Intrarenal oxygen tension measured by a modified Clark electrode at normal and low blood pressure and after injection of x-ray contrast media

Liss, Per; Nygren, Anders; Revsbech, Niels Peter; Ulfendahl, H. R.

doi:10.1007/s004240050455

Cited by 85 publications

(66 citation statements)

References 39 publications

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“…Urine and arterial blood samples were taken for subsequent analyses. Renal oxygen tension was thereafter measured using modified Clark-type microelectrodes (4-6 µm o.d., Unisense, Aarhus, Denmark) [18]. The electrodes were twopoint calibrated in water saturated with either Na 2 S 2 O 5 or air at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension

Palm

Cederberg²,

Hansell³

et al. 2003

Diabetologia

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Aims/hypothesis. Augmented formation of reactive oxygen species (ROS) induced by hyperglycaemia has been suggested to contribute to the development of diabetic nephropathy. This study was designed to evaluate the influence of streptozotocin (STZ)-induced diabetes mellitus, as well as the effects of preventing excessive ROS formation by α-tocopherol treatment, on regional renal blood flow, oxygen tension and oxygen consumption in anaesthetized Wistar Furth rats. Methods. Non-diabetic and STZ-diabetic rats were investigated after 4 weeks with or without dietary treatment with the radical scavenger DL-α-tocopherol (vitamin E, 5%). A laser-Doppler technique was used to measure regional renal blood flow, whilst oxygen tension and consumption were measured using Clarktype microelectrodes. Results. Renal oxygen tension, but not renal blood flow, was lower throughout the renal parenchyma of diabetic rats when compared to non-diabetic control rats. The decrease in oxygen tension was most pronounced in the renal medulla. Renal cellular oxygen consumption was markedly increased in diabetic rats, predominantly in the medullary region. Diabetes increased lipid peroxidation and protein carbonylation in the renal medulla. Treatment with α-tocopherol throughout the course of diabetes prevented diabetesinduced disturbances in oxidative stress, oxygen tension and consumption. The diabetic animals had a renal hypertrophy and a glomerular hyperfiltration, which were unaffected by α-tocopherol treatment. Conclusions/interpretation. We conclude that oxidative stress occurs in kidneys of diabetic rats predominantly in the medullary region and relates to augmented oxygen consumption and impaired oxygen tension in the tissue. [Diabetologia (2003[Diabetologia ( ) 46:1153[Diabetologia ( -1160

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Section: Methodsmentioning

confidence: 99%

Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension

Palm

Cederberg²,

Hansell³

et al. 2003

Diabetologia

Self Cite

275

288

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“…Cortical blood perfusion was measured with laser-Doppler flowmetry (probe 411, 0.45 mm optical density, PF 4001-2; Perimed, Stockholm, Sweden) (10). Oxygen tension (PO 2 ) was measured with a polarographic technique, using modified Clark-type microelectrodes (4 -6 m outer diameter; Unisense, Aarhus, Denmark) (18,19). Electrodes were two-point calibrated in water saturated with Na 2 S 2 O 5 or saturated with air at 37°C, respectively.…”

Section: Methodsmentioning

confidence: 99%

Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats

et al. 2005

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Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (PO 2 ). Streptozotocin-induced diabetic and control rats were injected with L-arginine followed by N-nitro-L-arginine-metyl-ester (L-NAME). NO and PO 2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical PO 2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 ؎ 15 nmol/l compared with 45 ؎ 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected PO 2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 ؎ 6.7 vs. 127.9 ؎ 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after L-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetesinduced alteration in renal oxygen metabolism and local blood flow regulation. Diabetes 54:3282-3287, 2005 N itric oxide (NO) regulates vascular tone in resistance vessels and thereby blood perfusion in most capillary beds. Systemic inhibition of NO synthase (NOS) decreases renal blood perfusion, both in the cortex and in the medulla (1-3), and increases mean arterial blood pressure (4). Previous investigations in vitro have also shown that NO is a potent competitive inhibitor of oxygen consumption (5) at the level of cytochrome oxidase, the terminal electron acceptor in mitochondria (6). Therefore, the magnitude of the inhibition of oxygen consumption by NO will increase at low PO 2 (7).Long-term hyperglycemia is associated with increased oxidative stress, i.e., increased production of reactive oxygen species (ROS) (8 -11). ROS can react with NO, forming peroxynitrite, and thus decrease the bioavailability of NO (11). The bioavailability of NO and formation of peroxynitrite are also highly dependent on superoxide dismutase, as modeled by Buerk et al. (12). Decreased influence of NO has therefore been suggested to be involved in the increased renal cortical cellular oxygen consumption closely associated with manifest diabetes (10,13,14). Furthermore, involvement of endogenous competitive NOS inhibitor asymmetric dimethylarginine (ADMA) in the development of vascular complications has gained increasing support over the last few decades (15).Because NO regulates the delivery of oxygen to tissue both by setting the level of vascular tone and blood pressure and by inhibiting cellular oxygen consumption, alterations in NO activity might ...

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“…Renal oxygen tension was thereafter measured using modified Clark-type microelectrodes (4-6 µm o.d. ; Unisense, Aarhus, Denmark) [13]. The electrodes were two-point calibrated in water, saturated with either Na 2 S 2 O 5 or with air at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Polyol-pathway-dependent disturbances in renal medullary metabolism in experimental insulin-deficient diabetes mellitus in rats

et al. 2004

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Aims/hypothesis. The renal medullary region is particularly vulnerable to reduced oxygen concentration because of its low blood perfusion and high basal oxygen consumption. This study investigated renal metabolic changes in relation to the previously observed decreased oxygen tension in streptozotocin-induced diabetic rats. Methods. Blood perfusion, oxygen tension and consumption, interstitial pH, and glycolytic and purinebased metabolites were determined in the renal cortex and the medulla of non-diabetic and diabetic animals by, respectively, laser Doppler flowmetry, oxygen and pH microelectrodes, and microdialysis. The importance of increased polyol pathway activity for the observed alterations was investigated by daily treatment with the aldose reductase inhibitor AL-1576 throughout the course of diabetes.Results. The diabetes-induced decrease in renal oxygen tension, due to augmented oxygen consumption, did not result in manifest hypoxia in either the cortical or the medullary region, as evaluated by microdialysis measurements of purine-based metabolites. The profound alterations in medullary oxygen metabolism were, however, associated with an increased lactate : pyruvate ratio and a concomitantly decreased pH. Notably, the renal medullary changes in oxygen tension, oxygen consumption, lactate : pyruvate ratio and pH were preventable by inhibition of aldose reductase. Conclusions/interpretation. Substantial metabolic changes were observed in the renal medulla in diabetic animals. These disturbances seemed to be mediated by increased polyol pathway activity and could be prevented by inhibition of aldose reductase.

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Intrarenal oxygen tension measured by a modified Clark electrode at normal and low blood pressure and after injection of x-ray contrast media

Cited by 85 publications

References 39 publications

Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension

Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension

Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats

Polyol-pathway-dependent disturbances in renal medullary metabolism in experimental insulin-deficient diabetes mellitus in rats

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