heart arrest/protease

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A protease-activated receptor 1 antagonist protects against global cerebral ischemia/reperfusion injury after asphyxial cardiac arrest in rabbits.

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Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1 (PAR1). However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the

Aprotinin and deep hypothermic cardiopulmonary bypass with or without circulatory arrest for craniotomy.

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Deep hypothermic cardiopulmonary bypass with or without circulatory arrest has been used to facilitate the surgical repair of complex cerebrovascular lesions. The advantages of deep hypothermia have been tempered by the occurrence of coagulopathy that is associated with substantial morbidity and

Activation of CPP-32 protease in hippocampal neurons following ischemia and epilepsy.

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Recent in vitro studies indicate an involvement of members of the interleukin-1beta converting enzyme (ICE) family of proteases in programmed neuronal cell death. Cell death of hippocampal neurons in animal models of cerebral ischemia and epilepsy shows morphological features of apoptosis and can be

The management of bleeding following surgery requiring hypothermic circulatory arrest.

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BACKGROUND Hemostasis is a significant problem in aortic surgery requiring profoundly hypothermic techniques. Aprotinin, a serine protease inhibitor, reduces blood loss in high-risk coronary and valve surgery, but its use in profound hypothermia is controversial. METHODS To evaluate the role of a

Use of aprotinin in patients undergoing deep hypothermic circulatory arrest: a review.

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Hemostatic derangements continue to be a major clinical challenge during thoracic aortic surgery using deep hypothermic circulatory arrest despite advances in surgical and pharmacologic therapy. Aprotinin, a broad-based, nonspecific serine protease inhibitor has been advocated for prophylactic use

The complement lectin pathway after cardiac arrest.

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The lectin pathway (LP) of the complement system may initiate inflammatory reactions when body tissue is altered. We aimed to investigate levels of the LP proteins in out-of-hospital cardiac arrest patients, and to compare these with healthy individuals. Furthermore, we aimed to clarify whether

Alpha II-spectrin breakdown products serve as novel markers of brain injury severity in a canine model of hypothermic circulatory arrest.

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BACKGROUND The development of specific biomarkers to aid in the diagnosis and prognosis of neuronal injury is of paramount importance in cardiac surgery. Alpha II-spectrin is a structural protein abundant in neurons of the central nervous system and cleaved into signature fragments by proteases

Use of protease inhibitor (trasylol) and heparin in cardiorespiratory resuscitation. II. Gasometric investigations of arterial blood.

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The purpose of the present work was to assess the effect of trasylol--an inhibitor of proteases--and heparin on gasometric values in arterial blood during cardio-respiratory resuscitation. The investigations were carried out on rabbits in three experimental groups. In group I the simplest

Aprotinin to improve cerebral outcome after hypothermic circulatory arrest: a study in a surviving porcine model.

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BACKGROUND Aprotinin is a serine protease inhibitor, which is usually used during cardiac surgery to reduce blood loss. There is evidence that aprotinin has neuroprotective effects during ischemia. We planned this study to evaluate its potential neuroprotective efficacy during hypothermic

A novel subtilisin-like serine protease of Batrachochytrium dendrobatidis is induced by thyroid hormone and degrades antimicrobial peptides.

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Batrachochytrium dendrobatidis (B. dendrobatidis), a chytrid fungus, is one of the major contributors to the global amphibian decline. The fungus infects both tadpoles and adult amphibians. Tadpoles are infected in their keratinized mouthparts, and infected adults exhibit hyperkeratosis and loss of

Calpain inhibition decreases endothelin-1 levels and pulmonary hypertension after cardiopulmonary bypass with deep hypothermic circulatory arrest.

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OBJECTIVE Cardiopulmonary bypass in infants and children can result in cardiopulmonary dysfunction through ischemia and reperfusion injury. Pulmonary hypertension and injury are particularly common and morbid complications of neonatal cardiac surgery. Inhibition of calpain, a cysteine protease, has

Aprotinin, blood loss, and renal dysfunction in deep hypothermic circulatory arrest.

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BACKGROUND The technique of deep hypothermic circulatory arrest (DHCA) for cardiothoracic surgery is associated with increased risk for perioperative blood loss and renal dysfunction. Although aprotinin, a serine protease inhibitor, reduces blood loss in patients undergoing cardiopulmonary bypass,

Effects of aprotinin on acute recovery of cerebral metabolism in piglets after hypothermic circulatory arrest.

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Brain protection during cardiopulmonary bypass and hypothermic circulatory arrest is incomplete. Activation of blood protease cascades may contribute to cellular injury under these conditions. To test this hypothesis, effects of the protease inhibitor aprotinin on recovery of brain energy metabolism

FSLLRY-NH2 Improves Neurological Outcome After Cardiac Arrest in Rats.

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We aimed to evaluate the effect of FSLLRY-NH2, a protease-activated receptor 2 (PAR2) inhibitor, on neurocognitive impairment and hippocampal neuronal degeneration in the setting of asphyxial cardiac arrest (ACA)-induced global cerebral ischemia (GCI) in

Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats.

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Global cerebral ischemia induced neuroinflammation causes neurofunctional impairment following cardiac arrest. Previous studies have demonstrated that the activation of protease activated receptor-2 (PAR-2) contributes to neuroinflammation. In the present study, we aimed to determine

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