September 1, 2001AJP Heart and Circulatory Physiology

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of α-fodrin

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Population

30 excised cross-circulated rat heart preparations

Design

Preclinical

Authors

TTTsuyoshi TsujiTokyo Medical and Dental University YOYoshimi OhgaOkayama University YYYoshiro YoshikawaUniversity of the Ryukyus

Discussion

Member takes

Implication

Calpain inhibition mitigates Ca2+-induced failure in animal tissue; hypothesis-generating and requires in vivo validation before clinical consideration.

Structured PICO

Population

30 excised cross-circulated rat heart preparations

Intervention

Exposure to high Ca2+ with or without a calpain inhibitor

Outcome

Contractile dysfunction, myocardial O2 consumption, and alpha-fodrin proteolysissurrogate

Ca2+ overload induces cardiac contractile dysfunction through calpain-mediated degradation of alpha-fodrin, suggesting a potential therapeutic target for preventing contractile failure.

Cite This Study

Tsuji et al. (2001) studied this question.

synapsesocial.com/papers/6a8799d286c445008eca814b https://doi.org/10.1152/ajpheart.2001.281.3.h1286

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Implication

Calpain inhibition mitigates Ca2+-induced failure in animal tissue; hypothesis-generating and requires in vivo validation before clinical consideration.

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of α-fodrin

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of α-fodrin

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider