Effects of endothelin-1 on resuscitation rate during cardiac arrest

Daniel J DeBehnke, Laurie Benson

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Objectives: Endothelin-1 (ET-1) is a potent peripheral and coronary artery vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during cardiac arrest. The effect of ET-1 on return of spontaneous circulation (ROSC) following cardiac arrest has not been studied. Our hypothesis was that ET-1 does not improve ROSC from cardiac arrest when compared to placebo. Methods: A total of 11 immature swine were used in this laboratory study. Animals were randomized to receive 300 μg ET-1 and standard dose epinephrine (SDE) or placebo and SDE during arrest. After a 10- min period of no-flow ventricular fibrillation (VF), CPR was performed for 3 min followed by ET-1/SDE or placebo/SDE administration. Following drug administration, standard ACLS was followed with SDE given every 3 min. Aortic pressure was monitored during resuscitation. ROSC was defined as any perfusing rhythm with a systolic pressure greater than 60 mmHg for 60 s. Animals received post-ROSC care as needed for 2 h post-ROSC. CPP and ROSC were analyzed using repeated measures ANOVA and Fischer's exact test respectively. P < 0.05 was considered significant. Results: Pre-arrest variables and CPP prior to ET-1 administration were not different between groups. Following ET-1 administration, CPP was significantly increased at all time points in ET-1/SDE versus placebo/SDE animals. ROSC was achieved in 1/5 (20%) ET-1/SDE versus 1/6 (16.7%) placebo/SDE animals (P > 0.05). The resuscitated ET-1/SDE animal survived 6.5 min compared to 120 min for the resuscitated placebo/SDE animal. Conclusions: In our study, ET-1 administration during cardiac arrest increases CPP but does not improve ROSC.

Original languageEnglish (US)
Pages (from-to)185-189
Number of pages5
JournalResuscitation
Volume47
Issue number2
DOIs
StatePublished - Jan 1 2000

Fingerprint

Endothelin-1
Heart Arrest
Resuscitation
Epinephrine
Placebos
Perfusion
Pressure
Cardiopulmonary Resuscitation
Vasoconstrictor Agents
Ventricular Fibrillation
Coronary Vessels
Analysis of Variance
Arterial Pressure
Swine
Blood Pressure
Pharmaceutical Preparations

Keywords

  • Cardiac arrest
  • Emergency medicine
  • Endothelin
  • Resuscitation

ASJC Scopus subject areas

  • Emergency Medicine
  • Emergency
  • Cardiology and Cardiovascular Medicine

Cite this

Effects of endothelin-1 on resuscitation rate during cardiac arrest. / DeBehnke, Daniel J; Benson, Laurie.

In: Resuscitation, Vol. 47, No. 2, 01.01.2000, p. 185-189.

Research output: Contribution to journalArticle

DeBehnke, Daniel J ; Benson, Laurie. / Effects of endothelin-1 on resuscitation rate during cardiac arrest. In: Resuscitation. 2000 ; Vol. 47, No. 2. pp. 185-189.
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abstract = "Objectives: Endothelin-1 (ET-1) is a potent peripheral and coronary artery vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during cardiac arrest. The effect of ET-1 on return of spontaneous circulation (ROSC) following cardiac arrest has not been studied. Our hypothesis was that ET-1 does not improve ROSC from cardiac arrest when compared to placebo. Methods: A total of 11 immature swine were used in this laboratory study. Animals were randomized to receive 300 μg ET-1 and standard dose epinephrine (SDE) or placebo and SDE during arrest. After a 10- min period of no-flow ventricular fibrillation (VF), CPR was performed for 3 min followed by ET-1/SDE or placebo/SDE administration. Following drug administration, standard ACLS was followed with SDE given every 3 min. Aortic pressure was monitored during resuscitation. ROSC was defined as any perfusing rhythm with a systolic pressure greater than 60 mmHg for 60 s. Animals received post-ROSC care as needed for 2 h post-ROSC. CPP and ROSC were analyzed using repeated measures ANOVA and Fischer's exact test respectively. P < 0.05 was considered significant. Results: Pre-arrest variables and CPP prior to ET-1 administration were not different between groups. Following ET-1 administration, CPP was significantly increased at all time points in ET-1/SDE versus placebo/SDE animals. ROSC was achieved in 1/5 (20{\%}) ET-1/SDE versus 1/6 (16.7{\%}) placebo/SDE animals (P > 0.05). The resuscitated ET-1/SDE animal survived 6.5 min compared to 120 min for the resuscitated placebo/SDE animal. Conclusions: In our study, ET-1 administration during cardiac arrest increases CPP but does not improve ROSC.",
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