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Electromechanical coupling in rat basilar artery in response to morphine
Neurosurgery
|December 1, 1983
Summary
Morphine sulfate causes rat basilar artery contraction by decreasing potassium conductance, leading to depolarization. Meperidine had minimal effects, and naloxone
Area of Science:
- Pharmacology
- Vascular Physiology
Background:
- Morphine and meperidine are narcotics with effects on the cardiovascular system.
- The rat basilar artery is a model for studying cerebral vascular smooth muscle.
Purpose of the Study:
- To investigate the mechanism of action of morphine sulfate and meperidine hydrochloride on rat basilar artery.
- To determine the effects of these agents on vascular smooth muscle contractility and electrical properties.
Main Methods:
- Measurements of force development, intracellular membrane potential (Em), and voltage-current curves in rat basilar artery.
- Application of morphine sulfate, meperidine hydrochloride, and naloxone.
- Electrical studies involving current pulses to assess input resistance (rin) and membrane potential changes (delta V).
Main Results:
- Morphine sulfate induced a dose-dependent contraction, reversible by naloxone.
- Morphine sulfate depolarized vascular smooth muscle cells and increased input resistance, suggesting decreased potassium conductance (gk).
- Meperidine hydrochloride exhibited significantly less effect on the preparation compared to morphine sulfate.
Conclusions:
- Morphine sulfate likely acts on rat basilar artery smooth muscle by reducing potassium conductance.
- The findings provide insight into the vascular effects of morphine.
- Naloxone's vehicle demonstrated in vitro vasodilator properties on cerebral vascular smooth muscle.