nger keep up. Less and less blood reaches the lungs, the heart enlarges to try to overcome the pressure, and damage to the overworked heart accumulates.
Although treatment for pulmonary hypertension has improved, long-term survival, even with therapy, is disappointing, similar to that for lung cancer. Because sorafenib inhibits the chemical signals that can trigger both cellular proliferation and new blood vessel growth, Gomberg-Maitland and colleagues suspected it might slow the growth and thickening of the pulmonary artery walls.
To test this theory they treated rats at high risk for pulmonary hypertension with sorafenib. The researchers studied five groups of rats. One group stayed in normal cages and received no medication. The other four groups spent three weeks in a low-oxygen environment–about half the normal level–which can trigger pulmonary hypertension. Rats in the reduced-oxygen chambers received: no medication, a drug called SU5416 (well known to cause severe pulmonary hypertension in this setting), SU5416 plus sorafenib, or sorafenib alone.
As expected, the unmedicated rats in a low-oxygen environment had mildly elevated pulmonary artery pressures after three weeks and those that received SU5416 developed severe pulmonary hypertension. But, those that received sorafenib or sorafenib plus S5416, had negligible pressure increases. Sorafenib appeared not only to counteract the effects of the low-oxygen environment but also to prevent the additional damage caused by SU5416.
"This was an encouraging sign," said Gomberg-Maitland. This is "one of the best models we have for this disease," she said.
The side effects of the drug in humans have been relatively mild. The most common adverse effects are: rashes of the face and arms or hands and feet, mild diarrhea, and fatigue.
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