Role of oxygen radicals in tourniquet-related ischemia-reperfusion injury of human patients

Friedl, H. P.; Till, Gerd O.; Trentz, O.; Ward, Peter A.

doi:10.1007/bf01645168

Cited by 51 publications

(25 citation statements)

References 17 publications

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“…Some hypertensive patients, especially those with severe ("malignant") hypertension, may have tissue ischemia with elevated lactate levels that similarly compete with urate transport in the proximal tubule [22]. Tissue ischemia can also result in increased generation of uric acid [30]. Hyperinsulinemia, which is common in obese and nonobese individuals with hypertension, is another factor associated with reduced urate excretion [31].…”

Section: Uric Acid Elevation Is Increased Secondary To Hypertensionmentioning

confidence: 98%

Uric Acid and Hypertension: Cause or Effect?

et al. 2010

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Uric acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, uric acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that uric acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which uric acid could initiate this response. It remains possible that uric acid is a marker for xanthine oxidase-associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that uric acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperuricemia might delay the development of essential hypertension.

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Section: Uric Acid Elevation Is Increased Secondary To Hypertensionmentioning

confidence: 98%

Uric Acid and Hypertension: Cause or Effect?

et al. 2010

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“…11 In addition to the release of lactate that blocks urate secretion in the proximal tubule, ischemia also results in increased uric acid synthesis. 16 With ischemia, ATP is degraded to adenine and xanthine, and there is also increased generation of xanthine oxidase. The increased availability of substrate (xanthine) and enzyme (xanthine oxidase) results in increased uric acid generation as well as oxidant (O 2 Ϫ ) formation.…”

Section: Hyperuricemia Is Increased In Subjects At Cardiovascular Riskmentioning

confidence: 99%

Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?

Kang²,

et al. 2003

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Abstract-Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal disease. Thus, it is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension and to design human studies to address this controversy. Key Words: antioxidants Ⅲ hypertension, essential Ⅲ cardiovascular diseases Ⅲ renin-angiotensin system Ⅲ vascular diseases Ⅲ renal disease U ric acid, a product of purine metabolism, is degraded in most mammals by the hepatic enzyme, urate oxidase (uricase), to allantoin, which is freely excreted in the urine. However, during the Miocene epoch (20 to 5 million years ago), 2 parallel but distinct mutations occurred in early hominoids that rendered the uricase gene nonfunctional. 1 As a consequence, humans and the great apes have higher uric acid levels (Ͼ2 mg/dL) compared with most mammals (Ͻ2 mg/dL).Uric acid levels also vary significantly within humans as the result of factors that increase generation (such as high purine or protein diets, alcohol consumption, conditions with high cell turnover, or enzymatic defects in purine metabolism) or decrease excretion. A reduction in glomerular filtration rate (GFR) increases serum uric acid, although a significant compensatory increase in gastrointestinal excretion occurs. 2 Hyperuricemia also may result from increased net tubular absorption. After filtration, uric acid undergoes both reabsorption and secretion in the proximal tubule, and this process is mediated by a urate/anion exchanger and a voltagesensitive urate channel. 3,4 Organic anions such as lactate decrease urate secretion by competing for urate through the organic anion transporter, whereas several substances, including probenacid and benziodarone, have opposite effects. 5 Hyperuricemia is usually defined as Ͼ6.5 or 7.0 mg/dL in men and Ͼ6.0 mg/dL in women.

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“…Hypertension can also lead to microvascular disease that can cause local tissue ischemia (Puig and Ruilope, 1999). Tissue ischemia can then lead to an increase in the synthesis of UA, ultimately resulting in an increased serum UA level (Friedl et al, 1991). These mechanisms indicate that the increase in the plasma UA level may be a consequence rather than a cause of hypertension.…”

Section: Hyperuricemia and Hypertensionmentioning

confidence: 99%