What question did this study set out to answer?

This study investigates the protective effects of cilazaprilat on rat cardiac myocytes during hypoxia/reoxygenation injury.

February 16, 1999CirculationOpen Access

Cardioprotective Effect of Angiotensin-Converting Enzyme Inhibition Against Hypoxia/Reoxygenation Injury in Cultured Rat Cardiac Myocytes

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Why the study?

Does cilazaprilat protect cultured neonatal rat cardiac myocytes against hypoxia/reoxygenation injury?

Population

Neonatal rat cardiac myocytes in primary culture exposed to hypoxia for 5.5 hours and subsequently…

Comparison

Cilazaprilat (ACE inhibitor) vs Untreated control, CV-11974, angiotensin II, and…

Design

Preclinical

Follow-up

6.5 hours (5.5 hours hypoxia + 1 hour reoxygenation)

Authors

SMSatoaki MatobaHeart Failure & Transplant TTTetsuya TatsumiNantan General Hospital NKNatsuya KeiraNantan General Hospital

Discussion

Member takes

Implication

Does not support clinical use; extends preclinical evidence for bradykinin-NO pathways in myocyte protection.

Key Points

This study investigates the protective effects of cilazaprilat on rat cardiac myocytes during hypoxia/reoxygenation injury.
Cilazaprilat and bradykinin were tested for their effects on CK release in cultured rat cardiac myocytes exposed to hypoxia/reoxygenation.
Inhibition substances such as Hoe 140, L-NMMA, and methylene blue were used to discern mechanisms of protection.
CGMP levels and bradykinin production during hypoxia were measured in cultured myocytes.
Cilazaprilat reduced CK release by 50% in response to hypoxia/reoxygenation, indicating significant protection.
Bradykinin production was enhanced in myocytes following cilazaprilat treatment after hypoxia.
Inhibition of NO synthase and guanylate cyclase reduced the protective effects of cilazaprilat, suggesting an NO and cGMP pathway involvement.

Structured PICO

Does cilazaprilat protect cultured neonatal rat cardiac myocytes against hypoxia/reoxygenation injury?

Population

Neonatal rat cardiac myocytes in primary culture exposed to hypoxia for 5.5 hours and subsequently reoxygenated for 1 hour

Intervention

Cilazaprilat (ACE inhibitor)

Comparator

Untreated control, CV-11974 (angiotensin II receptor antagonist), angiotensin II, and various pathway inhibitors (Hoe 140, L-NMMA, methylene blue, staurosporine, aminoguanidine, indomethacin)

Outcome

Myocyte injury determined by the release of creatine kinase (CK) and preservation of myocyte ATP contentsurrogate

Cilazaprilat directly protects cultured cardiac myocytes against hypoxia/reoxygenation injury via bradykinin accumulation and subsequent NO/cGMP pathway activation.

Cite This Study

Matoba et al. (1999) studied this question.

synapsesocial.com/papers/6a77c27d137c7dcc81be0bd4 https://doi.org/10.1161/01.cir.99.6.817

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Cardioprotective Effect of Angiotensin-Converting Enzyme Inhibition Against Hypoxia/Reoxygenation Injury in Cultured Rat Cardiac Myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Cardioprotective Effect of Angiotensin-Converting Enzyme Inhibition Against Hypoxia/Reoxygenation Injury in Cultured Rat Cardiac Myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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