Athens, Ga. – A new University of Georgia study suggests that commonly prescribed drugs used to lower blood pressure may help reduce brain damage when given within 24 hours of a stroke.
The finding, based on a study using rats and published in the April issue of the Journal of Hypertension, may ultimately revolutionize emergency stroke care by putting blood pressure-lowering medications alongside clot-busting drugs and blood thinners as front-line medications.
"There is a long-standing controversy about whether you should even treat elevated blood pressure in stroke victims," said lead author Susan Fagan, professor of clinical and administrative pharmacy at the UGA College of Pharmacy and the Medical College of Georgia. "We were able to show that lowering blood pressure in the 24 hours following a stroke can reduce brain damage."
Fagan and her team induced strokes in rats by occluding a major artery in the brain. After three hours, the suture was removed to simulate the effect of thrombolytic, or clot-busting, drugs. The rats were then given one of two common blood pressure lowering drugs or – for the control group – a saline solution.
When the researchers measured the amount of brain damage, they found that the rats that had received the blood pressure lowering drugs fared significantly better. While the control group showed damage in 50 percent of the brain, those receiving the drugs hydralazine and enalapril showed 30 percent damage.
The finding complements a study Fagan and her colleagues published last year in the same journal that found similar reductions in brain damage using the common blood pressure drug, candesartan, a popular drug in the class known as angiotensin receptor blockers (ARBs). The rats given candesartan, however, showed the additional benefit of improved function while the rats receiving the other blood pressure medications had less benefit. Fagan said that in addition to protecting the brain and blood vessels through lowering blood pressure, ARBs appear to provide additional benefits by blocking the damaging effects of angiotensin II, a molecule released from the brain and probably other tissues following stroke.
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