OBJECTIVES: Arrhythmias, including ventricular fibrillation (VF), occur in two phases after coronary obstruction, the first during the reversible stage of acute myocardial ischaemia (phase 1) and the second during evolution of the infarct (phase 2). We tested the hypothesis that phase 2 arrhythmias are mediated by actions of neutrophils accumulating within the infarct. METHODS: Male rats (n=10 per group) were randomized to receive 2 ml/kg i.p. of either rabbit anti-rat neutrophil anti-serum or normal rabbit serum. After 17 h, single stage left coronary artery ligation was performed under pentobarbitone anaesthesia, and ischaemia was maintained for 240 min. RESULTS: Anti-serum pretreatment caused almost total neutropenia, reducing neutrophils in circulating blood from 2096+/-274x10(3) to 8+/-8x10(3) per ml (p<0.05). It also blocked neutrophil accumulation in the infarct, reducing cardiac myeloperoxidase activity from 74.7+/-27.4 to 9+/-3 mU per mg protein (p<0.05). Despite this, there was no significant difference between control and anti-serum-treated rats in the incidence of phase 2 VF (30% in each group) tachycardia (VT; 60% vs 80%) or number of ventricular premature beats (VPBs). CONCLUSION: Neutrophil accumulation within the evolving myocardial infarct does not mediate phase 2 VF.
OBJECTIVES:Arrhythmias, including ventricular fibrillation (VF), occur in two phases after coronary obstruction, the first during the reversible stage of acute myocardial ischaemia (phase 1) and the second during evolution of the infarct (phase 2). We tested the hypothesis that phase 2 arrhythmias are mediated by actions of neutrophils accumulating within the infarct. METHODS: Male rats (n=10 per group) were randomized to receive 2 ml/kg i.p. of either rabbit anti-rat neutrophil anti-serum or normal rabbit serum. After 17 h, single stage left coronary artery ligation was performed under pentobarbitone anaesthesia, and ischaemia was maintained for 240 min. RESULTS: Anti-serum pretreatment caused almost total neutropenia, reducing neutrophils in circulating blood from 2096+/-274x10(3) to 8+/-8x10(3) per ml (p<0.05). It also blocked neutrophil accumulation in the infarct, reducing cardiac myeloperoxidase activity from 74.7+/-27.4 to 9+/-3 mU per mg protein (p<0.05). Despite this, there was no significant difference between control and anti-serum-treated rats in the incidence of phase 2 VF (30% in each group) tachycardia (VT; 60% vs 80%) or number of ventricular premature beats (VPBs). CONCLUSION: Neutrophil accumulation within the evolving myocardial infarct does not mediate phase 2 VF.
Authors: Aiilyan K Houng; Rachel A McNamee; Attila Kerner; Pallavi Sharma; Almois Mohamad; Jonathan Tronolone; Guy L Reed Journal: Am J Physiol Heart Circ Physiol Date: 2009-01-02 Impact factor: 4.733