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April 27, 2001Circulation Research

Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism

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Why the study?

Does diazoxide improve postischemic contractile function and alter ROS production in adult cardiomyocytes and perfused rat hearts?

Population

Adult cardiomyocytes and perfused rat hearts

Comparison

Diazoxide vs Untreated cells/hearts, N-acetylcysteine alone…

Design

Preclinical

Follow-up

20 minutes of global ischemia and 20 minutes of reflow

Authors

RFRobert A. ForbesOtsuka (United States)CSCharles SteenbergenCross-Cutting CardiologyEMElizabeth MurphyCross-Cutting Cardiology

Discussion

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Member takes

Overview

Diazoxide may precondition isolated rat hearts via ROS; leaves open clinical translation for ischemia-reperfusion injury.

Structured PICO

Does diazoxide improve postischemic contractile function and alter ROS production in adult cardiomyocytes and perfused rat hearts?

P
Population
Adult cardiomyocytes and perfused rat hearts
I
Intervention
Diazoxide (50 micromol/L in cells, 100 micromol/L in perfused hearts before ischemia)
C
Comparator
Untreated cells/hearts, N-acetylcysteine (NAC) alone, or diazoxide + NAC
O
Outcome
Reactive oxygen species (ROS) production in cells and postischemic contractile function (left ventricular developed pressure) in perfused heartssurrogate

Diazoxide-induced cardioprotection against ischemia-reperfusion injury is mediated by the generation of a pro-oxidant environment via reactive oxygen species signaling.

Cite This Study

Forbes et al. (2001) studied this question.

synapsesocial.com/papers/6a7fb58ca3d55be9ef9fe8a5https://doi.org/10.1161/hh0801.089342
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