• D DeBehnke.
• Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee 53226, USA. ddebehnk@mcw.edu
• Acad Emerg Med. 2000 Mar 1; 7 (3): 211-21.

BackgroundEndothelin-1 (ET-1) is a potent vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during arrest. The effects of ET-1 on organ blood flow during arrest have not been extensively studied.ObjectiveTo investigate the effects of ET-1 on myocardial and cerebral blood flow during cardiac arrest.MethodsSixty immature swine were anesthetized and instrumented. The animals were randomized to receive one of three doses of ET-1 (50, 150, or 300 microg) or placebo with/without standard-dose epinephrine (SDE) during cardiac arrest. After a 10-minute period of no-flow ventricular fibrillation (VF), cardiopulmonary resuscitation (CPR) was performed for 3 minutes, followed by drug administration. Placebo or SDE was given every 3 minutes. Myocardial and cerebral blood flow was measured using a fluorescent microsphere technique.ResultsPrearrest and CPR variables were not different between groups. Beginning 4 minutes after giving 300 microg ET-1 with or without SDE, CPP was significantly increased compared with SDE alone. Total myocardial blood flow following ET-1 administration was no different than myocardial blood flow following SDE alone. Cerebral blood flow increased 3.5 minutes after administration of 300 microg ET-1 with SDE and reached significance 9.5 minutes after drug administration when compared with SDE alone [92.5 (48.8-117.9) vs 15.6 (7.7-23) mL/min/100 g].ConclusionsThree hundred microg ET-1 with SDE increases CPP and improves cerebral blood flow but does not improve myocardial blood flow during cardiac arrest. The peripheral effects of ET-1 significantly improve CPP and cerebral blood flow, but myocardial blood flow is not increased due to coronary vasoconstriction.

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