Publications by authors named "Jaqueline Arias"

Background: Whole body periodic acceleration (pGz), the repetitive, head-foot sinusoidal motion of the body, increases pulsatile shear stress on the vascular endothelium producing increased release of endothelial derived nitric oxide (eNO) into circulation. Based upon prior CPR investigations, we hypothesized that pGz instituted prior to and during hemorrhagic shock (HS) should improve survival.

Materials And Methods: Sixteen anesthetized male pigs, 23 ± 5 kg, were randomized to receive 1 h pGz or no pGz (CONT) prior to and during severe controlled graded HS up to 2-1/2 h.

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Aims: Periodic acceleration (pGz) is a method that applies repetitive sinusoidal head-to-foot motion to the horizontally positioned body. pGz adds pulses to the circulation as a function of frequency, thereby increasing shear stress to the endothelium. Pulsatile shear stress increases release of cardioprotective endothelial-derived nitric oxide prostaglandin E-2 and prostacyclin into the circulation.

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Periodic acceleration (pGz), sinusoidal motion of the whole body in a head-foot direction in the spinal axis, is a novel noninvasive means for cardiopulmonary support and induction of pulsatile shear stress. pGz increases plasma nitrite levels, in vivo and in vitro. Additionally, pGz confers cardioprotection in models of ischemia reperfusion injury.

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Objective: To evaluate the use of a Na/H exchanger (NHE-1) inhibitor as a cardioprotective adjunct therapy to low-volume resuscitation in two different rat models of traumatic hemorrhagic shock.

Design: Experimental, prospective study.

Setting: Medical center research laboratory.

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Introduction: Periodic acceleration (pGz) is a non-invasive method of increasing pulsatile shear stress to the endothelium. pGz is achieved by the sinusoidal head to foot motion to the supine body. pGz increases endogenous production of nitric oxide in whole animal models and isolated perfused vessel preparations, and is cardioprotective when applied prior to, during and after ischemia reperfusion.

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Asphyxia cardiac arrest and shock are models for whole body ischemia reperfusion injury. Periodic acceleration (pGz) achieved by moving the body on a platform is a novel method for inducing pulsatile vascular shear stress and endogenous production of endothelial nitric oxide, prostaglandin E2, tissue plasminogen activator, and adrenomedullin. The aforementioned are cardioprotective during and after ischemia reperfusion injury.

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Whole body periodic acceleration (pGz) along the spinal axis is a novel method of cardiopulmonary resuscitation (CPR). Oscillatory motion of the supine body in a horizontal fashion provides ventilation and blood flow to vital organs during cardiac arrest and pulsatile shear stress to the vascular endothelium. We previously showed in pigs that pGz-CPR affords better overall survival, post resuscitation myocardial function, and neurological outcomes compared to conventional chest compression CPR.

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Background: Asphyxia is one of the most common causes of pediatric cardiac arrest, and becoming a more frequently recognized cause in adults. Periodic acceleration (pGz) is a novel method of cardiopulmonary resuscitation (CPR). pGz is achieved by rapid motion of the supine body headward-footward that generates adequate perfusion and ventilation during cardiac arrest.

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Periodic acceleration (pGz) is produced by a platform which moves the supine body repetitively in a headward to footward direction. The imparted motion produces pulsatile shear stress on the vascular endothelium. Pulsatile shear stress on the vascular endothelium has been shown to elicit production of a host of cardioprotective, cytoprotective mediators.

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Severe blood loss is a major cause of death occurring within hours of traumatic injury. Na+/H+ exchange (NHE-1) activity is an important determinant of the extent of ischemic myocardial injury. The goal of the present study was to test the hypothesis that NHE-1 inhibition delays the onset of hypovolemic circulatory shock, thereby preventing early death due to severe hemorrhage in pigs.

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Background: Nitric oxide (NO) is a critical regulator of vascular tone, and signal transduction. NO is produced via three unique synthases (NOS); endothelial (eNOS), and neuronal (nNOS) are both constitutively expressed and inducible (iNOS) produced primarily after stimulation. NO has been implicated during and after ischemia reperfusion injury as both a detrimental and cardioprotective mediator.

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The purpose of the present study was to identify the roles of the three nitric oxide synthase (NOS) isoforms on whole body ischemia-reperfusion injury during cardiopulmonary resuscitation (CPR) with periodic acceleration (pGz) in pigs. Thirty-two anesthetized pigs (27.6+/-3.

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The effects of whole body, periodic acceleration (pGz) on cardiopulmonary resuscitation outcome, organ blood flow and tissue inflammatory injury were examined in an experimental pig model, and compared with Thumper (TH)-CPR. VF was induced in 16 pigs, and remained untreated for 3 min, followed by either pGz-CPR or TH-CPR for 15 min. Defibrillation attempts were made at 18 min of VF.

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Na(+)/H(+) exchange (NHE) is involved in the myocardial injury that occurs during ischemia and reperfusion. The goal of the present study was to investigate the role of NHE in hypovolemic circulatory shock by using a potent NHE-1 selective inhibitor BIIB513. Acute rapid hemorrhage was induced in 14 pigs by bleeding (30 mL/kg over 30 min).

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