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Spontaneously hypertensive rats (SHR) with ventricular hypertrophy show an increased vulnerability for the development of potentially lethal ventricular arrhythmias such as ventricular fibrillation (VF). The mechanisms of this increased vulnerability are not fully understood but may be related to abnormal intracellular Ca2+ (Ca2+i) handling under stress conditions. We therefore investigated whether Ca2+i handling is abnormal in hypertrophied hearts of SHR without heart failure during stimulation stress, and if so whether abnormal Ca2+i handling is a determinant of the increased vulnerability to VF in SHR. Ca2+i was measured by indo-1 surface fluorescence in perfused hearts of 8- to 10-month-old control Wistar-Kyoto rats (WKY) and age-matched SHR. The state of Ca2+i handling was analyzed during three different forms of stimulation stress: rapid pacing, the long rest period after cessation of rapid pacing, and preprogrammed ventricular stimulation that was simultaneously used for the determination of VF threshold. The pulse number VF threshold was used as an index to determine vulnerability to VF and to analyze the relationship of Ca2+i handling to vulnerability. Although VF thresholds were lower in SHR than in WKY, we found that both demonstrated similar Ca2+i handling during stimulation stress. The extent and rate of Ca2+i accumulation during rapid pacing and those of the Ca2+i decline after cessation of pacing were similar in SHR and WKY. In addition, the relationship between Ca2+i and VF threshold was unaltered in SHR. Thus, we conclude that Ca2+i handling is normal in hypertrophied hearts of SHR without heart failure during stimulation stress and that it is not a determinant of the increased vulnerability to VF in SHR.
Zaugg et al. (Mon,) studied this question.