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For the relief and treatment of severe pain.
The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. Morphine first acts on the mu-opioid receptors. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. It has been shown that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream.
LD<sub>50</sub> = 461 mg/kg (rat, oral), 600 mg/kg (mouse, oral). Human lethal dose by ingestion is 120-250 mg of morphine sulfate. Symptoms of overdose include cold, clammy skin, flaccid muscles, fluid in the lungs, lowered blood pressure, "pinpoint" or dilated pupils, sleepiness leading to stupor and coma, slowed breathing, and slow pulse rate.
Bioavailability is approximately 30%.
2-4 hours
A small amount of glucuronide conjugates are excreted in bile, with minor enterohepatic recycling. Seven to 10% of administered morphine sulfate is excreted in the feces.
* 1 to 6 L/kg
* 20 – 30 mL/min/kg [Adult] * 1852 +/- 116 mL/min [Chinese] * 1495 +/- 80 mL/min [Caucasian]