phorbol/hemorrhage

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Separate administration of ammonium pyrrolidinedithiocarbamate and phorbol myristate acetate at early and late stages decreases secondary brain injury following intracerebral haemorrhage in rats via the NF-κB pathway

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Introduction: Nuclear factor-kB (NF-kB) is a critical regulator of inflammatory responses following intracerebral haemorrhage (ICH). According to our previous study, inhibiting the p65 subunit at an early stage after ICH can reduce cell

Toxicity of Jatropha curcas phorbol esters in mice.

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Phorbol esters are the main toxins in Jatropha curcas seed and oil. The aim of this study was to assess the acute toxicity of phorbol esters given by intragastric administration and to determine the LD50 for Swiss Hauschka mice. The LD50 and 95% confidence limits for male mice were 27.34 mg/kg body

Hydroxy-octadecenoic acids instead of phorbol esters are responsible for the Jatropha curcas kernel cake's toxicity.

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The toxic kernel cake of Jatropha curcas (KCakeJ) is an emerging health and environmental concern. Although phorbol esters are widely recognized as the major toxin of KCakeJ, convincing evidence is absent. Here, we show that rather than phorbol esters an isomeric mixture of

The protective effect of mepacrine on acute lung edema induced by phorbol myristate acetate in rats.

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A good model of adult respiratory distress syndrome is lung injury induced by phorbol myristate acetate (PMA). In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs. In the isolated lung, saline

The involvement of nitric oxide, nitric oxide synthase, neutrophil elastase, myeloperoxidase and proinflammatory cytokines in the acute lung injury caused by phorbol myristate acetate.

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Phorbol myristate acetate (PMA) causes acute lung injury (ALI). The present study was designed to elucidate the role of nitric oxide (NO), inducible NO synthase (iNOS), neutrophil elastase (NE) and other mediators in the ALI caused by PMA. In isolated rat's lungs, PMA at various doses (1, 2 and 4

Acute alcohol intoxication during hemorrhagic shock: impact on host defense from infection.

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BACKGROUND Acute alcohol intoxication is a frequent underlying condition associated with traumatic injury. Our studies have demonstrated that acute alcohol intoxication significantly impairs the immediate hemodynamic, metabolic, and inflammatory responses to hemorrhagic shock. This study

Lymph from a primate baboon trauma hemorrhagic shock model activates human neutrophils.

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We have reported that toxic factors in intestinal lymph are responsible for acute lung injury and bone marrow suppression and that they contribute to a systemic inflammatory state based on studies in rodent models of trauma-hemorrhagic shock. Rodent models may not completely reflect the responses of

Hemorrhage affects the ability of murine peritoneal macrophages to alkanize intracellular pH in acidic environments.

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Although departures from the normal physiologic pH range, associated with states of shock, injury, and/or infection are thought to impair phagocytic function and chemotaxis, it remains unknown if the ability of the peritoneal macrophage (pMø) to gate H+ is affected following hemorrhagic shock. To

Obligatory roles of protein kinase C and nitric oxide in the regulation of cerebral vascular tone: an implication of a pathogenesis of vasospasm after subarachnoid haemorrhage.

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We previously showed that a canine basilar artery manifested tonic and potent, protein kinase C (PKC)-dependent contractions when nitric oxide (NO) was inhibited. We also reported a linear correlation between chronological changes in the angiographic severity of vasospasm, enhanced PKC, and

Role of protein kinase C in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage.

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This study investigated the role of protein kinase C (PKC) in the pathogenesis of vasospasm after experimental subarachnoid hemorrhage (SAH). PKC activation by intracisternal injection of a phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TP)] induced dose-dependent, slowly developing, severe

Human CalDAG-GEFI deficiency increases bleeding and delays αIIbβ3 activation.

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Affinity regulation of integrin αIIbβ3 for fibrinogen by inside-out signaling plays a critical role in hemostasis. Calcium and diacylglycerol (DAG)-regulated guanine nucleotide exchange factor I (CalDAG-GEFI) was identified as a Rap1-activating molecule, and its role in inside-out αIIbβ3 activation

Entry of gut lymph into the circulation primes rat neutrophil respiratory burst in hemorrhagic shock.

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OBJECTIVE Endothelial cell injury by polymorphonuclear neutrophil (neutrophil [PMN]) respiratory burst after trauma and hemorrhagic shock (T/HS) predisposes subjects to acute respiratory distress syndrome and multiple organ failure. T/HS mesenteric lymph injures endothelial cell and lymph duct

High-dose methylprednisolone prevents vasospasm after subarachnoid hemorrhage through inhibition of protein kinase C activation.

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We have previously shown that the inflammatory process after subarachnoid hemorrhage causes vasospasm. The efficacy of methylprednisolone by suppression of the inflammatory process has been reported, although pharmacological mechanisms have not been clarified. The purpose of this study was to

The effects of IB4, a monoclonal antibody to the CD18 leukocyte integrin on phorbol myristate acetate (PMA)-induced polymorphonuclear leukocyte (PMN) accumulation and endothelial injury in rabbit lungs.

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A model of acute lung injury induced by intravenous phorbol myristate acetate (PMA) is described. The model is characterized by the accumulation of polymorphonuclear leukocytes (PMNs) and a hemorrhagic edema in bronchoalveolar lavage (BAL) fluid when measured 6 h following the administration of PMA

Luminol-chemiluminescence in free peritoneal cells in hemorrhagic shock in rats treated with PAF-receptor-antagonist BN 52021.

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The activity of rat peritoneal cells were assessed by the phorbol mirystinian acetate (PMA)-induced luminol chemiluminescence (LCL). Results in control groups (0 - no manipulation, and I - carotid artery cannulation) were compared with those in the untreated hemorrhagic shock (group II), in the

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