What is the clinical evidence from this study?

Study design: Other. Population: Metabolic acidosis. Intervention: Metabolic acidosis vs. Reequilibration at pH = 7.4. Primary outcome: Myocardial response (pHi, high-energy phosphates, coronary flow, developed pressure).

What question did this study set out to answer?

To identify mechanical and biochemical factors that influence myocardial functional tolerance and recovery during severe metabolic acidosis.

November 1, 1987AJP Heart and Circulatory Physiology

Factors influencing myocardial response to metabolic acidosis in isolated rat hearts

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Key result

Rat heart recovery after metabolic acidosis is linked to preserving ATP at ~75% of control.

Population

Isolated Langendorff rat hearts

Comparison

Metabolic acidosis under various conditions vs Baseline/reequilibration at pH = 7.4, and…

Design

Preclinical

Follow-up

45 minutes (30 min perfusion, 15 min reequilibration)

Authors

TWThomas A. WattersUniversity of California, San Francisco MWMichael F. WendlandQB3 WPWilliam W. ParmleyHeart Failure & Transplant

Discussion

Member takes

Implication

Biochemical thresholds predict recovery in acidotic rat hearts; leaves open translation to clinical myocardial protection.

Key Points

To identify mechanical and biochemical factors that influence myocardial functional tolerance and recovery during severe metabolic acidosis.
Perfused isolated Langendorff rat hearts for 30 minutes under metabolic acidosis (pH 6.8) followed by 15 minutes of reequilibration at physiological pH (7.4).
Simultaneously tracked intracellular pH, beta-ATP, phosphocreatine, and inorganic phosphate using 31P nuclear magnetic resonance spectroscopy alongside mechanical measurements of coronary flow and developed pressure across varying workloads and substrate conditions.
Under high workload, acidosis severely depressed intracellular pH, high-energy phosphates, coronary flow, and developed pressure, ultimately causing irreversible cessation of beating during reequilibration.
Lowering cardiac workload, sustaining baseline coronary flow using vasodilators, or substituting glucose with pyruvate substantially mitigated functional and biochemical decline during acidosis.
Full mechanical recovery required maintaining intracellular pH above 6.40, tissue ATP levels at or above 75% of control, and a phosphorylation potential (ln[ATP]/[ADP]f[Pi]) of at least 4.1.

Structured PICO

Population

Isolated Langendorff rat hearts

Intervention

Metabolic acidosis (perfusion at pH = 6.8 for 30 min) under various conditions (work load variations, vasodilators, pyruvate substitution, raised osmolality)

Comparator

Baseline/reequilibration at pH = 7.4, and comparison between different experimental conditions

Outcome

Intracellular pH (pHi), beta-ATP, phosphocreatine, inorganic phosphate (Pi) content, coronary flow, and developed pressuresurrogate

Myocardial tolerance to metabolic acidosis in isolated rat hearts is improved by lowering work load, maintaining coronary flow, substituting pyruvate for glucose, or raising perfusate osmolality.

Cite This Study

Watters et al. (1987) studied Metabolic acidosis. Metabolic acidosis vs. Reequilibration at pH = 7.4 was evaluated on Myocardial response (pHi, high-energy phosphates, coronary flow, developed pressure). Recovery of biochemical and mechanical performance in isolated rat hearts after 30 min of metabolic acidosis was directly related to ln[ATP]/[ADP]f[Pi] ≥ 4.1, pHi > 6.40, and ATP ≥ 75% of control.

synapsesocial.com/papers/6aa2c4da8adb575768fdd27f https://doi.org/10.1152/ajpheart.1987.253.5.h1261

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Factors influencing myocardial response to metabolic acidosis in isolated rat hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Factors influencing myocardial response to metabolic acidosis in isolated rat hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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