Merck & Co. opened its defense in the retrial of the first federal Vioxx lawsuit with testimony about the history and workings of the once-popular painkiller.

Jurors listened attentively as Dr. Briggs Morrison, who was on the “project team” coordinating Vioxx research that the drug and similar medicines reduce an enzyme called prostacyclin which helps keep blood from clotting. However, Morrison pointed out that prostacyclin is produced in many parts of the body because it has numerous other functions, and said that Vioxx didn’t affect its production in blood vessels.

The five men and three women will eventually have to decide whether they think Vioxx caused the blood clot that killed Richard “Dickie” Irvin in May 2001 and, if that answer is yes, whether Merck hid the drug’s dangers.

Irvin’s widow, Evelyn Irvin Plunkett, is among more than 9,600 state and federal court plaintiffs who claim that in a rush to get Vioxx to market and to keep it there, Merck hid its dangers from the public.

Vioxx was developed in the years before several of Merck’s other big money-makers were scheduled to lose their patents, allowing other companies to sell generic versions and driving down prices.

Vioxx, was approved in 1999, brought in $2.5 million in 2003. In September 2004, Merck pulled it from the market after a study found it doubled patients’ risk of heart attacks and strokes after 18 months. Merck contends that there is no danger in shorter periods. The U.S. Food and Drug Administration stated last year that class of drugs which encompasses Vioxx was safe for short-term use.

U.S. District Judge Eldon Fallon, who is overseeing pretrial matters for all 4,000-plus federal Vioxx cases, has said he hopes to work out a settlement after the first four trials and wants this one over in two to 2 1/2 weeks. Plunkett’s attorneys rested their case Monday evening, after just over five days of testimony.

Their witnesses included the editor of a prestigious medical journal, who said Merck scientists overstated a claim that has been central to their defense: that the drug is dangerous only after a year and a half of use. Another witness, a former FDA official, said the company could have changed the Vioxx label two years earlier than it did to note that, in one drug test, heart attacks occurred in five times as many patients taking Vioxx than those on another painkiller.

Morrison testified that, after an early study found an indication that Vioxx apparently decreased production of prostacyclin, the next question was to find out where the prostacyclin in question was created, because the body makes it in many places and its action is different in each.

When pieces of blood vessels from rabbits with healthy arteries and those with atherosclerosis were put into test tubes, and Vioxx added to match the concentration of a 250 or 1,000-milligram dose in humans, it had no effect on prostaglandin production, Morrison said.

“Wherever in the body Vioxx was decreasing production of prostaglandin, it wasn’t the blood vessels,” he said.

He said that invalidated the idea that an imbalance of prostaglandin and thromboxane, which makes blood cells clump together, made heart attacks more likely in people taking Vioxx.

Troy Rafferty’s cross-examination concentrated on pointing out that Morrison was not a cardiologist or pharmacologist, and that Merck had not done any of the studies suggested by outside scientists after the prostaglandin reduction was found.

There were “lots of ideas floating around,” Morrison said, and none of the studies would have pinpointed where in the body COX-2 inhibitors depress prostacyclin production.

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