What question did this study set out to answer?

This study explores whether increased Na+/H+-exchanger activity leads to elevated cytosolic sodium and impaired calcium handling in heart failure.

March 15, 2003Cardiovascular ResearchOpen Access

Increased Na+/H+-exchange activity is the cause of increased Na+i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model

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Why the study?

Does NHE inhibition with cariporide improve cytosolic sodium and calcium handling in a rabbit model of heart failure?

Population

Isolated left ventricular midmural myocytes from rabbits with heart failure induced by combined volume and…

Comparison

Cariporide to inhibit Na+/H+-exchanger, and… vs Age-matched control animals and untreated heart…

Design

Preclinical

Authors

ABAntonius BaartscheerOslo University Hospital

Discussion

Member takes

Implication

NHE inhibition should not yet change practice; leaves open therapeutic potential in clinical heart failure trials.

Key Points

This study explores whether increased Na+/H+-exchanger activity leads to elevated cytosolic sodium and impaired calcium handling in heart failure.
Heart failure induced in rabbits by volume and pressure overload.
Measurement of cytosolic sodium, calcium, and pH in isolated left ventricular myocytes.
Use of inhibitors cariporide and ouabain to assess sodium influx and calcium handling.
[Na+]i and diastolic [Ca2+]i significantly higher in heart failure than control.
Specific inhibition of NHE with cariporide normalized [Na+]i and [Ca2+]i, improving calcium handling.
Increased [Na+]i in control myocytes with ouabain led to calcium handling abnormalities similar to heart failure.

Structured PICO

Does NHE inhibition with cariporide improve cytosolic sodium and calcium handling in a rabbit model of heart failure?

Population

Isolated left ventricular midmural myocytes from rabbits with heart failure induced by combined volume and pressure overload, and age-matched controls.

Intervention

Cariporide (10 micromol/l for 5 min) to inhibit Na+/H+-exchanger (NHE), and ouabain (100 micromol/l) to inhibit Na+/K+-ATPase.

Comparator

Age-matched control animals and untreated heart failure myocytes.

Outcome

Cytosolic sodium ([Na+]i), cytosolic calcium ([Ca2+]i), and cytosolic pH (pHi) handling.surrogate

NHE inhibition with cariporide normalizes cytosolic sodium and calcium handling in a rabbit model of heart failure, suggesting a potential therapeutic target for developing hypertrophy and heart failure.

Cite This Study

Antonius Baartscheer (2003) studied this question.

synapsesocial.com/papers/6a227fe3ffccceb004b7321d https://doi.org/10.1016/s0008-6363(02)00809-x

Topics

Heart failure HFrEF treatment

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Increased Na+/H+-exchange activity is the cause of increased Na+i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Increased Na+/H+-exchange activity is the cause of increased Na+i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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