Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD)

Abstract

Histamine has inotropic, chronotropic, arrhythmogenic, and vasoactive effects, and is released from the heart in ischaemia-reperfusion injury. The effect of ventricular fibrillation (VF) and defibrillation (DEF) on histamine release was investigated in 9 anaesthetized patients undergoing transvenous implantation of ICD. Concomitant arterial and coronary sinus (CS) blood samples were drawn before induction of VF (duration 20 seconds), immediately after, and 2 and 5 min after DEF (18-24 Joules). Basal arterial histamine was 2.5 +/- 6 nmol/l, and did not increase after VF. The histamine level in CS was 1.1 +/- 0.2 nmol/l before VF (p < 0.008 compared to arterial), and increased to 2.5 +/- 0.6 nmol/l immediately after (p < 0.045 compared to basal), to 3 +/- 1.1 nmol/l 2 min after (p < 0.45), and to 2.4 +/- 0.8 nmol/l 5 min after VF. In the basal state there was an uptake of histamine across the coronary circulation. After VF/DEF the level of histamine increased in coronary venous blood, suggesting cardiac release of histamine.

Endothelin-1 induces organ-specific histamine liberation and neutrophil granulocyte accumulation in the rat

“…In addition, there are some data which suggest that cardiac histamine might be released from non-MC stores, too. Early studies of Valen et al showed that ischemia causes a sustained increase in cardiac histamine content [28,29], and similarly, Dai et al demonstrated an increase in histamine content in the right ventricle with unchanged cardiac MC numbers during acute myocardial ischaemia [30]. These results may indicate that non-MC sources are also involved in cardiac histamine liberation.…”