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Myocardial function and effect of serum in isolated heart from hypertriglyceridemic and hypertensive rats
Karla Carvajal1, Guadalupe Baños
1Department of Biochemistry, Instituto Nacional de Cardiología Ignacio Chávez, México, DF, Mexico. karla_ca@yahoo.com
Insights
Hypertriglyceridemia in rats impairs heart function and electrical conduction. It also worsens heart injury after ischemia-reperfusion, with serum containing factors affecting heart performance.
Area of Science:
- Cardiovascular Physiology
- Metabolic Disorders
Background:
- Hypertriglyceridemia (HTG) and hypertension are common metabolic conditions.
- Their combined effect on myocardial function requires further investigation.
Purpose of the Study:
- To evaluate myocardial function in rats with sugar-induced HTG and hypertension.
- To assess the impact of HTG serum on isolated heart performance.
- To investigate the response to ischemia-reperfusion injury in HTG hearts.
Main Methods:
- Isolated heart preparation from control rats (CR) and HTG rats.
- Measurement of ventricular pressure (VP) and perfusion pressure.
- Assessment of cardiac electrical conduction and response to global ischemia (30 minutes) and reperfusion.
Main Results:
- HTG rat hearts exhibited lower VP and faster conduction rates compared to CR.
- Recovery of VP after ischemia was significantly reduced in HTG hearts.
- HTG serum caused increased VP and perfusion pressure.
- Reperfusion led to higher incidence of arrhythmias (premature beats, ventricular fibrillation, tachycardia) in HTG hearts.
- A circulating factor in HTG serum induced a vasoactive response.
Conclusions:
- Hypertriglyceridemia induces significant alterations in myocardial mechanical and electrical properties.
- HTG exacerbates myocardial injury following ischemia-reperfusion.
- Serum from HTG rats contains a factor that negatively impacts cardiac performance and vasculature.
Abstract:
We evaluated the myocardial function of rats with sugar-induced hypertriglyceridemia (HTG) and hypertension, and the effect of serum on myocardial performance in the isolated heart preparation. Also, the response to reperfusion after 30 minutes of global ischemia was investigated. Hearts from HTG rats developed lower ventricular pressure (VP) and the conduction rate was higher than in hearts from control rats (CR). The recovery of VP after ischemia was significantly lower in HTG than in CR hearts (p < 0.05). The HTG sera produced a higher increase in the VP and in the perfusion pressure. During reperfusion, the incidence of premature beats, ventricular fibrillation and tachycardia in HTG hearts was increased so hypertriglyceridemia caused alterations in the mechanical and electrical conduction of the myocardium and exacerbated the injury produced by ischemia-reperfusion. Also a circulating factor in the HTG serum induced a vasoactive response of the heart which was reflected in its mechanical performance.