Open AccessEffects of Ketamine on In Vivo Cardiac Sympathetic Nerve Endings
Author(s) -
Hirotoshi Kitagawa,
Toji Yamazaki,
Tsuyoshi Akiyama,
Hiromu Mori,
Kenji Sunagawa
Publication year - 2001
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200110001-00009
Subject(s) - ketamine , anesthesia , medicine , desipramine , occlusion , dialysis , cardiology , chemistry , antidepressant , hippocampus
Using the dialysis technique, we examined the effect of ketamine on dialysate norepinephrine (NE) levels in the myocardial interstitial space in anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and we measured the dialysate NE levels serving as an indicator of NE output at the cardiac sympathetic nerve endings. During local administration of ketamine (10 mM), we examined the time-course of the change in dialysate NE levels and the dialysate NE response to coronary occlusion. Dialysate NE levels significantly increased from 39+/-7 pg/ml at control to 133+/-22 pg/ml 30 min after beginning the ketamine administration. Addition of either omega-conotoxin GVIA (N-type calcium channel blocker) at 10 microg/kg intravenously or desipramine (neuronal NE transport blocker) at 100 microM did not inhibit the increment in dialysate NE evoked by ketamine. These findings suggest that the increase in dialysate NE evoked by ketamine is dependent neither on the activity of NE exocytosis nor on the neuronal NE transport. Left descending coronary artery occlusion evoked increments in dialysate NE. The addition of ketamine augmented the dialysate NE response to coronary occlusion. A ketamine-induced increment in dialysate NE might occur as a consequence of NE exocytosis independent or membrane NE transport insensitive efflux of NE.