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Title: Modeling sickle cell vasoocculsion in the rat leg: Quantification of trapped sickle cells and correlation with sup 31 P metabolic and sup 1 H magnetic resonance imaging changes

Journal Article · · Proceedings of the National Academy of Sciences of the United States of America; (USA)
; ; ; ; ; ;  [1]
  1. Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY (USA)

The authors have developed an animal model to elucidate the acute effects of perfusion abnormalities on muscle metabolism induced by different density-defined classes of erythrocytes isolated from sickle cell anemia patients. Technetium-99m ({sup 99m}Tc)-labeled, saline-washed normal (AA), homozygous sickle (SS), or high-density SS (SS4) erythrocytes were injected into the femoral artery of the rat and quantitative {sup 99m}Tc imaging, {sup 31}P magnetic resonance spectroscopy by surface coil at 2 teslas, and {sup 1}H magnetic resonance imaging at 0.15 tesla were performed. Between 5 and 25 {mu}l of SS4 cells was trapped in the microcirculation of the thigh. In contrast, fewer SS discocytes (SS2) or AA cells were trapped. After injection of SS4 cells an initial increase in inorganic phosphate was observed in the region of the thigh served by the femoral artery, intracellular pH decreased, and subsequently the proton relaxation time T{sub 1} reached a broad maximum at 18-28 hr. When T{sub 1} obtained at this time was plotted against the volume of cells trapped, an increase of T{sub 1} over the control value of 411 {plus minus} 48 msec was found that was proportional to the number of cells trapped. They conclude that the densest SS cells are most effective at producing vasoocclusion. The extent of the change detected by {sup 1}H magnetic resonance imaging is dependent on the amount of cells trapped in the microcirculation and the magnitude of the initial increase of inorganic phosphate.

OSTI ID:
5299064
Journal Information:
Proceedings of the National Academy of Sciences of the United States of America; (USA), Vol. 86:10; ISSN 0027-8424
Country of Publication:
United States
Language:
English

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