Abstract

In vivo measurements of gadodiamide (Gd-DTPA-BMA) T(1) relaxivity were performed at 4.7 T in injured and normal rat brains. Cerebral lesions were induced in nine rats by a localized freezing method. T(1) maps of the lesions were generated before and after injection of Gd-DTPA-BMA (0.1-0.6 mmol/kg). Samples of normal and necrotic brain were collected postmortem; the wet and dry weights were determined, and Gd content was measured by inductively coupled plasma mass spectroscopy. The in vivo relaxivity was determined by a linear fit of a plot of the change in relaxation rate following injection of the contrast agent as a function of Gd content. This analysis yielded a relaxivity in the injured brain of 2.8 sec(-1) mmol(-1) kg tissue water at 36 degrees C. The water weight fraction was 0.90 +/- SD 0.02 wt/wt in injured brain and 0.79 +/- 0.02 in normal brain. Relaxivity measurements were also performed on solutions of Gd-DTPA-BMA (0.0-0.6 mmol) and albumin (0-30% wt/wt) in normal saline at room and physiologic temperatures. The relaxivity in the albumin/saline increased with increasing solids content with values of 4.0-4.9 sec(-1) mmol(-1)kg at 21 degrees C and 3.4-4.5 sec(-1) mmol(-1) kg at 37 degrees C. The relaxivity of the tissues differed significantly from that of the saline solutions of comparable solids content, suggesting that the solids content of a tissue is not the only factor that determines in vivo relaxivity.

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