Key result
Oral administration of sodium thiosulfate improved ejection fraction from 51.0% to 60.9% and ameliorated hypertension, left ventricular hypertrophy, and cardiac fibrosis in a rat model of heart disease.
Why the study?
Despite existing antihypertensive therapies, some patients still develop heart failure, necessitating novel cardioprotective approaches.
Does oral sodium thiosulfate improve cardiac dysfunction and remodeling in a rat model of L-NNA-induced hypertension?
Does oral sodium thiosulfate improve cardiac dysfunction and remodeling in a rat model of L-NNA-induced hypertension?
Absolute Event Rate: 60.9% vs 51%
p-value: p=<0.05
Oral sodium thiosulfate provides cardioprotective effects comparable to ACE inhibition in a rat model of NO-deficient hypertension, without causing metabolic acidosis.
Hypothesis-generating in this rat model; leaves open translation of oral sodium thiosulfate to human hypertensive heart disease.
Hypertension contributes to cardiac damage and remodeling. Despite the availability of renin-angiotensin system inhibitors and other antihypertensive therapies, some patients still develop heart failure. Novel therapeutic approaches are required that are effective and without major adverse effects. Sodium Thiosulfate (STS), a reversible oxidation product of hydrogen sulfide (H 2 S), is a promising pharmacological entity with vasodilator and anti-oxidant potential that is clinically approved for the treatment of calciphylaxis and cyanide poisoning. We hypothesized that Sodium Thiosulfate improves cardiac disease in an experimental hypertension model and sought to investigate its cardioprotective effects by direct comparison to the ACE-inhibitor lisinopril, alone and in combination, using a rat model of chronic nitric oxide (NO) deficiency. Systemic nitric oxide production was inhibited in Sprague Dawley rats by administering N-ω-nitro- l -arginine (L-NNA) with the food for three weeks, leading to progressive hypertension, cardiac dysfunction and remodeling. We observed that STS, orally administered via the drinking water, ameliorated L-NNA-induced heart disease. Treatment with STS for two weeks ameliorated hypertension and improved systolic function, left ventricular hypertrophy, cardiac fibrosis and oxidative stress, without causing metabolic acidosis as is sometimes observed following parenteral administration of this drug. STS and lisinopril had similar protective effects that were not additive when combined. Our findings indicate that oral intervention with a H 2 S donor such as STS has cardioprotective properties without noticeable side effects.
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Nguyen et al. (2021) studied L-NNA-Induced Heart Disease (Hypertension) (n=25). Sodium Thiosulfate (STS) vs. L-NNA only (control) was evaluated on Ejection fraction (p=<0.05). Oral administration of sodium thiosulfate improved ejection fraction from 51.0% to 60.9% and ameliorated hypertension, left ventricular hypertrophy, and cardiac fibrosis in a rat model of heart disease.
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