March 1, 1992AJP Heart and Circulatory Physiology

EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle

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Why the study?

Does EDRF blockade with hydroquinone prevent sepsis-induced arteriole dilation in skeletal muscle in rats?

Population

Rats with high cardiac output bacteremia and low cardiac output live Escherichia coli sepsis

Comparison

Local chemical blockade of EDRF by hydroquinone vs Unblocked state (implied)

Design

Preclinical

Authors

ALA.S. LübbeUniversity of the Witwatersrand RGR. Neal GarrisonUnited States Department of Veterans Affairs HCHenry M. CryerUniversity of California, Los Angeles

Discussion

Member takes

Implication

Suggests EDRF drives sepsis microcirculatory changes in rats; leaves open human translation and therapeutic targeting.

Structured PICO

Does EDRF blockade with hydroquinone prevent sepsis-induced arteriole dilation in skeletal muscle in rats?

Population

Rats with high cardiac output bacteremia (HOB) and low cardiac output live Escherichia coli sepsis (LOS) (cremaster muscle model)

Intervention

Local chemical blockade of EDRF by hydroquinone (HQ)

Comparator

Unblocked state (implied)

Outcome

Small arteriole (6-22 microns) dilation and large arteriole (55-135 microns) constrictionsurrogate

EDRF mediates small arteriole vasodilation in skeletal muscle during bacteremia, highlighting the endothelium's role in microcirculatory responses to sepsis.

Cite This Study

Lübbe et al. (1992) studied this question.

synapsesocial.com/papers/6a6fead5e71d69abee08452b https://doi.org/10.1152/ajpheart.1992.262.3.h880

View Full Paper

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EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle

Discussion

Member takes

Implication

Structured PICO

Cite This Study

EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider