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Published on: September 18, 2017
Sodium overload during postnatal phases impairs diastolic function and exacerbates reperfusion arrhythmias in adult
Marina Conceição Dos Santos Moreira1, Allancer Divino de Carvalho Nunes2, Paulo Ricardo Lopes3
1Department of Academic Areas, Federal Institute of Education, Science, and Technology of Goiás, Formosa, Brazil.
Insights
Childhood sodium overload harms adult heart function, increasing risks during reperfusion events. This high-salt diet exposure during development leads to impaired relaxation and more severe arrhythmias.
Area of Science:
- Cardiovascular Physiology
- Developmental Toxicology
- Cardiac Electrophysiology
Background:
- Childhood sodium overload is known to impair baroreflex sensitivity and elevate blood pressure and heart rate in adulthood, with lasting effects.
- Existing research has not fully detailed the impact of high-salt diet (HSD) exposure during postnatal development on adult cardiac ischemia/reperfusion (I/R) responses.
Purpose of the Study:
- To investigate the long-term effects of HSD during infancy and adolescence on isolated heart function and cardiac I/R responses in adult rats.
- To determine if HSD in early life compromises the heart's ability to recover from ischemic events later in life.
Main Methods:
- Male Wistar rats (21 days old) were fed a high-salt diet (0.3M NaCl) or tap water for 60 days.
- Following the treatment period, both groups were switched to a normal sodium diet for 30 days.
- Isolated hearts were perfused using the Langendorff technique and subjected to 20 minutes of anoxia followed by 20 minutes of reperfusion.
Main Results:
- High-salt diet (HSD) did not affect basal contractile function of the isolated hearts.
- However, HSD significantly elevated left ventricular end-diastolic pressure during reperfusion (23.1 ± 5.2 mmHg vs. 11.6 ± 1.4 mmHg, p < 0.05).
- The incidence of ectopic beats during reperfusion was significantly increased in the HSD group (208.8 ± 32.9s vs. 75.0 ± 7.8s, p < 0.05).
Conclusions:
- Postnatal sodium overload adversely affects cardiac function following reperfusion injury in adulthood.
- HSD during development diminishes ventricular relaxation and exacerbates arrhythmias during reperfusion.
- These findings suggest a potential arrhythmogenic effect of early-life high-salt diet exposure.
Abstract:
Sodium overload during childhood impairs baroreflex sensitivity and increases arterial blood pressure and heart rate in adulthood; these effects persist even after high-salt diet (HSD) withdrawal. However, the literature lacks details on the effects of HSD during postnatal phases on cardiac ischemia/reperfusion responses in adulthood. The current study aimed to elucidate the impact of HSD during infancy adolescence on isolated heart function and cardiac ischemia/reperfusion responses in adulthood. Male 21-day-old Wistar rats were treated for 60 days with hypertonic saline solution (NaCl; 0.3M; experimental group) or tap water (control group). Subsequently, both groups were maintained on a normal sodium diet for 30 days. Subsequently, the rats were euthanized, and their hearts were isolated and perfused according to the Langendorff technique. After 30 min of the basal period, the hearts were subjected to 20 min of anoxia, followed by 20 min of reperfusion. The basal contractile function was unaffected by HSD. However, HSD elevated the left ventricular end-diastolic pressure during reperfusion (23.1 ± 5.2 mmHg vs. 11.6 ± 1.4 mmHg; p < 0.05) and increased ectopic incidence period during reperfusion (208.8 ± 32.9s vs. 75.0 ± 7.8s; p < 0.05). In conclusion, sodium overload compromises cardiac function after reperfusion events, diminishes ventricular relaxation, and increases the severity of arrhythmias, suggesting a possible arrhythmogenic effect of HSD in the postnatal phases.
