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O2 Extraction (o2 + extraction)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short-term maximal exercise

EQUINE VETERINARY JOURNAL, Issue S36 2006
M. MANOHAR
Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with N,-nitro-L-arginine methyl ester [l -NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the l -NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion. [source]

Impaired oxygen extraction in metabolic myopathies: Detection and quantification by near-infrared spectroscopy

MUSCLE AND NERVE, Issue 4 2007
Bruno Grassi MD
Abstract Patients with mitochondrial myopathies (MM) or myophosphorylase deficiency (McArdle's disease, McA) show impaired capacity for O2 extraction, low maximal aerobic power, and reduced exercise tolerance. Non-invasive tools are needed to quantify the metabolic impairment. Six patients with MM, 6 with McA, 25 with symptoms of metabolic myopathy but negative biopsy (patient-controls, P-CTRL) and 20 controls (CTRL) underwent an incremental cycloergometric test. Pulmonary O2 uptake (V,O2) and vastus lateralis oxygenation indices (by near-infrared spectroscopy, NIRS) were determined. Concentration changes of deoxygenated hemoglobin and myoglobin (,[deoxy(Hb + Mb)]) were considered an index of O2 extraction. ,[deoxy(Hb + Mb)] peak (percent limb ischemia) was lower in MM (25.3 ± 12.0%) and McA (18.7 ± 7.3) than in P-CTRL (62.4 ± 3.9) and CTRL (71.3 ± 3.9) subjects. V,O2 peak and ,[deoxy(Hb + Mb)] peak were linearly related (r2 = 0.83). In these patients, NIRS is a tool to detect and quantify non-invasively the metabolic impairment, which may be useful in the follow-up of patients and in the assessment of therapies and interventions. Muscle Nerve, 2006 [source]

RENAL OXYGEN DELIVERY: MATCHING DELIVERY TO METABOLIC DEMAND

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2006
Paul M O'Connor
SUMMARY 1The kidneys are second only to the heart in terms of O2 consumption; however, relative to other organs, the kidneys receive a very high blood flow and oxygen extraction in the healthy kidney is low. Despite low arterial,venous O2 extraction, the kidneys are particularly susceptible to hypoxic injury and much interest surrounds the role of renal hypoxia in the development and progression of both acute and chronic renal disease. 2Numerous regulatory mechanisms have been identified that act to maintain renal parenchymal oxygenation within homeostatic limits in the in vivo kidney. However, the processes by which many of these mechanisms act to modulate renal oxygenation and the factors that influence these processes remain poorly understood. 3A number of such mechanisms specific to the kidney are reviewed herein, including the relationship between renal blood flow and O2 consumption, pre- and post-glomerular arterial,venous O2 shunting, tubulovascular cross-talk, the differential control of regional kidney blood flow and the tubuloglomerular feedback mechanism. 4The roles of these mechanisms in the control of renal oxygenation, as well as how dysfunction of these mechanisms may lead to renal hypoxia, are discussed. [source]