SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Journal of Cardiovascular Pharmacology and Therapeutics
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Wann, S.-r.
Right arrow Articles by Yu, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wann, S.-r.
Right arrow Articles by Yu, T.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Cariporide for Pharmacologic Defibrillation After Prolonged Cardiac Arrest

Shue-ren Wann, MD

Institute of Critical Care Medicine, Palm Springs, CA

Max Harry Weil, MD, PhD

Shijie Sun, MD

Wanchun Tang, MD

Institute of Critical Care Medicine, Palm Springs, CA; The Keck School of Medicine of the University of Southern California, Los Angeles, CA

Ting Yu, MD

Institute of Critical Care Medicine, Palm Springs, CA

Background: We hypothesized that cariporide, a sodium-hydrogen exchange inhibitor, would be as cardioprotective during the global myocardial ischemia of prolonged cardiac arrest as it is in settings of coronary occlusion.

Methods and Results: Fifteen Sprague-Dawley rats were randomized to receive bolus injections of cariporide or placebo in a dose of 3 mg.kg-1 into the right atrium either 5 minutes before, or at 8 minutes after, onset of ventricular fibrillation. Ventricular fibrillation was electrically induced and untreated for 8 minutes. Precordial compression, together with mechanical ventilation, was then started and continued for an interval of 8 minutes prior to attempted resuscitation. All but one placebo-treated animal were successfully resuscitated. Spontaneous defibrillation with restoration of circulation was observed in both cariporide-pretreatment and post-treatment groups but in none of the placebo-treated animals. Postresuscitation cardiac index, end-tidal CO2, mean aortic pressure, left ventricular systolic pressure, left ventricular end-diastolic pressure, and left ventricular contractile and lusitropic functions (dP/dt40, and -dP/dt) were significantly less impaired after cariporide, especially in the pretreated group, compared to electrically defibrillated controls. Postresuscitation ventricular premature beats were significantly reduced after cariporide. The duration of postresuscitation survival was significantly increased in animals pretreated with cariporide.

Conclusions: Cariporide, when administered prior to and during cardiac arrest, improved both the success of resuscitation and postresuscitation myocardial function.

Key Words: cardiopulmonary resuscitation • postresuscitation myocardial dysfunction • postresuscitation survival • Na+/H+ exchanger inhibitor • cariporide

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 7, No. 3, 161-169 (2002)
DOI: 10.1177/107424840200700306


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
S. Wang, J. Radhakrishnan, I. M. Ayoub, J. D. Kolarova, D. M. Taglieri, and R. J. Gazmuri
Limiting sarcolemmal Na+ entry during resuscitation from ventricular fibrillation prevents excess mitochondrial Ca2+ accumulation and attenuates myocardial injury
J Appl Physiol, July 1, 2007; 103(1): 55 - 65.
[Abstract] [Full Text] [PDF]



Advertisement