Plasma histamine determination in man and dog following the infusion of plasma substitutes: Models for histamine release under pathophysiological conditions

1973 ◽  
Vol 3 (3) ◽  
pp. 183-184 ◽  
Author(s):  
W. Lorenz ◽  
A. Doenicke ◽  
H. -J. Reimann ◽  
M. Thermann ◽  
R. Tauber ◽  
...  
Keyword(s):  
Histamine Release ◽  
Plasma Histamine ◽  
Plasma Substitutes

Plasma histamine levels during plasmapheresis: difficult interpretation of adverse reactions to plasma substitutes

2001 ◽  
Vol 50 (2) ◽  
pp. 65-67 ◽  
Author(s):  
I. Celik ◽  
W. Krack ◽  
T. Zeiler ◽  
V. Kretschmer ◽  
S. Solinas ◽  
...  
Keyword(s):  
Adverse Reactions ◽  
Plasma Histamine ◽  
Plasma Substitutes

Inhibition of Histamine Release in Experimental Diabetes

1957 ◽  
Vol 191 (1) ◽  
pp. 25-28 ◽  
Author(s):  
Andres Goth ◽  
W. L. Nash ◽  
Mary Nagler ◽  
James Holman
Keyword(s):  
Histamine Release ◽  
Intravenous Injection ◽  
Experimental Diabetes ◽  
Egg White ◽  
Diabetic Rats ◽  
Plasma Histamine ◽  
Elevated Plasma ◽  
Edema Formation

Alloxan diabetic rats failed to show the characteristic edema and elevated plasma histamine levels which follow the intravenous injection of dextran or egg white. Pretreatment with insulin restored the ability of these rats to respond in a normal fashion. Insulin in normal rats promotes edema formation and histamine release induced by dextran or egg white. In contrast to these findings, neither diabetes nor insulin pretreatment exerted an influence on the response of rats to intravenously injected compound 48/80. These results suggest a hitherto unrecognized role of insulin in certain types of inflammation and histamine release.

Definition of histamine release in human subjects and experimental animals using plasma histamine determinations in the whole individual

1979 ◽  
Vol 9 (1) ◽  
pp. 35-35 ◽  
Author(s):  
W. Lorenz ◽  
A. Doenicke ◽  
E. Neugebauer ◽  
B. Schwarz ◽  
A. Schmal ◽  
...  
Keyword(s):  
Histamine Release ◽  
Human Subjects ◽  
Plasma Histamine ◽  
Experimental Animals ◽  
Definition Of

scholarly journals Potentiation of Vancomycin-Induced Histamine Release by Muscle Relaxants and Morphine in Rats

1999 ◽  
Vol 43 (12) ◽  
pp. 2881-2884 ◽  
Author(s):  
Hideki Shuto ◽  
Masanori Sueyasu ◽  
Shuji Otsuki ◽  
Tomoko Hara ◽  
Yuki Tsuruta ◽  
...  
Keyword(s):  
Histamine Release ◽  
Intravenous Injection ◽  
Subcutaneous Administration ◽  
In Vitro Study ◽  
Muscle Relaxants ◽  
Plasma Histamine ◽  
Peritoneal Mast Cells ◽  
Anaphylactoid Reactions

The intravenous injection of vancomycin sometimes causes anaphylactoid reactions, in which histamine release may play a major role. These reactions are more frequently manifested when vancomycin is injected into anesthetized patients. We examined the vancomycin-induced histamine release and the interaction of vancomycin with muscle relaxants or opioid in rats. In an in vitro study with rat peritoneal mast cells, treatment with vancomycin at concentrations of greater than 1.25 mM produced significant histamine release. Tubocurarine, vecuronium, pancuronium, succinylcholine, and morphine up to concentrations of 0.25, 1, 5, 30, and 5 mM, respectively, produced no significant histamine release. However, the nonsignificant histamine release induced by 0.5 mM vancomycin was clearly enhanced by combining vancomycin with any of these agents. In the in vivo study, the intravenous injection of vancomycin significantly increased the plasma histamine levels in rats when vancomycin was injected at 200 mg/kg of body weight (63.2 ± 34.0 ng/ml [mean ± standard deviation]) but not when it was injected at 100 mg/kg (30.8 ± 20.2 ng/ml) compared with that in the saline-treated rats (22.5 ± 11.4 ng/ml). Although the subcutaneous administration of morphine (10 mg/kg) never increased the plasma histamine levels, the intravenous injection of vancomycin (100 mg/kg) 30 min after this morphine treatment markedly increased the plasma histamine levels (56.0 ± 26.9 ng/ml). These findings provide experimental evidence that the combination of muscle relaxants or an opioid with vancomycin may increase the risk of anaphylactoid reactions by enhancing the release of histamine.

Amomum xanthiodes Inhibits Mast Cell-Mediated Allergic Reactions Through the Inhibition of Histamine Release and Inflammatory Cytokine Production

2005 ◽  
Vol 230 (9) ◽  
pp. 681-687 ◽  
Author(s):  
Sang-Hyun Kim ◽  
Tae-Yong Shin
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Proinflammatory Cytokines ◽  
Immunoglobulin E ◽  
Ionophore A23187 ◽  
Allergic Reactions ◽  
Disodium Cromoglycate ◽  
Plasma Histamine ◽  
Intracellular Ca

In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell-mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80-induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)-stimulated tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-κB (NF-κB)-dependent. In addition, AXE decreased PMA plus A23187-induced degradation of IκBα and the nuclear translocation of NF-κB. Our findings provide evidence that AXE inhibits mast cell-derived immediate-type allergic reactions, and that cAMP, intracellular Ca2+, proinflammatory cytokines, and NF-κB are involved in these effects.

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