2011;50:951C963. decrease was blunted in infliximab-treated swine (1-hour between group difference in MAP 21 mmHg, 95% CI 3C38 mmHg and SW 6.7 gm-m, 95% CI 0.4C13 at 1 hour). Remaining ventricular systolic dp/dt fell in the vehicle group (-437 mm Hg/sec, 95% CI -183 to -690) but did not in the infliximab group. Tau rose only in the vehicle group (44 msec, 95% Prinomastat CI 1C87). Short-term survival was higher in the infliximab group (Kaplan-Meier p = 0.022). Conclusions Blockade of TNF- in the Prinomastat immediate post-ROSC period improved survival and hemodynamic guidelines with this swine model of ischemic VF. strong class=”kwd-title” Keywords: cardiopulmonary resuscitation, ventricular fibrillation, post-resuscitation period, inflammatory response Intro Emergency medical solutions (EMS) respond to approximately 300,000 out-of-hospital Prinomastat cardiac arrests (OOHCA) each year in the United States.1 A 5-fold variation in survival to hospital discharge following EMS-treated cardiac arrest was reported among the 10 municipalities reporting from your Resuscitation Outcomes Consortium.2 Several studies have shown that post-cardiac arrest care and attention is an important determinant of survival.3C6 Myocardial ischemia is a common cause of cardiac arrest, especially among individuals with ventricular fibrillation (VF) as their initial arrest rhythm.7,8 Furthermore, ongoing ischemia likely contributes to post-cardiac arrest myocardial dysfunction in individuals achieving return of spontaneous blood circulation (ROSC).9 Management of post-resuscitation myocardial dysfunction has focused on prevention and, more recently, on early intervention, particularly early percutaneous coronary intervention, following resuscitation.10.11 Optimal pharmacologic management has not been defined nor has a goal-directed approach been verified.9 An increase in blood proinflammatory cytokines have been reported following resuscitation and plasma levels of TNF- have been shown to be inversely correlated with myocardial function.12,13 Using an electrical model of VF, we previously demonstrated that early administration of infliximab, an anti-TNF-alpha monoclonal antibody, following a return of Prinomastat spontaneous blood circulation (ROSC) in swine, ameliorates subsequent myocardial dysfunction.14 However, with this swine arrest model, post-arrest cardiac dysfunction is brief and moderate in severity.15 The purpose of this study was to determine if early blockade of TNF-alpha would prevent early post-cardiac arrest death and attenuate myocardial dysfunction following resuscitation PLCB4 from ischemically induced VF, a more clinically relevant arrest model with more profound post-resuscitation hemodynamic failure. METHODS This investigation was authorized by the Animal Care and Utilization Review Committee of our institution and adheres to the American Physiological Societys Guiding Principles in the Care and Use of Animals. Male home swine (Yorkshire and Yorkshire/Hampshire crossbreed) three to four months of age (mean excess weight 38 5 kg) were premedicated with IM ketamine (20 mg/kg) and xylazine (2 mg/kg). General anesthesia was induced with isoflurane via nose cone and, following endotracheal intubation, managed with inhaled isoflurane (Mac pc 1.0C2.5%) and nitrous oxide inside a 1 to 1 1 mixture with oxygen. End-tidal CO2 was continually monitored via side-stream capnography and minute air flow was adjusted to keep up end-tidal CO2 at 35C45 mm Hg. Standard lead II of the surface ECG was monitored continually during instrumentation and throughout the study protocol. Under fluoroscopic guidance, high fidelity, micro-manometer tipped catheters (Millar Tools, Houston, TX) were positioned in the ascending aorta and remaining ventricle (LV) via the femoral arteries and in the right atrium (RA) via a jugular vein. A thermistor-tipped catheter (Edwards Lifesciences, Irvine, CA) was positioned in a branch of the pulmonary artery for thermodilution cardiac output (CO) determinations. Commercially available, standard adhesive defibrillation electrode patches were applied to the remaining and right lateral aspects of the shaved thorax. Transthoracic impedance was measured using a tetrapolar constant current impedance measuring system (THRIM?, Morro Bay, CA). A small value non-inductive resistor (30) was then placed in series with the truncated exponential biphasic defibrillation waveform defibrillator (LifePak 12, Medtronic Emergency Response Systems, Redmond, WA). Following instrumentation, heart rate, systolic and diastolic aortic and LV pressure, imply RA pressure, LV systolic (maximum) and diastolic (min) dP/dt, and CO were recorded and arterial blood was analyzed (I-Stat CG8+, I-Stat Corp, Princeton, NJ). Mean arterial pressure (MAP), stroke volume (SV), and LV stroke work were derived using standard formulae. Using a 6 French HS-1 guiding catheter put via a carotid artery, a 4 mm 20 mm angioplasty catheter (Abbott Vascular, Temecula CA) was situated over a standard 0.014 coronary wire in the remaining anterior descending (LAD) coronary.
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- Furthermore, the indirect assay showed an amplification with a factor of about three as compared to the signal obtained with the direct assay
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- Initial results also exhibit superb efficacy of the vaccine in preventing hospitalization and severe disease in healthy individuals (7, 8)
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