Cyanide intoxication induced exocytotic epinephrine release in rabbit myocardium

Cyanide intoxication, which has been used as a model of energy depletion at cardiac sympathetic nerve terminals, causes non-exocytotic release of nore pinephrine (NE). However, the effect of cyanide intoxication on cardiac epi nephrine (Epi) release remains unknown. Using cardiac microdialysis in the rabbit, we measured dialysate Epi and NE concentrations as indices of myoca rdial interstitial Epi and NE levels, respectively. Local administration of sodium cyanide (30 mM) through the dialysis probe increased both Epi and N E levels (from 11.3+/-2.3 to 32.3+/-4.4 pg/ml and from 33.6+/-6.1 to 389.0/-71.8 pg/ml, respectively, mean+/-S.E., P<0.01). Local desipramine (100 mu M) administration suppressed the cyanide induced NE response without affec ting the Epi response. In contrast, local omega-conotoxin GVIA (10 mu M) ad ministration partially suppressed the cyanide induced NE response and total ly abolished the Epi response. In conclusion, cyanide intoxication causes N -type Ca2+ channel dependent exocytotic Epi release as well as inducing N-t ype Ca2+ channel independent non-exocytotic NE release. (C) 2000 Elsevier S cience B.V. All rights reserved.