• YAKHAK HOEJI
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• v.51 no.1
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• pp.63-67
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• 2007

To investigate the relation between extracellular Ca$^{2+}$ and histamine release, we observed agonist-induced histamine release from RBL 2H3 mast cells in the presence or absence of extracellular Ca$^{2+}$ concentration. Histamine release induced by melittin and thapsigargin were greater in the presence of extracellular Ca$^{2+}$ than in the absence of extracellular Ca$^{2+}$. Econazole-induced histamine release had nothing to do with extracellular Ca$^{2+}$, whereas arachidonic acid-induced histamine release increased in the absence of extracellular Ca$^{2+}$. Calmodulin antagonists did not affect melittin-induced histamine release but they may potentiate arachidonic acid-induced histamine release. These data suggest that arachidonic acid-induced histamine release may be mediated via Ca$^{2+}$-independent pathway and may be potentiated by the block of Ca$^{2+}$-dependent pathway.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.14 no.3
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• pp.122-129
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• 1981

Histamine has been known to be one of the causative materials of allergy-like food poisoning from eating of the meat of the dark-fleshed fishes. In the previous study, we had reported the changes of histamine contents fin three kinds of the dark-fleshed fishes. The present paper was also conducted to investigate the changes of the histamine contents in the mackerel pike, and compare with the white-fleshed fish, spanish mackerel, under different condition of storage and processing. The formation of histamine in the muscle of mackerel pike was markedly higher than spanish mackerel. Referring to temperature, the formation of histamine at $12^{\circ}C$ was observed more rapid than that at $2^{\circ}C$. In the muscle of mackerel pike, the histamine contents reached the levels of 98.3mg/100g for at the storage for 5 days at $12^{\circ}C$. But in that of spanish mackerel, the content showed the level of 4.9mg/100g at the storage 7 days at $12^{\circ}C$. The histamine contents in sun dried products of the samples were higher than those of rat-materials, salted or hot-air dried products.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.83-91
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• 1996

The present study was designed to determine the effect of hydrocortisone on CA secretion evoked by histamine from the isolated perfused rat adrenal glands. Histamine (150 ug) given into an adrenal vein produced significantly CA secretion from the rat adrenal medulla. This histamine-evoked CA secretion was enhanced markedly by the pretreatment with the natural glucocorticoid hydrocortisone (30 uM) or the synthetic glucocorticoid dexamethasone 30 (uM) for 20 min, respectively. Hydrocortisone-induced potentiation of CA secretion evoked by histamine was inhibited by preloading with heparin (3.56 U/ml), an $IP_3$ receptor antagonist while more enhanced by forskolin (0.2 uM), a potent stimulator of adenylate cyclase. From the experiment result taken together, it is thought that hydrocortisone (glucocorticoids) can enhance the releasing effect of CA evoked by histamine from the isolated perfused rat adrenal medulla, which seems to be associated to accumulation of inositol phosphate as well as cyclic AMP in the rat adrenomedullary chromaffin cells.

• Korean Journal of Pharmacognosy
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• v.9 no.1
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• pp.41-47
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• 1978

Total saponins and ether extracts of red and white ginseng were obtained and their effects on blood pressure in cat and their histamine liberating activities in rabbits were measured. 1) Ether extract of red ginseng showed a transient hypotensive effect and subsequently showed a remarkable and persistent hypotensive effect, whereas other three fractions, such as saponin fractions of red and white ginseng and ether extract of white ginseng showed only a initial transient hypotensive effects. 2) Histamine levels liberated into blood after administration of each fractions measured by the bioassay with guinea pig ileum. Ether extract of red ginseng immediately increased histamine contents in plasma but the histamine levels decreased to normal level within 10min in spite of decreased blood pressure was sustained. Although white ginseng saponin lowered blood pressure immediately when it is administered, histamine release was observed after 10min. The results suggest that hypotensive effects of ginseng seems to have no correlation with the histamine liberating activity. Ginseng appears to show hypotensive effect via some other mechanisms.

• Tuberculosis and Respiratory Diseases
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• v.39 no.3
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• pp.228-235
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• 1992

Background: Although polymorphonuclear leukocytes (PMN) are important in protecting the airways and alveolar surfaces, there is evidence that they can also injure the lung while exercising their defensive role. However it has been unclear whether PMN-induced pneumocyte injury is mediated by their direct cytotoxic effect on target cells or by PMN-derived cytotoxic mediators. On the other hand histamine was known not only to act as an important chemical mediator participated in the pathogenesis of some atotic and allegic disorders, but also to have an inhibitory effect on normal PMN functions. Method: To study the mechanism by which PMN induce pneumocyte injury, we cocultured PMN from four healthy nonsmokers or their PMN-derived supernatants (PMN-SPN) with monolayers of $^{51}Cr$-labeled human A549 pneumocytes and compared PMN-and PMN-SPN-mediated pneumocyte injuries measured by $^{51}Cr$ release assay. We also compared the effects of histamine on each pneumocyte injury. Results: 1) PMN-SPN showed more injurious effect on A549 pneumocytes than that of PMN itself regardless histamine pretreatment of PMN. 2) Pneumocyte injury by PMN with histamine pretreatment was increased or decreased compared with that by PMN without histamine pretreatment, according to histamine concentrations, and PMN stimulating agents and their concentrations. 3) Pneumocyte injury by PMN-SPN with histamine pretreatment tended to be decreased compared with that by PMN-SPN without histamine pretreatment. Conclusion: Our results suggest that PMN-SPN may play more important role in mediating pneumocyte injury than PMN itself and that histamine may partially play a protective role on PMN-induced pneumocyte injury. Alternatively we conclude that the effects of histamine on PMN-induced pneumocyte injury may be affected by microenvironment in vivo.

• The Korean Journal of Physiology
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• v.2 no.2
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• pp.33-43
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• 1968

Histamine, 0.5 mg as histamine base in 4 ml of normal saline solution, was injected into rabbits anesthetized with nembutal and the mean blood pressure was kept in the range of $52{\sim}80\;mmHg$ for over one hour by supplemental additions. Following the injection of the test substances, 300 mg of urea and 200 mg of antipyrine intravenously, serial blood samples were obtained from the femoral artery and the internal jugular vein at $0.5{\sim}3$ minutes interval. The decreasing patterns in the concentrations of arterial and venous blood plasma samples were compared with each other. The ratio of the concentration of brain tissue to that of the final arterial plasma was also studied. By these measures the degrees of penetration of the test substances in the brain in the control and in the histamine treated rabbits were observed. The concentrations of antipyrine and urea in the arterial blood plasma were decreasing exponentially with respect to the time elapsed. The venous concentrations were anticipated to increase initially and to cross the arterial concentration curve in the point of equlibrium between the plasma and the tissue. On the contrary to the expectation venous concentration also revealed the decreasing tendency similar to that of arterial plasma. The similarity between these two curves, arterial and venous, would be atributable to the fact that the cerebral blood flow rate was large enough and the rising phase in the venous concentration curve was instantly over before serial blood samples were taken. Inspite of some similarity in the decreasing tedency in both concentration curves there were appreciable discrepancies between the arterial and venous plasma which would reflect the situation far from the equlibria among several compartments in the brain. Changes in plasma potassium levels caused by the injection of histamine or bleeding were observed, too. Using 8 rabbits as the control and 12 rabbits for the histamine treated group following results were obtained: 1. Both of the concentration curves, arterial and venous, declined rapidly at_first and slowly later on and approached same equilibrium concentration with the passage of time after a single injection. The time at which attained the same concentration was $2.0{\pm}0.54\;min.$ in the control and $4.3{\pm}1.92\;min.$ in the histamine treated group with respect to antipyrine. On the other hand in the case of urea they were $2.4{\pm}0.59\;min.$ in the control and $4.4{\pm}1.31\;min.$ in the histamine group, respectively. In the histamine treated group enlarged spaces for distribution of test substances were postulated. 2. The concentration of antipyrine in the brain tissue water revealed no significant differences between the control and experimental groups, showing $212{\pm}40.2\;mg/l$ in the control and $206{\pm}64.1\;mg/l$ in the histamine treated group. On the other hand urea revealed higher value in the histamine treated group than in the control, showing an enhanced penetration of urea into the tissue after injection of histamine. Urea concentration in the brain water was $32.3{\pm}3.36\;mg%$ in the control and $39.2{\pm}4.25\;mg%$ in the histamine treated group. 3. The distribution ratio of antipyrine in the brain tissue was very close to unity in the histamine treated animals as well as in the control. 4. The average of the distribution ratio of urea in the control animals was 0.77 and it showed the presence of blood-brain barrier with regard to urea. However in the histamine treated animals the distribution ratios climbed up to 0.86 and they were closer to unity than in the control animals. Out of 12 cases 5 were greater than 0.9 and 8 exceeded 0.85. It appeared that histamine enhanced the penetration of urea through the barrier. 5. Histamine injection and or hemorrhage caused an elevation of the concentration of potassium in plasma. In the event that histamine and hemorrhage were applied together the elevation of potassium exceed the elevation seen at the histamine alone. There was no evidence that the leakage of potassium from the brain tissue was dominant in comparison with the general leakage from the whole body.

• The Korean Journal of Pain
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• v.5 no.2
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• pp.234-238
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• 1992

We compared the effectiveness of vasodilator therapy with histamine and stellate ganglion block(SGB) for the treatment of sudden sensoryneural hearing impairment retrospctively. 24 patients were treated with histamine and nicotinic acid(histamine group), and 30 patients were treated with SGB(SGB group). Corticosteroids and low molecular weight dextran($Rheomacrodex^{(R)}$) were given to all patients. The degree of hearing impairment and the evidence of improvement were checked with audiogram. 52.8%(10 out of l9 follow-up ckecked patients) of patients in histamine group and 56.7%(17 out of 30) of patients in SGB group had improved within three weeks of treatment, which means both histamine and SGB are equally effective. As a consequence, we concluded that SGB ia a good substitute for histamine as a vasodilator therapy for sudden sensoryneural hearing impairment with minimal complication, few absolute contraindications, and simple and safe technique.

• Microbiology and Biotechnology Letters
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• v.33 no.4
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• pp.260-266
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• 2005

IgE-dependent histamine releasing factor (HRF), previously known as P23/P21 or translationally controlled tumor protein (TCTP), induces the degranulation of histamine in mast cell and basophil. Yeast two hybrid results showed that HRF interacts with the alpha subunit of Na, K-ATPase, suggesting that HRF is a regulator for governing the activity of Na, K-ATPase. In this study, we examined the interaction of HRF and Wa,K-ATPase after treatments of various PKC isotype inhibitors. Membrane fractionation, pull-down assay and immunoprecipitation results showed that PKC $\alpha,\;PKC\;\beta,\;\delta$ subunits are involved in the phosphorylation of HRF. However, these results did not correlate with the results of histamine release assay since histamine release assay results suggested that some PKC isotype inhibitors induced the histamine release in RBL-2H3 cell.

• Microbiology and Biotechnology Letters
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• v.33 no.3
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• pp.231-235
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• 2005

Histamine-releasing factors (HRFs) are soluble mediators that can release histamine and other mediators from basophils and mast cells and their activity can vary, depending on the type of IgE. The activity of HRFs is affected by the presence of IgE, although HRF is thought to bind to a specific receptor other than IgE. Until now, HRF signaling pathway including its receptor remains unclear in spite of numerous studies. Since there had been many reports about reactive oxygen species (ROS) as a signaling molecule rather than as a by-product of metabolism, we investigated the possibility of ROS as an intracellular messenger involved in HRF-mediated histamine degranulation. In RBL-2H3 cells, ROS was generated by HRF using $H_2O_2$-sensitive fluorescence of fluorescent 2', 7'-dichlorofluorescein ($H_2DCFDA$). These effects were blocked by anti-oxidant N-acetylcysteine (NAC). These results suggest that ROS generation could play a role as an intracellular messenger in histamine release by HRF.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.313-322
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• 1998

In a myocyte freshly isolated from rabbit cerebral artery, the characteristics of $Ca^{2+}$ release by histamine or caffeine were studied by microspectrofluorimetry using a $Ca^{2+}-binding$ fluorescent dye, fura-2. Histamine (5 ${\mu}M$) or caffeine (10 mM) induced a phasic rise of cytoplasmic free $Ca^{2+}$ concentration $([Ca^{2+}]_C)$ which could occur repetitively with extracellular $Ca^{2+}$ but only once or twice in $Ca^{2+}-free$ bathing solution. Also, the treatment with inhibitor of sarcoplasmic reticulum $Ca^{2+}-ATPase$ suppressed the rise of $[Ca^{2+}]_C$ by histamine or caffeine. In $Ca^{2+}-free$ bathing solution, short application of caffeine in advance markedly attenuated the effect of histamine, and vice versa. In normal $Ca^{2+}-containing$ solution with ryanodine (2 ${\mu}M$), the caffeine-induced rise of $[Ca^{2+}]_C$ occurred only once and in this condition, the response to histamine was also suppressed. On the other hand, in the presence of ryanodine, histamine could induce repetitive rise of $[Ca^{2+}]_C$ while the amplitude of peak rise became stepwisely decreased and eventually disappeared. These results suggest that two different $Ca^{2+}-release$ mechanisms (caffeine-sensitive and histamine-sensitive) are present in rabbit cerebral artery myocyte and the corresponding pools overlap each other functionally. Increase of $[Ca^{2+}]_C$ by histamine seems to partially activate ryanodine receptors present in caffeine-sensitive pool.