What question did this study set out to answer?

To evaluate how increased hydrogen ion concentration and proton-calcium competition alter myocardial contractility and cellular metabolism.

January 12, 1976Acta Medica Scandinavica

Effects of Acidosis on Myocardial Contractility and Metabolism*

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Population

Perfused rat heart model (working heart preparation) and isolated cardiac sarcolemma

Comparison

Respiratory acidosis to pH 6.6, metabolic… vs Normal pH (7.4) perfusion

Design

Preclinical

Authors

JWJohn WilliamsonUniversity of Virginia BSBrian SaferNational Institutes of Health TRT. L. RichUniversity of California, Los Angeles

Discussion

Member takes

Implication

Animal models distinguish rapid respiratory vs slower metabolic acidosis effects on contractility; leaves open translation to clinical acid-base management.

Key Points

To evaluate how increased hydrogen ion concentration and proton-calcium competition alter myocardial contractility and cellular metabolism.
Perfused isolated working rat hearts under respiratory acidosis (high carbon dioxide) or metabolic acidosis (low bicarbonate) down to pH 6.6, testing responses to extracellular calcium, verapamil, and epinephrine.
Rapidly freeze-clamped heart tissue at intervals up to 3 minutes following acidosis induction to quantify glycolytic intermediates, adenine nucleotides, and citric acid cycle metabolites.
Measured high- and low-affinity calcium binding in isolated cardiac sarcolemma preparations at pH 6.6 compared with pH 7.4.
Respiratory acidosis to pH 6.6 caused left ventricular pressure to drop rapidly with a half-time of 5 seconds, an effect completely reversed by elevating extracellular calcium.
At the 5-second mark of contractile decline, ATP and creatine phosphate levels increased while ADP decreased, indicating that impaired energy production does not cause the initial loss of contractility.
Prolonged acidosis suppressed glycolytic flux, oxygen consumption, and citric acid cycle turnover, leading to total adenine nucleotide depletion and irreversible failure when calcium rescue was attempted without acetate.

Structured PICO

Population

Perfused rat heart model (working heart preparation) and isolated cardiac sarcolemma

Intervention

Respiratory acidosis (high pCO2) to pH 6.6, metabolic acidosis (low HCO3-), and calcium addition

Comparator

Normal pH (7.4) perfusion

Outcome

Left ventricular pressure development and metabolic intermediate levels (ATP, ADP, creatine phosphate, citric acid cycle intermediates)surrogate

Respiratory acidosis rapidly depresses myocardial contractility primarily by competing with calcium for intracellular binding sites, an effect that precedes and is independent of a fall in the rate of energy production.

Cite This Study

Williamson et al. (1976) studied this question.

synapsesocial.com/papers/6a766eec3da069e66cbd3101 https://doi.org/10.1111/j.0954-6820.1976.tb05871.x

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Implication

Animal models distinguish rapid respiratory vs slower metabolic acidosis effects on contractility; leaves open translation to clinical acid-base management.

Effects of Acidosis on Myocardial Contractility and Metabolism*

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Effects of Acidosis on Myocardial Contractility and Metabolism*

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider