ribose/hemorrhage

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Combined therapy with PJ34, a poly(ADP-ribose)polymerase inhibitor, reduces tissue plasminogen activator-induced hemorrhagic transformations in cerebral ischemia in mice.

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Recombinant tissue-type plasminogen activator (rt-PA) is presently the only pharmacological treatment approved for thrombolysis in patients suffering from ischemic stroke. Although reperfusion of ischemic tissue is essential, the use of rt-PA is limited due to its narrow therapeutic window and risk

Role of nitrosative stress and activation of poly(ADP-ribose) polymerase-1 in cardiovascular failure associated with septic and hemorrhagic shock.

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Reactive oxygen and nitrogen species, particularly peroxynitrite, are potent inducers of tissue damage during systemic inflammatory response and circulatory shock. Recent evidence indicates that the toxicity of these species largely depends on their ability to trigger activation of the nuclear

Increased poly(ADP-ribose) polymerase activity during porcine hemorrhagic shock is transient and predictive of mortality.

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OBJECTIVE The aim of our study was to compare poly(ADP-ribose) polymerase (PARP) activity levels in a porcine model of hemorrhagic shock and resuscitation. METHODS We designed a prospective, comparative randomized survival study of hemorrhagic shock using 20 male Yorkshire-Landrace pigs (15-25 kg).

Inhibition of poly(ADP-ribose) synthetase improves vascular contractile responses following trauma-hemorrhage and resuscitation.

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Hyporeactivity of vessels to constrictor agents is thought to contribute to cardiovascular decompensation following trauma-hemorrhage and resuscitation. In this study, we determined if inhibition of poly(ADP-ribose) synthetase (PARS) activity prevented the development of vascular hyporeactivity in

Effects of inhibitors of the activity of poly (ADP-ribose) synthetase on the organ injury and dysfunction caused by haemorrhagic shock.

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1 Poly (ADP-ribose) synthetase (PARS) is a nuclear enzyme activated by strand breaks in DNA, which are caused by reactive oxygen species (ROS). Here we investigate the effects of the PARS inhibitors 3-aminobenzamide (3-AB), nicotinamide and 1,5-dihydroxyisoquinoline (ISO) on the circulatory failure

Effects of 5-aminoisoquinolinone, a water-soluble, potent inhibitor of the activity of poly (ADP-ribose) polymerase on the organ injury and dysfunction caused by haemorrhagic shock.

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Poly (ADP-ribose) synthetase (PARP) is a nuclear enzyme activated by strand breaks in DNA, which are caused inter alia by reactive oxygen species (ROS). Here we report on (i) a new synthesis of a water-soluble and potent PARP inhibitor, 5-aminoisoquinolinone (5-AIQ) and (ii) investigate the effects

3-Aminobenzamide, an inhibitor of poly (ADP-ribose) synthetase, improves hemodynamics and prolongs survival in a porcine model of hemorrhagic shock.

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Hypoxia, energy deficit, and oxidative damage are principal mechanisms of injury in hemorrhagic shock (HS). Oxidant-induced cellular energetic failure and cell dysfunction is mediated, in part, via the activation of the nuclear enzyme poly (ADP-ribose) synthetase (PARS). Here we examine the effect

Activation of poly(ADP-ribose) polymerase in severe hemorrhagic shock and resuscitation.

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This study examines activation of poly(ADP-ribose) polymerase (PARP) in the ileum during hemorrhage and resuscitation and determines if inhibition of PARP reduces organ dysfunction and metabolic acidosis. Awake, nonheparinized rats were hemorrhaged (40 mmHg, 60 min). Resuscitation used Ringer's

Poly(ADP-ribose) polymerase activation and brain edema formation by hemoglobin after intracerebral hemorrhage in rats.

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Brain edema induced by intracerebral hemorrhage (ICH) is a serious problem in the treatment of ICH. However, the mechanisms of brain edema formation following ICH are not well-understood. We have found that hemoglobin plays an important role in edema development after ICH. In this study, we sought

Reduction of hemorrhagic transformation by PJ34, a poly(ADP-ribose)polymerase inhibitor, after permanent focal cerebral ischemia in mice.

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Hemorrhagic transformation is an aggravating event that occurs in 15 to 43% of patients suffering from ischemic stroke. This phenomenon due to blood-brain barrier breakdown appears to be mediated in part by matrix metalloproteinases (MMPs) among which MMP-2 and MMP-9 could be particularly involved.

The poly-ADP ribose polymerase-1/apoptosis-inducing factor pathway may help mediate the protective effect of electroacupuncture on early brain injury after subarachnoid hemorrhage.

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Subarachnoid hemorrhage (SAH) is a clinically common, acute, critical cerebrovascular disease associated with high mortality. Here, we investigated the effects of electroacupuncture on early brain injury after SAH. We successfully established a Sprague-Dawley rat model of the SAH model, and randomly

Potential role of the peroxynitrate-poly(ADP-ribose) synthetase pathway in a rat model of severe hemorrhagic shock.

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Peroxynitrite (a potent oxidant produced by nitric oxide and superoxide) and hydroxyl radical, reactive oxidants produced during hemorrhagic shock, are potent triggers of DNA single-strand breakage. DNA injury triggers the activation of the nuclear enzyme poly(ADP-ribose) synthetase (PARS), which

Inhibition of poly(ADP-ribose) polymerase attenuates cerebral vasospasm after subarachnoid hemorrhage in rabbits.

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OBJECTIVE Poly(ADP-ribose) polymerase (PARP) is important in modulating inflammation, which has been implicated in cerebral vasospasm after subarachnoid hemorrhage (SAH). We investigated the role of PARP in vasospasm using 3-aminobenzamide (3-AB), a PARP inhibitor, in a rabbit

Potential role of poly (ADP-ribose) polymerase in delayed cerebral vasospasm following subarachnoid hemorrhage in rats.

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Poly (ADP-ribose) polymerase (PARP) serves a key role in several neurological disorders, however, the specific role of PARP in delayed cerebral vasospasm (DCVS) following subarachnoid hemorrhage (SAH) remains unclear. The present study was conducted to clarify the possible mechanism of PARP in DCVS

Protection against hemorrhagic shock in mice genetically deficient in poly(ADP-ribose)polymerase.

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Hemorrhagic shock (HS) and resuscitation leads to widespread production of oxidant species. Activation of the enzyme poly(ADP-ribose) polymerase (PARP) has been shown to contribute to cell necrosis and organ failure in various disease conditions associated with oxidative stress. We tested the

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