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Renovascular spasm

The mechanism by which these patients develop ALPE also remains to be clarified. However, two hypotheses have been put forward, and active oxygen/renovascular spasm or tubular obstruction may be involved. One hypothesis is that patients with renal hypouricemia are exposed to active oxygen because the level of an active oxygen... [Pg.63]

If several candidates are purified and identified in the future, some ALPE-specific markers maybe found. However, the pathogenesis of patchy renovascular spasm may involve several factors, not just a single factor. [Pg.74]

We speculate that ischemia induces changes in the tubulo-interstitium by such factors as oxidative stress, apoptosis, an increase in intracellular Ca, complement activation, ICAM-1 expression, and inflammation, in a region controlled by the blood vessels, thereby influencing the blood vessels and prolonging vascular spasm. Coronary spasm persists for 15min, and cerebrovascular spasm in the presence of subarachnoid hemorrhage persists for a week in some patients. Therefore, renovascular spasm may persist for a long period. [Pg.78]


See other pages where Renovascular spasm is mentioned: [Pg.71]    [Pg.77]    [Pg.71]    [Pg.77]    [Pg.64]   
See also in sourсe #XX -- [ Pg.74 ]




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