New clue on Jackson killer drug
Wednesday September 16th, 2009
By Jane Collingwood
Experts may be closer to explaining why people vary in their risk heart
failure when exposed to anaesthestic drugs such as propofol.
The drug is sometimes used for its short-term effects which include mild euphoria, hallucinations, and disinhibition, but it may lead to addiction.
Propofol has been in the news recently due to its suspected role in the death of Michael Jackson. A Los Angeles County coroner concluded that the singer died from a mixture of propofol and a benzodiazepine drug.
Now, a team from the Medical College of Wisconsin, USA, has found the genetic causes of variation in sensitivity to collapse of the heart during anaesthesia.
They administered the drug to two groups of rats, one very sensitive to anaesthetics and one much less sensitive. A small region on chromosome 13 was identified, which contained the genetic switch responsible for the difference in the response.
Researcher Dr Richard Roman says: "By identifying a genetic susceptibility for cardiovascular collapse to low dose propofol, our findings may provide a key to better understand the underlying cause of the mysterious death of Michael Jackson."
Details are published in the Journal of Pharmacology and Experimental Therapeutics.
Co-author Dr Carol Moreno Quinn added: "The next step is to identify the exact gene and see if it is also responsible for cardiovascular collapse with propofol in humans. We can then test which persons with this gene would be sensitive to anaesthesia and prevent deaths and accidents due to cardiovascular collapse in the operating room."
The team believes that people whose blood pressure is more responsive to salt may be more sensitive to propofol, through its effects on the smooth muscle of the blood vessels.
Stadnicka, A. et al. Mechanism of Differential Cardiovascular Response to Propofol in Dahl Salt-Sensitive, Brown Norway, and Chromosome 13-Substituted Consomic Rat Strains: Role of Large Conductance Ca2+ and Voltage-Activated Potassium Channels. The Journal of Pharmacology and Experimental Therapeutics, Vol. 330, September 2009, pp. 727-35.
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