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Jon D. Levine - One of the best experts on this subject based on the ideXlab platform.
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sympathetic dependence in bradykinin induced synovial plasma Extravasation is dose related
Neuroscience Letters, 1996Co-Authors: Frederick Jia-pei Miao, W. Janig, Paul Green, Terence J Coderre, Jon D. LevineAbstract:Abstract While previous studies have implicated a role for sympathetic postganglionic neuron-terminals in bradykinin-induced plasma Extravasation, a recent report by Cambridge and Brain [Br. J. Pharmacol., 115 (1995) 641–647] has suggested that it is sympathetic-independent. However, the doses of bradykinin used in these two groups of studies were considerably different. Therefore, in the present study, we characterized the sympathetic-dependence of plasma Extravasation at varying doses of bradykinin. By measuring the concentration of Evans blue dye Extravasation into the joint perfusate following its intravenous injection, bradykinin-induced plasma Extravasation in the knee joint cavity was determined spectrophotometrically. To examine the role of sympathetic postganglionic neuron terminals in mediating bradykinin-induced plasma Extravasation, we used surgical ablation of the lumbar sympathetic chain. Intra-articular perfusion of BK dose-dependently increased synovial plasma Extravasation. After surgical sympathectomy, the dose-response curve for bradykinin-induced plasma Extravasation was significantly shifted to the right. We conclude that at concentrations observed in inflamed tissues (between 10−8 and 10−7 M), bradykinin-induced plasma Extravasation is largely mediated by sympathetic postganglionic neuron terminals.
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modulation of bradykinin induced plasma Extravasation in the rat knee joint by sympathetic co transmitters
Neuroscience, 1993Co-Authors: Paul Green, J Luo, Philip H Heller, Jon D. LevineAbstract:We describe the contribution of various sympathetic post-ganglionic neuron mediators to bradykinin-induced plasma Extravasation in the knee joint of the rat. Co-perfusion of the sympathetic post-ganglionic neuron mediators, norepinephrine or neuropeptide Y with bradykinin resulted in diminished plasma Extravasation. In contrast, the putative sympathetic post-ganglionic neuron mediators of bradykinin-induced plasma Extravasation, namely prostaglandin E2, ATP, the selective adenosine A2-receptor agonist, CGS21680 or the endothelium-derived relaxing factor (as its precursor L-arginine) all greatly enhanced bradykinin-induced plasma Extravasation, but produced little or no increase in plasma Extravasation administered alone. The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma Extravasation induced by bradykinin, and we hypothesize that differential release of mediators from the sympathetic post-ganglionic neuron terminal, in response to varying stimuli, regulates local plasma Extravasation during inflammation.
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increasing sympathetic nerve terminal dependent plasma Extravasation correlates with decreased arthritic joint injury in rats
Neuroscience, 1991Co-Authors: Terence J Coderre, Allan I Basbaum, A K Chan, Clyde A Helms, Jon D. LevineAbstract:This study compared the pharmacology of adrenergic agents that influence plasma Extravasation in normal animals with those agents that influence tissue injury in an inflammatory disease model. Specifically we studied the effects of beta 2- and alpha 2-adrenergic receptor agonists and antagonists on bradykinin-induced plasma Extravasation in normal Sprague-Dawley rats and on joint injury in rats with experimental arthritis. Plasma Extravasation induced by infusion of bradykinin in the rat knee joint was attenuated by the beta 2-agonist salbutamol or by the alpha 2-antagonist yohimbine, and was enhanced by the beta 2-antagonist, ICI-118,551, or by the alpha 2-agonist, clonidine. In rats that had undergone chemical symphathectomy, bradykinin-induced plasma Extravasation was markedly reduced, and there was no enhancement of bradykinin-induced plasma Extravasation by either ICI-118,551 or clonidine. Although ICI-118,551 and clonidine enhanced bradykinin-induced plasma Extravasation, these drugs significantly reduced joint injury in rats with adjuvant-induced arthritis. Neither salbutamol nor yohimbine, however, significantly increased joint injury in the arthritic rats, presumably because arthritis severity is already high in these animals. Consistent with this hypothesis, both salbutamol and yohimbine did significantly increase the joint injury associated with experimental arthritis in Wistar-Kyoto rats, a strain which develops a mild adjuvant arthritis. The fact that increased plasma Extravasation is associated with decreased arthritis severity suggests that plasma Extravasation, a major sign of acute inflammation, contributes to tissue reparative processes.
Lisa Schulmeister - One of the best experts on this subject based on the ideXlab platform.
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vesicant chemotherapy Extravasation management
British journal of nursing, 2011Co-Authors: Lisa SchulmeisterAbstract:Extravasation is a potentially harmful complication of vesicant chemotherapy administration. Although nurses strive to prevent Extravasations from occurring, they cannot always be prevented. Vesicant chemotherapy Extravasations must be promptly detected and appropriately treated in order to reduce the severity of tissue destruction that occurs when vesicants inadvertently enter the tissue. Recently approved treatments have demonstrated safety and efficacy, and have enabled patients to maintain their skin integrity and adhere to their planned chemotherapy treatment schedules. Nurses need to be knowledgeable about advances in Extravasation management so that they can provide optimal care to patients receiving vesicant chemotherapy.
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Extravasation management clinical update
Seminars in Oncology Nursing, 2011Co-Authors: Lisa SchulmeisterAbstract:Objective To present a clinical update on the prevention, detection, and evidence-based management of vesicant chemotherapy Extravasations. Data Sources Journal articles, published and unpublished case reports, personal experience. Conclusion In the 4 years that have elapsed since the publication of the original article, much more is known about vesicant chemotherapy Extravasation, and effective evidence-based treatments now are available. The antidotes sodium thiosulfate for mechlorethamine Extravasations and hyaluronidase for plant alkaloid Extravasations are recommended by the manufacturers of these vesicants and cited in nursing guidelines. The anthracycline Extravasation treatment dexrazoxane for injection, the first and only Extravasation treatment with proven effectiveness, is now available as Totect (dexrazoxane; TopoTarget USA, Rockaway, NJ, USA) in the US and Savene (SpePharm, Amsterdam, The Netherlands) in Europe. Implications for Nursing Practice Nurses who administer vesicant chemotherapy agents need to be aware of the most current evidence (or lack of evidence) for various types of Extravasation treatment. Well-informed nurses are patient advocates and instrumental in detecting, managing, and documenting Extravasations. Most importantly, nurses play a key role in preventing vesicant chemotherapy Extravasations.
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preventing and managing vesicant chemotherapy Extravasations
The journal of supportive oncology, 2010Co-Authors: Lisa SchulmeisterAbstract:Although vesicant chemotherapy Extravasations cannot be entirely prevented, the risk of Extravasation can be reduced by adhering to guidelines for safe vesicant administration. These include engaging patients in Extravasation-prevention efforts, thoroughly assessing patients receiving vesicants, selecting an appropriate administration site for peripheral vesicant administration, and checking for a blood return prior to and during vesicant administration. In addition, whenever an Extravasation occurs or is suspected, vesicant administration must immediately cease, and the appropriate antidote or treatment needs to be promptly administered.
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managing vesicant Extravasations
Oncologist, 2008Co-Authors: Lisa SchulmeisterAbstract:Extravasation is an unusual but potentially severe complication of vesicant chemotherapy administration. Some Extravasation injuries prompt litigation and the oncologist's actions, or lack of action, are scrutinized in the courtroom. This article presents advice and recommendations for treating patients who receive vesicants and includes a discussion of FDA-approved vesicant Extravasation treatments and antidotes.
Tetsuro Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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roles of leukocytosis and cysteinyl leukotriene in polymorphonuclear leukocyte dependent plasma Extravasation
Journal of Leukocyte Biology, 2006Co-Authors: Kazutaka Tokita, Yasuhiro Uchida, Tetsuro YamamotoAbstract:The PMN-dependent plasma Extravasation is a major mechanism of permeability enhancement in acute inflammation. To reveal the pathophysiological significance of the PMN-dependent plasma Extravasation, we prepared a systemic leukocytotic guinea pig model by a daily injection of recombinant human (rh)G-CSF. The extent of the PMN-dependent plasma Extravasation, regarded as the late-phase permeability induced by an intradermal injection of zymosan-activated guinea pig plasma (ZAP) or of rhC5a, clearly correlated to the circulating PMN number. The augmentation of local response following the systemic response seemed to be the characteristic feature of the PMN-dependent plasma Extravasation. We then revealed the molecular mechanism of the PMN-dependent plasma Extravasation. Neither the antihistaminic agent diphenhydramine, nor the bradykinin B2 receptor antagonist, HOE140, affected the ZAP-induced, late-phase Extravasation. In contrast to this, pretreatment with an antagonist of cysteinyl leukotriene (cys-LT) 1 receptor, pranlukast, significantly reduced the late-phase Extravasation. Similarly, it was reduced by pretreatment with a 5-lipoxygenase inhibitor, MK-886, indicating the participation of cys-LTs in the PMN-dependent plasma Extravasation. Histologically, pretreatment with pranlukast or MK-886 did not affect the ZAP-induced PMN infiltration. Consistently, a combined treatment with pranlukast and diphenhydramine completely suppressed the early-phase Extravasation. As pranlukast pretreatment did not affect plasma Extravasation induced by mast cell degranulation, and depletion of platelets did not influence the pranlukast-inhibitable plasma Extravasation induced by rhC5a injection, cys-LTs are most likely produced by transcellular biosynthesis involving PMNs and vascular wall cells.
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Differential role of neutrophils and monocytes during subcutaneous plasma Extravasation
Laboratory Investigation, 2004Co-Authors: Kazutaka Tokita, Tetsuro YamamotoAbstract:We examined the behavior of polymorphonuclear leukocytes (PMNs) and monocytes during subcutaneous plasma Extravasation in guinea-pigs. Plasma Extravasation was induced by intradermal injection of zymosan-activated plasma (ZAP). The degree of Extravasation correlated logarithmically with the concentration of injected ZAP, and was composed of PMN-dependent and -independent components. The latter was mediated primarily by histamine. The former accounted for 40–50% of the total plasma Extravasation, peaked within 15 min, and then rectilinearly decreased with a half-life between 30 and 40 min. Histological examination of skin at 15 min after ZAP injection demonstrated PMN attachment to the luminal surface of venule endothelial cells, without evidence of PMN Extravasation. We next examined whether monocyte infiltration of subcutaneous tissue played a causal role in plasma Extravasation. Monocyte-predominant infiltration was initially caused by an intradermal injection of a monocyte-specific chemotactic factor, the S19 ribosomal protein (RP S19) dimer. Monocyte infiltration did not induce plasma Extravasation even in guinea-pigs with elevated peripheral blood monocyte levels following administration of a macrophage-colony stimulating factor. A simultaneous injection of prostaglandin E_2, a vasodilating agent, with RP S19 dimer also did not induce plasma Extravasation. In contrast, a simultaneous injection of RP S19 dimer with ZAP changed the leukocyte infiltration pattern from PMN-predominant to monocyte-predominant, and almost completely suppressed the PMN-dependent component of the ZAP-induced plasma Extravasation. The lack of plasma Extravasation in the monocyte-predominant pattern was reproduced when a strong monocyte infiltration was induced by an intradermal injection of apoptotic cells. We conclude that leukocyte-induced plasma Extravasation is specific for PMN, and is not due to a physical leakage of plasma during leukocyte emigration. Rather, plasma Extravasation is probably caused by a cognate interaction between PMNs and postcapillary venule endothelial cells.
Dominick Corbi - One of the best experts on this subject based on the ideXlab platform.
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vesicant Extravasation part ii evidence based management and continuing controversies
Oncology Nursing Forum, 2006Co-Authors: Rita Wickham, Constance Engelking, Carmel Sauerland, Dominick CorbiAbstract:Purpose/objectives To review the literature, synthesize current recommendations, and discuss remaining controversies regarding vesicant Extravasation management. Data sources Published evidence-based reports, clinical articles, and anecdotal case reports about antineoplastic and nonantineoplastic vesicant agent management. Data synthesis Prevention of vesicant Extravasation sequelae requires knowledge about vesicant Extravasation manifestations and differentiation of vesicant Extravasation from other local IV site reactions. When evidence is weak or missing, logical application of data-based or empirical management strategies is critical. Actions may include timely administration of subcutaneous or topical antidotes, comfort measures, and surgical interventions to minimize the extent of tissue damage and morbidity should Extravasation occur. Conclusions Vesicant Extravasation and sequelae constitute a complex patient problem. Clinicians should strive to prevent Extravasation or seek to minimize injury should it occur. To this end, clinicians must demonstrate awareness of its risks and use specialized knowledge when administering vesicant agents. Implications for nursing Nurses who administer vesicant agents should understand the nursing and collaborative actions that should be taken to minimize patient morbidity, pain, and disability.
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vesicant Extravasation part i mechanisms pathogenesis and nursing care to reduce risk
Oncology Nursing Forum, 2006Co-Authors: Carmel Sauerland, Rita Wickham, Constance Engelking, Dominick CorbiAbstract:Purpose/Objectives: To review the literature regarding the incidence, current practice, guideline recommendations, nursing management, and knowledge gaps relevant to vesicant Extravasation. Data Sources: Published research articles, books, case reports, and national guidelines. Data Synthesis: Vesicant Extravasation is a relatively rare but signifi cant complication of chemotherapy administration. Extravasation may have a range of consequences that can cause serious physical and quality-of-life effects. Knowledge of risk factors and preventive measures can reduce patient risk. Data-based and empirical management strategies such as immediate local measures (agent withdrawal, comfort measures, and medical interventions) may minimize risk for Extravasation, as well as lead to timely recognition and management and decreased morbidity should Extravasation occur. Conclusions: Vesicant Extravasation and sequelae constitute a complex patient problem that clinicians should strive to prevent or to minimize injury should it occur. To this end, clinicians must demonstrate awareness of risks and use specialized knowledge while administering vesicant agents. Implications for Nursing: Only nurses knowledgeable about Extravasation and skilled in associated techniques should assume responsibility for vesicant administration.
Paul Green - One of the best experts on this subject based on the ideXlab platform.
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sympathetic dependence in bradykinin induced synovial plasma Extravasation is dose related
Neuroscience Letters, 1996Co-Authors: Frederick Jia-pei Miao, W. Janig, Paul Green, Terence J Coderre, Jon D. LevineAbstract:Abstract While previous studies have implicated a role for sympathetic postganglionic neuron-terminals in bradykinin-induced plasma Extravasation, a recent report by Cambridge and Brain [Br. J. Pharmacol., 115 (1995) 641–647] has suggested that it is sympathetic-independent. However, the doses of bradykinin used in these two groups of studies were considerably different. Therefore, in the present study, we characterized the sympathetic-dependence of plasma Extravasation at varying doses of bradykinin. By measuring the concentration of Evans blue dye Extravasation into the joint perfusate following its intravenous injection, bradykinin-induced plasma Extravasation in the knee joint cavity was determined spectrophotometrically. To examine the role of sympathetic postganglionic neuron terminals in mediating bradykinin-induced plasma Extravasation, we used surgical ablation of the lumbar sympathetic chain. Intra-articular perfusion of BK dose-dependently increased synovial plasma Extravasation. After surgical sympathectomy, the dose-response curve for bradykinin-induced plasma Extravasation was significantly shifted to the right. We conclude that at concentrations observed in inflamed tissues (between 10−8 and 10−7 M), bradykinin-induced plasma Extravasation is largely mediated by sympathetic postganglionic neuron terminals.
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modulation of bradykinin induced plasma Extravasation in the rat knee joint by sympathetic co transmitters
Neuroscience, 1993Co-Authors: Paul Green, J Luo, Philip H Heller, Jon D. LevineAbstract:We describe the contribution of various sympathetic post-ganglionic neuron mediators to bradykinin-induced plasma Extravasation in the knee joint of the rat. Co-perfusion of the sympathetic post-ganglionic neuron mediators, norepinephrine or neuropeptide Y with bradykinin resulted in diminished plasma Extravasation. In contrast, the putative sympathetic post-ganglionic neuron mediators of bradykinin-induced plasma Extravasation, namely prostaglandin E2, ATP, the selective adenosine A2-receptor agonist, CGS21680 or the endothelium-derived relaxing factor (as its precursor L-arginine) all greatly enhanced bradykinin-induced plasma Extravasation, but produced little or no increase in plasma Extravasation administered alone. The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma Extravasation induced by bradykinin, and we hypothesize that differential release of mediators from the sympathetic post-ganglionic neuron terminal, in response to varying stimuli, regulates local plasma Extravasation during inflammation.
