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Published on: February 17, 2018
Chronic administration of carvedilol improves cardiac function in 6-month-old Syrian cardiomyopathic hamsters
Nildris Cruz1, Luz Arocho, Luis Rosario
1Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, P.R., USA.
Insights
Carvedilol improved cardiac function in older cardiomyopathic hamsters by reducing blood pressure and peripheral resistance, but did not prevent ventricular dilation. This suggests vasodilation, not sympathetic overactivation, drives improved heart function in this model.
Area of Science:
- Cardiology
- Pharmacology
- Animal Models
Background:
- Heart failure (HF) is a progressive condition linked to renin-angiotensin and sympathetic system activation.
- Beta-blockers show promise in HF treatment, but mechanisms require clarification.
- Carvedilol's cardiovascular effects in cardiomyopathic hamsters are evaluated.
Purpose of the Study:
- To assess the impact of carvedilol on cardiovascular function in young and aged cardiomyopathic hamsters (SCH).
- To investigate the mechanisms behind carvedilol's effects on heart failure progression.
Main Methods:
- Carvedilol (1 mg/kg/day) administered to 2- and 6-month-old SCH hamsters.
- Treatment durations of 1 month (young) and 5 months (aged).
- Evaluated systolic blood pressure (SBP) and echocardiographic parameters (LVESV, LVEDV, EF, COI, HR, LVPWT).
Main Results:
- In 2-month-old SCH, carvedilol reduced SBP but did not alter cardiac parameters.
- In 6-month-old SCH, carvedilol decreased SBP, HR, and LVESV, while increasing EF and COI.
- Carvedilol did not affect LVEDV or LVPWT, indicating no prevention of ventricular dilatation.
Conclusions:
- Carvedilol significantly enhances cardiac function in aged cardiomyopathic hamsters.
- Improved function is linked to reduced peripheral resistance via carvedilol's vasodilator properties.
- Sympathetic overactivation is unlikely to be the primary cause of dilated cardiomyopathy in this model.
Abstract:
Heart failure (HF) is a multifactorial and progressive disease that has been linked to activation of the renin-angiotensin and sympathetic systems. In recent years, beta-blockers have been shown to improve the status of HF patients, although the precise mechanisms remain unclear. The present study evaluates the effect of beta-blockade with carvedilol (1 mg/kg/day) on cardiovascular function in 2- and 6-month-old cardiomyopathic hamsters (SCH) after 1-month and 5-month treatment periods with the drug, respectively. Age-matched golden hamsters were used as controls (CT). Systolic blood pressure (SBP) and echocardiographic studies were evaluated. The latter studies included left ventricular end-systolic (LVESV) and end-diastolic (LVEDV) volumes, ejection fraction (EF), cardiac output index (COI), heart rate (HR), and left ventricular posterior wall thickness (LVPWT). In 2-month-old SCH, carvedilol administration during a 1-month period reduced SBP from 107.59 +/- 3.49 to 77.26 +/- 3.49 mm Hg (n = 5, p < 0.05). At this stage, cardiac parameters in SCH were similar to those of controls and were not affected by carvedilol administration. In 6-month-old SCH, 5-month administration of carvedilol decreased SBP from 102.16 +/- 3.61 to 90.60 +/- 2.80 mm Hg (n = 5, p < 0.05), HR from 363 +/- 14 to 324 +/- 14 bpm (n = 5, p < 0.05), and LVESV from 0.18 +/- 0.01 to 0.13 +/- 0.01 ml/100 g BW (n = 5, p < 0.05), and increased EF and COI by 14 and 23%, respectively (n = 5, p < 0.05). The drug did not modify LVEDV or LVPWT. These results reveal that carvedilol significantly improves cardiac function in 6-month-old cardiomyopathic hamsters, but it does not prevent ventricular dilatation. Improved cardiac function appears to be secondary to decreased total peripheral resistance, due mainly to the vasodilator properties of the drug. Thus, overactivation of the sympathetic system is not likely to be a determining factor in the etiology of dilated cardiomyopathy in this animal model.
