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AIM: The present study was designed to test a hypothesis that nonfatal ventricular arrhythmia such as ventricularpremature beats (VPB) is a contributing factor in the elevation of blood pressure variability (BPV). METHODS:Blood pressure (BP) and electrocardiogram were continuously recorded. The relation between VPB and BPV wasobserved under conscious state in chronic myocardial infarction (MI) rats one month after ligation of the leftcoronary artery, and further verified under anesthetized state in rat model of ventricular arrhythmia produced byacute intravenous infusion of aconitine. RESULTS: MI rats exhibited a big difference in the count and pattern ofVPB, and were divided into no VPB, occasional VPB, and frequent VPB groups. Among the three groups, therewere no differences in BP, heart period (HP), and MI size. However, BPV was markedly higher in frequent notoccasional VPB rats, and HP variability (HPV) was larger in both frequent and occasional VPB rats, when comparedwith no VPB rats. In the whole population of MI rats, BPV was positively correlated with VPB and HPV, not withBP, HP and MI size. Infusion of aconitine had no effect on BP, HP, BPV, and HPV during the period without VPB.Frequent VPB after several minutes of aconitine infusion induced significant increase in BPV and HPV with nochange in BP and HP. BPV was also positively correlated with VPB and HPV, not with BP and HP. Hemodynamicsin aconitine-evoked ventricular tachycardia was characterized as lower BP, higher BPV, and higher HPV.CONCLUSION: High BPV can be caused by frequent not occasional VPB in rats.
AIM: The present study was designed to test a hypothesis that nonfatal ventricular arrhythmia such as ventricular premature beats (VPB) is a contributing factor in the elevation of blood pressure variability (BPV). METHODS: Blood pressure (BP) and electrocardiogram were continuously recorded. The relation between VPB and BPV wasobserved under conscious state in chronic myocardial infarction (MI) rats one month after ligation of the left coronary artery, and further verified under anesthetized state in rat model of ventricular arrhythmia produced by intravenous infusion of aconitine. RESULTS: MI rats Among the three groups, therewere no differences in BP, heart period (HP), and MI size. However, BPV was markedly higher in frequent notoccasional VPB rats, and HP variability (HPV) was larger in both frequent and occasional VPB rats, when compared with no VPB rats. In the whole population of MI rats, BPV was positively correlated with VPB and HPV, not with BP, HP and MI size. Infusion of aconitine had no effect on BP, HP, BPV, and HPV during the period without VPB.Frequent VPB after several minutes of aconitine infusion induced significant increase in BPV and HPV with nochange in BP and HP. BPV was also positively associated with VPB and HPV, not with BP and HP. Hemodynamicsin aconitine-evoked ventricular tachycardia was characterized as lower BP, higher BPV, and higher HPV. CONCLUSION: High BPV can be caused by frequent not occasional VPB in rats.