Acidosis and cardiac muscle contractility: comparative aspects

Area of Science:

• Physiology
• Cardiovascular Biology
• Evolutionary Biology

Background:

• Transition to air-breathing increases risk of cellular acidosis due to carbon dioxide (CO2) buildup.
• Acidosis negatively impacts cardiac muscle contractility by interfering with calcium ion function.
• This effect is particularly relevant for cardiac muscle, where hydrogen ions can inhibit calcium's inotropic action.

Purpose of the Study:

• To investigate the inherent ability of cardiac muscle to resist the negative inotropic effects of hydrogen ions.
• To determine the prevalence of this resistance in air-breathers versus water-breathers.
• To elucidate the cellular mechanisms underlying this acidotic resistance in cardiac muscle.

Main Methods:

• Comparative analysis of cardiac muscle properties in air-breathing and water-breathing vertebrates.
• Measurement of intracellular pH and tissue buffer capacity.
• Calcium-flux measurements and analysis of cellular calcium distribution, including mitochondrial stores.

Main Results:

• Cardiac muscle's ability to resist acidosis is prevalent in air-breathers but largely absent in water-breathers (fish).
• This resistance does not involve neutralization or excretion of excess hydrogen ions.
• Acidosis-induced intracellular calcium deficits are compensated by an expanded calcium pool regulating cardiac force.

Conclusions:

• Vertebrate cardiac muscle exhibits an evolved mechanism to maintain contractility during CO2-induced acidosis.
• This adaptation appears linked to increased intracellular calcium availability, potentially involving mitochondrial calcium stores.
• The findings highlight a key physiological difference between air-breathing and water-breathing vertebrates concerning cardiac function under acidic conditions.