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February 1974

Pulmonary Anatomic Arteriovenous Shunting Caused by Epinephrine

Author Affiliations

Akron, Ohio
From the Surgical Research Laboratories, Akron General Medical Center (Drs. Nomoto and Berk, and Mesdames Hagen and Koo), and the Case Western Reserve University Medical School (Dr. Berk), Akron, Ohio. Dr. Nomoto is a fellow of the American Heart Association.

Arch Surg. 1974;108(2):201-204. doi:10.1001/archsurg.1974.01350260055012

Pulmonary anatomic arteriovenous (A-V) shunting was measured with technetium Tc 99m human albumin microspheres in 44 anesthetized dogs. In untreated dogs, after a 15- to 30-minute observation period following the first microsphere injection, no significant changes in heart rate, arterial pressure, cardiac output, or the pH occurred, but there was a small increase in arterial oxygen pressure and a small decrease in arterial carbon dioxide pressure. These were attributed to preanesthetic excitement or reactions to the anesthetic itself. The second microsphere injection showed no significant change in pulmonary shunting.

Infusions of epinephrine hydrochloride at the rate of 2μg/kg/min and 4μg/kg/min showed significant increases in the pulmonary shunting to 320% and 573% of control values, respectively, during the same time intervals. Epinephrine in amounts that can be produced endogenously under conditions of stress may cause the opening of anatomic pulmonary A-V shunts.