Resuscitation
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Comparative Study
Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide.
The post-cardiac arrest syndrome includes a decline in myocardial microcirculation function. Inhibition of the platelet IIb/IIIa glycoprotein receptor has improved myocardial microvascular function post-percutaneous coronary intervention. Therefore, we evaluated such inhibition with eptifibatide for its effect on myocardial microcirculation function post-cardiac arrest and resuscitation. ⋯ Inhibition of platelet IIb/IIIa glycoprotein receptors with eptifibatide post-resuscitation prevented myocardial microcirculation dysfunction. Left ventricular dysfunction post-resuscitation was not improved with eptifibatide, and perhaps transiently worse at 30min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.
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Comparative Study
Genetic deletion of NOS3 increases lethal cardiac dysfunction following mouse cardiac arrest.
Cardiac arrest mortality is significantly affected by failure to obtain return of spontaneous circulation (ROSC) despite cardiopulmonary resuscitation (CPR). Severe myocardial dysfunction and cardiovascular collapse further affects mortality within hours of initial ROSC. Recent work suggests that enhancement of nitric oxide (NO) signaling within minutes of CPR can improve myocardial function and survival. We studied the role of NO signaling on cardiovascular outcomes following cardiac arrest and resuscitation using endothelial NO synthase knockout (NOS3(-/-)) mice. ⋯ Genetic deletion of NOS3 decreases ROSC rate and worsens post-ROSC left-ventricular function. Poor cardiovascular outcomes are associated with differences in NOS3-dependent myocardial cGMP signaling and circulating NO metabolites.
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Comparative Study
Effects of arterial oxygen content on oxidative stress during resuscitation in a rat hemorrhagic shock model.
To examine whether reactive oxygen species (ROS) production is affected by arterial oxygen content (CaO(2)) in attempted resuscitation to restore blood pressure from hemorrhagic shock (HS) or not. ⋯ In a rat HS model, attempted resuscitation to restore blood pressure increased O(2) UC as well as %CoQ9. However, the magnitude of %CoQ9 increase that represents ROS production is not affected by CaO(2) during resuscitation from HS.