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Inhalation anaesthetics decrease calcium content of cardiac sarcoplasmic reticulum
1Membrane Research Institute, University City Science Center, Philadelphia, PA 19104.
British Journal of Anaesthesia
|June 1, 1989
Summary
Inhalation anesthetics, like halothane and enflurane, reduce heart muscle contractility by decreasing sarcoplasmic reticulum calcium content. This effect is similar to caffeine, suggesting increased SR calcium permeability.
Area of Science:
- Cardiology
- Anesthesiology
- Molecular Pharmacology
Background:
- Inhalation anesthetics are known to cause negative inotropic effects.
- Caffeine also exhibits a negative inotropic effect.
- The precise mechanisms underlying these effects require further elucidation.
Purpose of the Study:
- To investigate the impact of inhalation anesthetics on cardiac calcium content.
- To compare the effects of inhalation anesthetics and caffeine on myocardial contractility and calcium handling.
- To determine the correlation between sarcoplasmic reticulum (SR) calcium content and the negative inotropic effects of anesthetics.
Main Methods:
- Utilized a Langendorff perfused rat heart model.
- Administered halothane and enflurane at specific concentrations.
- Measured left ventricular pressure and myocardial calcium content using atomic absorption spectroscopy.
- Assessed sarcoplasmic reticulum (SR) calcium content via caffeine-induced calcium release.
Main Results:
- Halothane (2.8%) and enflurane (5.1%) significantly decreased left ventricular pressure (75.4% and 72.4%, respectively).
- Both anesthetics reduced myocardial calcium content by approximately 30-31%.
- A strong correlation was observed between the negative inotropic effect and decreased SR calcium content (r=0.95 for halothane, r=0.91 for enflurane).
Conclusions:
- Inhalation anesthetics induce a negative inotropic effect by reducing cardiac sarcoplasmic reticulum (SR) calcium content.
- These findings suggest that anesthetics increase the calcium permeability of the SR.
- This increased permeability leads to a diminished SR calcium store, ultimately impairing myocardial contractility.