Whole Body Periodic Acceleration (pGz) Improves Survival and Allows for Resuscitation in a Model of Severe Hemorrhagic Shock in Pigs

Bassuk, Jorge; Wu, Heng; Arias, Jaqueline; Kurlansky, Paul; Adams, José A.

doi:10.1016/j.jss.2010.07.047

Cited by 8 publications

(7 citation statements)

References 82 publications

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“…Despite the richness of this literature, however, a direct link from shear stress on endothelial cells to HSP expression to the resilience of blood vessels has not been defined, although the work of Adams and colleagues 389,390 comes close to demonstrating it. Working in a pig model of ventricular fibrillation, they exposed the anesthetized animal to mechanical head-to-foot shaking, at frequencies designed to create a sinusoidal shear stress on endothelial cells of blood vessels, additional to the pulse.…”

Section: Physical Stressesmentioning

confidence: 99%

Acquired Resilience: An Evolved System of Tissue Protection in Mammals

et al. 2018

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This review brings together observations on the stress-induced regulation of resilience mechanisms in body tissues. It is argued that the stresses that induce tissue resilience in mammals arise from everyday sources: sunlight, food, lack of food, hypoxia and physical stresses. At low levels, these stresses induce an organised protective response in probably all tissues; and, at some higher level, cause tissue destruction. This pattern of response to stress is well known to toxicologists, who have termed it hormesis. The phenotypes of resilience are diverse and reports of stress-induced resilience are to be found in journals of neuroscience, sports medicine, cancer, healthy ageing, dementia, parkinsonism, ophthalmology and more. This diversity makes the proposing of a general concept of induced resilience a significant task, which this review attempts. We suggest that a system of stress-induced tissue resilience has evolved to enhance the survival of animals. By analogy with acquired immunity, we term this system ‘acquired resilience’. Evidence is reviewed that acquired resilience, like acquired immunity, fades with age. This fading is, we suggest, a major component of ageing. Understanding of acquired resilience may, we argue, open pathways for the maintenance of good health in the later decades of human life.

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Section: Physical Stressesmentioning

confidence: 99%

Acquired Resilience: An Evolved System of Tissue Protection in Mammals

et al. 2018

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“…Pulsatile flow has also been shown to improve cerebral hemodynamic status in other clinically relevant states, including prolonged cerebral ischemia as a model of stroke (Allen et al, 2012), and severe hemorrhage (Bassuk et al, 2010). In a pig model of prolonged (30-min) isolated global normothermic brain ischemia, Allen et al (Allen et al, 2012) demonstrated that 20-min of pulsatile perfusion at a frequency of 1.3 Hz (80 cycles/min) and a flow rate of 750 ml/min resulted in reduced neurological deficit and cerebral tissue edema, no post-ischemic seizures (compared to 100% of animals in the non-pulsatile perfusion group), and an attenuated increases in oxygen radical damage.…”

Section: “Friend”mentioning

confidence: 99%

“…While these studies show benefit with pulsatile perfusion at or around the cardiac frequency, Adams et al (Adams et al, 2000, 2001) have introduced a novel approach to induce pulsatile flow by applying whole body periodic acceleration in the head-to-foot axis (Gz) at a frequency of approximately 3–4 Hz (180–240 cycles/min) and an acceleration of ±0.4 m/s 2 . These investigators have demonstrated that periodic acceleration can increase vital organ blood flow in pigs, including the brain, heart, kidneys, and liver at rest (Adams et al, 2001), and following significant clinical events such as severe hemorrhage (Bassuk et al, 2010), and cardiac arrest (Adams et al, 2011); subsequent survival from hemorrhage also increased from 0 to 50% (Bassuk et al, 2010). In studies using rats and piglets, these protective effects have been shown to be mediated by shear-stress induced release of vasoactive mediators including endothelial nitric oxide, prostacyclin, and prostaglandin E2, with subsequent vasodilation leading to improved tissue perfusion (Adams et al, 2005; Uryash et al, 2009).…”

Section: “Friend”mentioning

confidence: 99%

Arterial pressure and cerebral blood flow variability: friend or foe? A review

Rickards

Tzeng

2014

Front. Physiol.

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Variability in arterial pressure and cerebral blood flow has traditionally been interpreted as a marker of cardiovascular decompensation, and has been associated with negative clinical outcomes across varying time scales, from impending orthostatic syncope to an increased risk of stroke. Emerging evidence, however, suggests that increased hemodynamic variability may, in fact, be protective in the face of acute challenges to perfusion, including significant central hypovolemia and hypotension (including hemorrhage), and during cardiac bypass surgery. This review presents the dichotomous views on the role of hemodynamic variability on clinical outcome, including the physiological mechanisms underlying these patterns, and the potential impact of increased and decreased variability on cerebral perfusion and oxygenation. We suggest that reconciliation of these two apparently discrepant views may lie in the time scale of hemodynamic variability; short time scale variability appears to be cerebroprotective, while mid to longer term fluctuations are associated with primary and secondary end-organ dysfunction.

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“…Despite 10 hundreds of treatment trials dating to the 1960s, interventions to improve survival from 11 sepsis have not significantly lowered mortality. 12 Administration of lipopolysaccharide (LPS), the endotoxin derived from the 13 purified outer membrane of E. Coli, produces systemic inflammatory effects of sepsis in 14 mice. Exposure to LPS causes a dose-dependent activation of a widespread cascade of 15 inflammatory mediators that disrupt the endothelial barrier.…”

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confidence: 99%

“…We and others reported that pulsatile shear increases expression of 32 both endothelial derived nitric oxide synthase (eNOS) and neuronal derived nitric oxide 33 synthase (nNOS) both which are produced in nanomolar concentrations, and are 34 important in modulating the anti-inflammatory response in sepsis (9)(10)(11). We have 35 previously shown in animal models of whole body and focal ischemia reperfusion injury 36 of the heart, brain, and skeletal muscles, that pGz improves outcomes, (12)(13)(14)(15)(16)(17)(18)(19). In part, 37 the effects of pGz are related to increased release of eNOS into the circulation as well as 38 prostaglandins, adrenomedullin, and signaling via Phosphoinositide 3-kinase protein 39 kinase B pathway (PI3K-AKT).…”

mentioning

confidence: 99%

Whole Body Periodic Acceleration Improves Survival and Microvascular Leak in a Murine Endotoxin Model

Adams¹,

Uryash²,

López

et al. 2018

Preprint

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Sepsis is a life threatening condition which produces multi-organ dysfunction with profound circulatory and cellular derangements. Administration of E.Coli endotoxin (LPS) produces systemic inflammatory effects of sepsis including disruption of endothelial barrier, and if severe enough death. Whole body periodic acceleration (pGz) is the headward-footward motion of the body. pGz has been shown to induce pulsatile shear stress to the endothelium, thereby releasing vascular and cardio protective mediators. The purpose of this study was to determine whether or not pGz performed as a pre-treatment or post-treatment strategy improves survival in a lethal murine endotoxin model. This study was designed as a prospective randomized controlled study in mice. pGz was performed in mice as pre-treatment (pGz-LPS, 3 days prior to LPS), post-treatment (LPS-pGz, 30 min after LPS ) strategies or Control (LPS-CONT), in a lethal murine model of endotoxemia. Endotoxemia was induced with intraperitoneal injection of E.Coli (40mg/kg). In a separate group of mice, a nonspecific nitric oxide synthase inhibitor (L-NAME) was provided in their drinking water and pGz-LPS and LPS-pGz performed to determine the effect of nitric oxide (NO) inhibition on survival. In another subset of mice, micro vascular leakage was determined. Behavioral scoring around the clock was performed in all mice at 30 min intervals after LPS administration, until 48 hrs. survival or death. LPS induced 100% mortality in LPS-CONT animals by 30 hrs. In contrast, survival to 48 hrs. occurred in 60% of pGz-LPS and 80% of LPS-pGz. L-NAME abolished the survival effects of pGz. Microvascular leakage was markedly reduced in both pre and post pGz treated animals and was associated with increased TIE2 and p-

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Whole Body Periodic Acceleration (pGz) Improves Survival and Allows for Resuscitation in a Model of Severe Hemorrhagic Shock in Pigs

Cited by 8 publications

References 82 publications

Acquired Resilience: An Evolved System of Tissue Protection in Mammals

Acquired Resilience: An Evolved System of Tissue Protection in Mammals

Arterial pressure and cerebral blood flow variability: friend or foe? A review

Whole Body Periodic Acceleration Improves Survival and Microvascular Leak in a Murine Endotoxin Model

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