1971
DOI: 10.1152/ajplegacy.1971.220.6.1991
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Exchange of free and albumin-bound Evans blue in interstitium of hamster kidney

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Cited by 11 publications
(4 citation statements)
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“…The free dye crosses blood vessel walls more readily than does dye bound to albumin (Levick & Michel, 1973). During the remainder of the first hour after injection, Evans blue dye (now bound to albumin) leaves the circulation at about the same rate as ~31I-labelled albumin (Sear et al, 1953;Wilde et al, 1971).…”
Section: Why Paraganglia Are Stained By Evans Bluementioning
confidence: 99%
See 1 more Smart Citation
“…The free dye crosses blood vessel walls more readily than does dye bound to albumin (Levick & Michel, 1973). During the remainder of the first hour after injection, Evans blue dye (now bound to albumin) leaves the circulation at about the same rate as ~31I-labelled albumin (Sear et al, 1953;Wilde et al, 1971).…”
Section: Why Paraganglia Are Stained By Evans Bluementioning
confidence: 99%
“…Although the capacity of rat plasma albumin to bind Evans blue dye is unknown, one mole of human, bovine or rabbit albumin binds 11-14 moles of dye at pH 7.4 (Allen & Orahovats, 1950;Freedman & Johnson, 1969;Levick & Michel, 1973). In addition, even when the dos~ of Evans blue is sufficient to saturate only one-third of the circulating albumin, the dye leaves the circulation much more rapidly than does ~31I-labelled albumin during the first 2 min after injection (Wilde et al, 1971). The initially rapid loss of dye results, presumably, from the delay in uniform mixing of the solutiort with blood, which in turn retards .binding of the dye to plasma proteins.…”
Section: Why Paraganglia Are Stained By Evans Bluementioning
confidence: 99%
“…The dye binds spontaneously and avidly to albumin (32,48). When injected into the blood, most of the free dye is bound to albumin within 2 min, provided the amount of dye is below saturation as in the present experiments (53,62).…”
Section: Discussionmentioning
confidence: 55%
“…The fate of BMSPCs is ultimately determined by the nature of the myocardial microenvironment. The onset of ischemic injury and subsequent reperfusion results in a robust proinflammatory state with elevated levels of locally activated complement [7577] and ROS [78]. The induction of ROS and subsequent cytokine cascade contributes to rapid neutrophil infiltration of the infarct region, with neutrophil levels peaking between 24 and 72 hours after MI [76, 79, 80].…”
Section: Fate Of Adults Stem Cells After MImentioning
confidence: 99%