RT Journal Article
SR Electronic
T1 Tyramine neurotoxicity and first-pass brain technetium-99m-diethylenetriamine penta-acetic acid.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 42
OP 47
VO 241
IS 1
A1 Faraj, B A
A1 Schmidt, F H
A1 Sarper, R
A1 Camp, V M
A1 Malveaux, E
YR 1987
UL http://jpet.aspetjournals.org/content/241/1/42.abstract
AB Tyramine induces coma in phenelzine-treated dogs with liver disease. The objective of the present investigation was to examine the influence of tyramine in these monoamine oxidase-inhibited dogs on the kinetics of Tc-99m-diethylenetriamine penta-acetic acid (Tc-99m-DTPA) during its first passage through the brain by nuclear imaging techniques. The study began with anesthetized mongrel dogs (n = 10) in a supine position over the camera detector. Data acquisition was started simultaneously after the rapid intracarotid injection of Tc-99m-DTPA (5 mCi) and 60 0.5-sec images of the brain were taken. Tyramine induced increased uptake with a concomitant impairment in the elimination of Tc-99m-DTPA from the brain of these phenelzine-treated animals with hepatic injury (n = 5) as compared to pretreated animals serving as a control group or phenelzine-treated animals without liver disease. This was accompanied by an appreciable reduction in hemispheric cerebral blood flow (50.5 +/- 19.3 vs. 110 +/- 16 ml/100 g/min), respectively. Increased cerebrovascular permeability of Tc-99m-DTPA and decreased cerebral blood flow occurred concomitantly with increased cerebrospinal fluid pressure and elevation in cerebrospinal fluid catecholamines of monoamine oxidase-inhibited animals with hepatic injury.