What question did this study set out to answer?

To assess whether the release of alpha-hydroxybutyrate dehydrogenase (HBDH) quantitatively corresponds to cellular necrosis and contractile failure in heart cells exposed to anoxia and reoxygenation.

June 1, 1979Cardiovascular Research

Release of alpha hydroxybutyrate from neonatal rat heart cell cultures exposed to anoxia and reoxygenation: comparison with impairment of structure and function of damaged cardiac cells

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Population

Spontaneously beating monolayer cultures of neonatal rat heart cells

Design

Preclinical

Follow-up

Up to 7 hours of anoxia followed by reoxygenation

Authors

ALA. van der LaarseLeiden University Medical Center LHL. HollaarLeiden University Medical Center LVLizet J.M. Van der ValkLeiden University Medical Center

Discussion

Member takes

Implication

HBDH may quantify necrosis in anoxia/reoxygenation models; leaves open translation to clinical ischemia-reperfusion biomarkers.

Key Points

To assess whether the release of alpha-hydroxybutyrate dehydrogenase (HBDH) quantitatively corresponds to cellular necrosis and contractile failure in heart cells exposed to anoxia and reoxygenation.
Spontaneously beating monolayer cultures of neonatal rat heart cells were subjected to oxygen and substrate depletion (anoxia) for 1 to 7 hours, followed by reoxygenation.
Quantified extracellular HBDH activity release, the extent of morphological necrosis, and alterations in spontaneous contractile function across time points.
HBDH release began after 1 hour of anoxia and progressively increased to 84% of total intracellular activity by 7 hours.
Reoxygenation of anoxic heart cells accelerated the rate of HBDH leakage, demonstrating the oxygen paradox phenomenon.
Enzyme release, necrotic cell counts, and loss of spontaneous beating capacity displayed an identical dependence on the duration of anoxia.

Structured PICO

Population

Spontaneously beating monolayer cultures of neonatal rat heart cells

Intervention

Depletion of oxygen and metabolic substrates for 1 to 7 hours (anoxia) followed by reoxygenation

Outcome

Release of alpha-hydroxybutyrate dehydrogenase (HBDH), extent of necrosis, and changes in spontaneous contractile activitysurrogate

Cardiac cell death in anoxia/reoxygenation models can be reliably quantified by measuring released HBDH activity.

Cite This Study

Laarse et al. (1979) studied this question.

synapsesocial.com/papers/6a76566464b2b4ebb108801c https://doi.org/10.1093/cvr/13.6.345

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Release of alpha hydroxybutyrate from neonatal rat heart cell cultures exposed to anoxia and reoxygenation: comparison with impairment of structure and function of damaged cardiac cells

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Release of alpha hydroxybutyrate from neonatal rat heart cell cultures exposed to anoxia and reoxygenation: comparison with impairment of structure and function of damaged cardiac cells

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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