April 8, 2004AJP Heart and Circulatory Physiology

Increases in brain and cardiac AT₁ receptor and ACE densities after myocardial infarct in rats

Q: What is the clinical evidence from this study?

Population: Myocardial infarction. Intervention: Intracerebroventricular infusion of Fab fragments to block brain OLC vs. Untreated post-MI rats. Primary outcome: ACE and AT1 receptor binding densities in brain, heart, and kidneys.

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Key result

Intracerebroventricular infusion of Fab fragments to block brain OLC markedly inhibited the post-MI increases in ACE and AT1 receptors in the brain and heart of rats.

Why the study?

Does intracerebroventricular infusion of Fab fragments reduce brain and cardiac ACE and AT1 receptor densities in rats after myocardial infarction?

Population

Rats after myocardial infarction (MI)

Design

Preclinical

Follow-up

8 weeks

Authors

JTJunhui TanChangi General Hospital HWHao WangJiangsu University FLFrans H. H. LeenenPreventive Cardiology

Discussion

Member takes

Implication

Brain OLC blockade attenuates post-MI RAS upregulation in rats; hypothesis-generating for central RAS targeting in human HF.

Structured PICO

Does intracerebroventricular infusion of Fab fragments reduce brain and cardiac ACE and AT1 receptor densities in rats after myocardial infarction?

Population

Rats evaluated 4 and 8 weeks after myocardial infarction to determine changes in ACE and AT1 receptor binding densities.

Intervention

Intracerebroventricular infusion of Fab fragments to block brain ouabain-like compounds (OLC) from 0.5 to 4 weeks after MI

Outcome

Angiotensin-converting enzyme (ACE) and angiotensin type 1 (AT1) receptor binding densities measured by 125I-labeled 351A and 125I-labeled ANG II binding at 4 and 8 weeks after MIsurrogate

Brain ouabain-like compounds play a major role in activating the brain and cardiac renin-angiotensin systems in rats after myocardial infarction.

Cite This Study

Tan et al. (2004) studied Myocardial infarction. Intracerebroventricular infusion of Fab fragments to block brain OLC vs. Untreated post-MI rats was evaluated on ACE and AT1 receptor binding densities in brain, heart, and kidneys. Intracerebroventricular infusion of Fab fragments to block brain OLC markedly inhibited the post-MI increases in ACE and AT1 receptors in the brain and heart of rats.

synapsesocial.com/papers/6a23878d412756072fa5dfd7 https://doi.org/10.1152/ajpheart.00858.2003

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Increases in brain and cardiac AT₁ receptor and ACE densities after myocardial infarct in rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Increases in brain and cardiac AT₁ receptor and ACE densities after myocardial infarct in rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider