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Effects of acid-base changes, hypoxia, and catecholamines on ventricular performance
The American Journal of Physiology
|May 1, 1975
Summary
Tris (hydroxymethyl)-aminomethane (Tris) and sodium bicarbonate (NaHCO3) affect ventricular performance (VP) during induced acidosis. Tris enhanced VP more than NaHCO3, suggesting a direct effect beyond pH alteration, possibly via catecholamines.
Area of Science:
- Cardiovascular Physiology
- Acid-Base Balance
- Pharmacology
Background:
- Extracellular pH significantly impacts cardiac function.
- The role of buffering agents in modulating ventricular performance during acidosis is complex.
- Beta-adrenergic pathways are crucial in regulating myocardial contractility.
Purpose of the Study:
- To investigate the effects of tris (hydroxymethyl)-aminomethane (Tris) and sodium bicarbonate (NaHCO3) on ventricular performance (VP) during induced acidosis in dogs.
- To determine if hypoxemia influences VP during acidosis.
- To evaluate the impact of beta-adrenergic blockade on the response to buffering agents.
Main Methods:
- Utilized a canine right heart bypass preparation with controlled hemodynamic parameters.
- Induced extracellular pH changes using Tris or NaHCO3, with and without hypoxemia.
- Administered propranolol for beta-adrenergic blockade.
- Measured maximal rate of rise of left ventricular pressure (dp/dt max) and left ventricular end-diastolic pressure to assess VP.
Main Results:
- Low extracellular pH diminished VP.
- Tris increased VP significantly more than NaHCO3 at elevated pH.
- Beta-adrenergic blockade reduced the VP response to Tris.
- Prior reserpine administration abolished the inotropic effect of Tris, indicating a role for endogenous catecholamines.
Conclusions:
- Tris (hydroxymethyl)-aminomethane (Tris) influences ventricular performance (VP) independently of its pH-altering effects.
- The observed inotropic effect of Tris is likely mediated through interaction with myocardial beta-adrenergic receptors and endogenous catecholamines.
- These findings highlight a potential direct myocardial action of Tris beyond simple acid-base correction.