Histamine storage

Mast Cells and Basophils. The chief sites of histamine storage are mast cells in the tissues and basophils in blood. These cells synthesize histamine and store it in secretory granules along with a heparin-protein complex. In response to specific antigens, mast cells or basophils are sensitized. Histamine is then secreted from the storage granules. Besides the histamine stores in mast cells and basophils, there is evidence of non-mast cell histamine in some tissues, particularly gastric and intestinal mucosa (60). 

A second important nonneuronal site of histamine storage and release is the enterochromaffin-like (ECL) cells of the fundus of the stomach. ECL cells release histamine, one of the primary gastric acid secretagogues, to activate the acid-producing parietal cells of the mucosa (see Chapter 62). 

The histamine release in the brain, and perhaps other sites, involves exocytosis, as this potassium-induced release is a calcium-dependent process. Histamine is released by many factors. For example, histamine is released by numer-ons drugs including reserpine, codeine, meperidine, hydralazine, morphine, d-tnbocurarine, dextrans, papaverine, and compound 48/80. However, the different histamine storage sites show certain degrees of specificity. For example, the histamine in mast cells is not released following potassium-induced depolarization or by reserpine, factors that release histamine from nenrons. Conversely, compound 48/80, which releases histamine from mast cells, is not able to release histamine from nenrons. 

On the neutrophil, the major selectin expressed is L-selectin. This molecule is constitutively expressed on mature neutrophils but may be expressed at low levels (50% of adult) in neonates. Stimulation of endothelial cells with thrombin, histamine, IL-1 and some other agents induces neutrophils (and other leukocytes) to leave the circulation and adhere to the endothelium. They do this by rolling onto the surface of the endothelium, to which they attach via P-selectin translocated from storage sites in Weibel-Palade bodies to the surface of the endothelium upon activation. The expression of P-selectin is short-lived and is replaced on the endothelial surface by E-selectin (whose expression is also regulated by some cytokines), which continues the endothelial-leukocyte interaction. 

The effect of temperature on histamine formation has been the subject of many studies (Table 6.5). Different studies reported 100-fold variations in histamine concentrations in skipjack tuna allowed to spoil under similar conditions. Although the information in Table 6.5 contains substantial variation, it is obvious that longer storage times and higher temperatures seem to induce histamine production. Control of biogenic amine production by low temperatures (for example 0°C) is consistently observed. 

Relationship of Bacterial Histidine Decarboxylase Production to Histamine Formation. Many studies have been completed with the objective of understanding factors such as storage time and temperature that influence production of histamine in fish. The majority of the investigations have considered only the histamine content of the product, and, consequently, only limited information is available concerning the relationship of histidine decarboxylase formation by the microflora to histamine build-up. 

Edmunds and Eitenmiller (38) in a study of the effect of storage time and temperature on histamine content and histidine decarboxylase activity of several fresh water and marine species... 

Rapid enzyme and histamine formation occurred in the inoculated fillets stored at 24 and 30°C. (Table 2 and Table 3). Maximal histidine decarboxylase activity occurred after 12 h of storage at both temperatures and decreased threafter. Histamine levels reached 520 mg/100 g and 608 mg/100 g at 24 and 30°C after 24 h of storage. At 24°C, the free histidine content decreased to 279 mg/100 g. In the uninoculated fillets, histidine decarboxylase activity was somewhat higher than noted in fillets stored at 15 C however, histamine content remained low after 24 h at 24°C and 30°C. 

Conceivably, histamine might be produced during a fishing voyage when fish are stored under inadequate refrigeration in the storage wells of tuna seiners. 

Sinus problems, hay fever, bronchial asthma, hives, eczema, contact dermatitis, food allergies, and reactions to drugs are all allergic reactions associated with the release of histamine and other autocoids, such as serotonin, leukotrienes, and prostaglandins. Histamine release is frequently associated with various inflammatory states and may be increased in urticarial reactions, mastocytosis, and basophilia. Histamine also acts as a neurotransmitter in the central nervous system (CNS). Upon release from its storage sites, histamine exerts effects ranging from mild irritation and itching to anaphylactic shock and eventual death. 

Virtually all of the histamine found in individual organs and tissues is synthesized locally and stored in sub cellular secretory granules. Within the tissues, the mast cells are the principal sites of storage in the blood, the ba-... 

Drugs, particularly organic bases, may release histamine from mast cells by physically displacing the amine from its storage sites. Morphine, codeine, d-tubocu-rarine, guanethidine, and radiocontrast media can release histamine from mast cells. Basic polypeptides, such as bradykinin, neurotensin, substance P, somatostatin, polymyxin B, and the anaphylatoxins resulting from complement activation, also stimulate histamine release. Venoms often contain basic polypeptides as well as the histamine-releasing enzyme phospholipase A. 

The effects of histamine on body tissues and organs can be diminished in four ways inhibition of histamine synthesis, inhibition of histamine release from storage granules, blockade of histamine receptors, and physiological antagonism of histamine s effects. Of these approaches, only the inhibition of histamine synthesis has not been employed clinically. The focus of this chapter is on Hi histamine receptor antagonists it provides a brief overview of the H2 blockers and the inhibitors of histamine release. More details can be found in Chapters 39 and 40. 

Histamine metabolism differs from that of classical neurotransmitters because histamine is so widely distributed in the body. The highest concentrations in human tissues are found in the lung, stomach, and skin (upto 33 ug/g tissue). Histamine metabolic pathways are simple histamine is produced from histidine in just one step (see figure 4.11). The principal production takes place in the mast cells of the peritoneal cavity and connective tissues. The gastric mucosa is another major storage tissue. Histamine can be found in the brain as well. 

Lack of histamine-immunoreactive mast cells suggests that the observed changes occur in the neuronal pool. Obviously, the postmortem time and storage... 

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