Detail of "80663-95-2"

Reference

Kinetics of meta-[131I]-iodobenzylguanidine in normal subjects: compartmental analysis

Kinetics of meta-[131I]-iodobenzylguanidine in normal subjects: compartmental analysis. Chambon, C.; Baulieu, J. L.; Guilloteau, D.; Valat, C.; Baulieu, F.; Itti, R.; Besnard, J. C. (Tours, Fr.). J. Biophys. Med. Nucl., 8(2-3), 198-200 (French) 1984. CODEN: JBMND6. ISSN: 0243-3354. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 8 Pharmacokinetic anal. of 131I-labeled meta-iodobenzylguanidine [80663-95-2] in normal subjects showed that the drug is distributed in 32 compartments. Kinetic parameters are tabulated for each subject and each compartment. Urinary elimination of radioactivity was 62-76% of the injected dose within 72 h.

Detection of abnormal cardiac adrenergic neuron activity in adriamycin-induced cardiomyopathy with iodine-125-metaiodobenzylguanidine

Detection of abnormal cardiac adrenergic neuron activity in adriamycin-induced cardiomyopathy with iodine-125-metaiodobenzylguanidine. Wakasugi, Shigetoshi; Wada, Akira; Hasegawa, Yoshihisa; Nakano, Shunichi; Shibata, Nobuhiko (Div. Cardiol., Pathol. Nucl. Med., Cent. Adult Dis., Osaka, Japan). J. Nucl. Med., 33(2), 208-14 (English) 1992. CODEN: JNMEAQ. ISSN: 0161-5505. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 9, 14 Radiolabeled metaiodobenzylguanidine (MIBG), an analog of norepinephrine (NE), serves as an index of adrenergic neuron integrity and function. 23214-92-8 and 80663-95-2 which are cas registry numbers are also used here. Using rat model of adriamycin-induced cardiomyopathy, the authors tested the hypothesis that abnormal cardiac adrenergic neuron activity may appear and be exacerbated dose dependently in adriamycin cardiomyopathy. The degree of vacuolar degeneration of myocardial cells was analyzed in relation to the duration of adriamycin treatment (2 mg/kg, once a wk). There were no abnormalities or only isolated degeneration in the 1- or 2-wk treatment groups, isolated or scattered degeneration in half of the 3-wk group, frequent scattered degeneration in the 4-wk group, scattered or focal degeneration in the 5-wk group, and extensive degeneration in the 8-wk group. Myocardial accumulation of [125I]MIBG 4 h after i.v. injection did not differ between the controls and the group treated 3 wk or less. However, the 4-wk group had a slightly lower accumulation in the right ventricular wall (82% of the control) and significantly lower accumulation in the left ventricular. In the 5-wk group, MIBG accumulation in the right and left ventricular wall was 35% and 27% of that in controls, resp. (p < 0.001). In the 8-wk group, MIBG accumulation in the right and left ventricular wall was 18% and 14% of that in controls, resp. Thus, MIBG accumulation in the myocardium decreased in an adriamycin dose-dependent manner. The appearance of impaired cardiac adrenergic neuron activity in the presence of slight myocardial impairment (scattered or focal vacuolar degeneration) indicates that MIBG scintigraphy may be a useful method for detection of adriamycin-induced cardiomyopathy. .