled crossover study involving exposure to both normoxia and acute (60 min) hypoxia (Fi = 0.14), followed by oral administration of 50 mg sildenafil and placebo (double-blinded).
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Biomedicine Research Center of Strasbourg (CRBS), UR 3072, "Mitochondria, Oxidative Stress and Muscle Plasticity", Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France.
Peripheral blood mononuclear cells' (PBMCs) mitochondrial respiration is impaired and likely involved in myocardial injury and heart failure pathophysiology, but its response to acute and severe hypoxia, often associated with such diseases, is largely unknown in humans. We therefore determined the effects of acute hypoxia on PBMC mitochondrial respiration and ROS production in healthy volunteers exposed to controlled oxygen reduction, achieving an inspired oxygen fraction of 10.5%.
View Article and Find Full Text PDFAnn Clin Lab Sci
November 2024
Department of Internal Medicine-Cardiovascular, Hangzhou Xixi Hospital, Hangzhou Sixth People's Hospital, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
Objective: To explore the influence of abietic acid on the autophagy and apoptosis of cardiomyocytes in rats with acute myocardial infarction (AMI).
Methods: A rat model of AMI was built by ligation of the anterior descending branch of left coronary artery, and a model of hypoxic cardiomyocyte injury was constructed by treating cardiomyocytes with hypoxia. Western blot assay was used to detect the abundance of proteins related to autophagy and apoptosis, MTT assay was used to measure the viability of cardiomyocytes, and the expression level of miR-30a-5p was detected by qRT-PCR.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!