Comparison of Cellular Mechanisms Underlying Histamine Release From Rat Mast Cells Induced by Ionic and Nonionic Radiographic Contrast Media

Itoh, Yoshinori; Sendo, Toshiaki; Yano, Tomoaki; Saito, Mami; Kubota, Takeshi; Oishi, Ryozo

doi:10.1097/01.rli.0000128656.13658.60

Cited by 6 publications

(6 citation statements)

References 38 publications

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“…The extremely low K D value found (18.7 mM) questions the specificity of these IgE for this patient [104]. It has recently been suggested that the higher histamine release from rat pulmonary mast cells found in vitro with ionic CM may result from the reduction in cAMP/A kinase pathway by ionic CM whereas the secretory phospholipase A 2 contributes to both ionic-and non-ionic CM-induced histamine release [113]. It has recently been suggested that the higher histamine release from rat pulmonary mast cells found in vitro with ionic CM may result from the reduction in cAMP/A kinase pathway by ionic CM whereas the secretory phospholipase A 2 contributes to both ionic-and non-ionic CM-induced histamine release [113].…”

Section: Pros Consmentioning

confidence: 75%

“…Finally, the complement system was not found to be involved in histamine release [104,112]. It has recently been suggested that the higher histamine release from rat pulmonary mast cells found in vitro with ionic CM may result from the reduction in cAMP/A kinase pathway by ionic CM whereas the secretory phospholipase A 2 contributes to both ionic-and non-ionic CM-induced histamine release [113]. In conclusion, there are several convergent data to suggest that some reactions to CM may belong to the hypersensitivity type-I.…”

Section: Pros Consmentioning

confidence: 95%

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Allergy‐like reactions to iodinated contrast agents. A critical analysis

Idée

Pinès

Prigent

et al. 2005

Fundamemntal Clinical Pharma

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Allergy-like reactions may occur following administration of iodinated contrast media (CM), mostly in at-risk patients (patients with history of previous reaction, history of allergy, co-treated with interleukin-2 or beta-blockers, etc.) but remain generally unpredictable. Severe and fatal reactions are very rare events. All categories of CM may induce such reactions, although first generation (high osmolar CM) have been found to induce a higher rate of adverse events than low osmolar CM. However, no differences were found between the two categories of CM with respect to mortality. Delayed reactions can also occur. There are no differences between the various categories of CM except for non-ionic dimers, which are more likely to induce such effect. Numerous clinical studies have evaluated the prophylactic value of drugs (mostly antihistamines and corticosteroids). Results are unclear and highly variable. Any prevention depends upon the mechanism involved. However, the mechanism of CM-induced allergy-like reaction remains disputed. Relatively recent data revived the hypothesis of a type-I hypersensitivity mechanism. Positive skin tests to CM have been reported. However, the affinity of IgE towards CM has been found to be very low in the only study which actually evaluated it. Other pathophysiological mechanisms (involving direct secretory effects on mast cells or basophils, or activation of the complement system associated or not with the plasma contact system) are also much debated. Anaphylaxis and anaphylactoid reactions are, in the end, clinically undistinguishable.

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Section: Pros Consmentioning

confidence: 75%

Section: Pros Consmentioning

confidence: 95%

Allergy‐like reactions to iodinated contrast agents. A critical analysis

Idée

Pinès

Prigent

et al. 2005

Fundamemntal Clinical Pharma

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“…Apart from adolescent effects, it would be of interest to examine the contribution of the arachidonic acid pathway to ethanol tolerance in both ages as studies have shown arachidonic acid and cPLA2 to be decreased following ethanol exposure (Basavarajappa et al 1998; Rubin 1989). However, cPLA 2 /AA inhibition does not exclusively modulate PKC, as AA activity also influences monoaminergic (Hellstrand et al 2002; LaBelle & Polyak 1998; T. et al 1997), cholinergic (Almeida et al 1999) and histaminergic (Itoh et al 2004) transmission. Future studies aim to investigate the specific relationship between AA and PKC in ethanol sensitivity through co-modulation of systems involved in the cPLA/AA cascade…”

Section: Discussionmentioning

confidence: 99%

Molecular and behavioral characterization of adolescent protein kinase C following high dose ethanol exposure

et al. 2013

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Rationale Ethanol is commonly used and abused during adolescence. Although adolescents display differential behavioral responses to ethanol, the mechanisms by which this occurs are not known. The PKC pathway has been implicated in mediating many ethanol-related effects in adults, as well as GABAA receptor regulation. Objectives The present study was designed to characterize cortical PKC isoform and GABAA receptor subunit expression during adolescence relative to adults as well as assess PKC involvement in ethanol action. Results Novel PKC isoforms were elevated, while PKCγ was lower during mid-adolescence relative to adults. Whole cell lysate and synaptosomal preparations correlated for all isoforms except PKC δ In parallel, synaptosomal GABAA receptor subunit expression was also developmentally regulated, with GABAAR δ and α4 being lower while α1 and γ2 were higher or similar, respectively, in adolescents compared to adults. Following acute ethanol exposure, synaptosomal novel and atypical PKC isoform expression was decreased only in adolescents. Behaviorally, inhibiting PKC with calphostin C, significantly increased ethanol-induced loss of righting reflex (LORR) in adolescents but not adults, whereas activating PKC with phorbol-dibutyrate was ineffective in adolescents but decreased LORR duration in adults. Further investigation revealed that inhibiting the cytosolic phospholipase A2/arachidonic acid (cPLA2/AA) pathway increased LORR duration in adolescents, but was ineffective in adults. Conclusions These data indicate that PKC isoforms are variably regulated during adolescence and may contribute to adolescent ethanol-related behavior. Furthermore, age-related differences in the cPLA2/AA pathway may contribute to age-related ethanol’s effects on novel and atypical PKC isoform expression and behavior.

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“…The role of the ionic strength of CM has also been investigated. Although some studies found that ionic CM are more toxic than non‐ionic CM, 25–28,37,38,41,45,49,51 others have not found such differences 29,34,44,47,48 . These discrepancies could be due to peculiarities in the methodology used in the different studies (e.g.…”

Section: Cellular Toxicity Of Contrast Media: Cell Culture Modelsmentioning

confidence: 97%

“…Numerous studies have investigated the toxicity of CM in cell culture models. Various cell types have been investigated, including renal epithelial (tubular) cells, [25][26][27][28][29][30][31][32][33][34][35][36] endothelial cells, 26,37-46 mesangial cells, 32,47,48 pulmonary mast cells, 49 smooth muscle cells, 50 hepatic cells, 32 human fibroblasts, 47 human neutrophils 51 and human embryonic kidney cells. 36,52 Table 1 summarizes the findings of these studies.…”

Section: Cellular Toxicity Of Contrast Media: Cell Culture Modelsmentioning

confidence: 99%

Pathophysiology of renal tissue damage by iodinated contrast media

Sendeski

2011

Clin Exp Pharma Physio

149

119

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1. The present review focuses on the cytotoxic effects of iodinated contrast media (CM) that are shared by all types of CM. 2. Although the clinical nephrotoxicity of CM has been progressively improved, all currently available CM still possess a level of cytotoxicity, which is probably caused by iodine. 3. The toxicity caused by specific CM properties, such as osmolarity, viscosity and ionic strength, can be differentiated from the cytotoxicity common to all CM in studies using cell culture, isolated blood vessels and isolated tubules. 4. The cytotoxicity induced by CM leads to apoptosis and cell death of endothelial and tubular cells and may be initiated by cell membrane damage, together with oxidative stress. 5. Cell damage may be aggravated by factors such as tissue hypoperfusion and hypoxia, properties of individual CM, such as ionic strength, high osmolarity and/or viscosity, and clinically unfavourable conditions. 6. Clinically detectable renal failure may result from the summation of all these factors.

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Comparison of Cellular Mechanisms Underlying Histamine Release From Rat Mast Cells Induced by Ionic and Nonionic Radiographic Contrast Media

Cited by 6 publications

References 38 publications

Allergy‐like reactions to iodinated contrast agents. A critical analysis

Allergy‐like reactions to iodinated contrast agents. A critical analysis

Molecular and behavioral characterization of adolescent protein kinase C following high dose ethanol exposure

Pathophysiology of renal tissue damage by iodinated contrast media

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