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PubMed1978

Pruritus as a manifestation of systemic disorders.

A significant internal disorder is present in only a limited number of patients with essential pruritus. The mechanisms for the production of pruritus in these disorders are poorly understood and frequently are unrelated to liberation of histamine. Proteolytic enzymes in lymphoproliferative disorders, bile acids in obstructive hepatobiliary disease, parathyroid hormone in chronic renal failure, and prostaglandins and kinins are but a few of the chemicals that may ultimately be responsible for the development of pruritus in these and other purely cutaneous disorders. Patients with essential pruritus should have a comprehensive physical and laboratory evaluation, but psychologic, environmental, and other factors must be considered when thorough clinical evaluation is unrewarding. Treatment should be directed towards elimination of the underlying alteration, control of the additional factors, and alleviation of the symptom.

Biliary Tract Diseases↗
PubMed1996

[Occupational asthma in an agricultural setting].

The prevalence of asthma in a farming environment is significant (from 3-7.7% according to various studies). The clinical picture has not been specified. The responsible agents are multiple and polysensitization frequent. Numerous substances of vegetable origin may be a cause, pollens, moulds, cereals, oil and protein producing plants, fibrous textiles, diverse plants and wood, etc. Amongst substances of animal origin the most frequent allergens incriminated are: allergens from mammals (horses, cattle, pigs), allergens from chickens and birds, arthropod allergens, insect allergens. Amongst chemical products those which are at risk to the respiratory system include insecticides, herbicides, fungicides, antibiotics and antiparasites. The diagnosis of the occupational character of asthma is sometimes difficult because of other causes of lung diseases in farm workers. The aetiological diagnosis is achieved by the clinical history, cutaneous tests, a level of specific serum IgE, and bronchial provocation tests which contrary to asthma in the industrial environment are not fundamental to the diagnosis except where chemical products are suspected. The mechanisms are sometimes intricate (IgE dependant mechanisms, non-specific liberation of histamine, activation of complement, intervention of endotoxins and pharmacological mechanisms...). Prevention may be carried out on behalf of the victim (for example wearing filtration masks in dusty work) and also carry out various methods to reduce the level of exposure to the allergen.

Agriculture↗
PubMed1979

Microvascular permeability to macromolecules in thermal injury.

Thermal injury of the skin causes an inflammatory reaction with formation of edema, mainly due to vasodilatation, increased extravascular osmotic activity and increased microvascular permeability to macromolecules. These reactions are due to local and systemic effects . At the site of injury heat itself causes microvascular damage. Vascular changes may also be mediated by vasoactive compounds, e.g. liberation of histamine and increased synthesis of prostaglandins. Reflex mechanisms elicited via the nervous system must also be considered. Morphological studies revealed increased number of vacuoles, a large number of open endothelial intercellular junctions and changes of the interstitial tissue at the site of thermal injury. The vascular reactions described can be modified by drugs, especially indomethacin which inhibits the synthesis of prostaglandins and drugs which competitively antagonize the effects of histamine at H2-receptors.

Animals↗
PubMed1975

[Pulmonary edemas due to acute heroin poisoning].

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.

Acute Disease↗
PubMed1977

Release of histamine and formation of prostaglandins in human lung tissue and rat mast cells.

Release of histamine and prostaglandins (PGs) from human lung tissue and rat mast cells was investigated. Passively sensitized lung fragments released PGE, PGF2alpha and the 15-ketodihydro metabolites into the media with time alone. Antigen challenge liberated 20% tissue histamine and there was a twofold increase in PGs. Twice as much PGF2alpha as PGE was found. beta-Adrenergic agonists inhibited the anaphylactic release of mediators and this action was blocked by propranolol. Both PGF2alpha and PGE were consistently found in the mast cell media, demonstrating that mast cells can synthesize PGs. Anaphylaxis induced a marked liberation of histamine but not of PGs. The results indicate that the release of histamine may precede the major release of PGs and suggest that the bulk of PGs may derive from cells in the proximity of the mast cells.

Adrenergic Agonists↗
PubMed1986

Amine transport in isolated rat mast cells treated with betaadrenoceptor blocking drugs.

Histamine and serotonin uptake in isolated rat mast cells is decreased in the presence of betaadrenoceptor blocking (BAB) drugs. Such inhibition is dose-dependent and is evidently higher for the inhibition of serotonin uptake. The most potent drugs were the highly lipophilic compounds Kö 1124 and propranolol. No difference was found among the various BAB drugs in their ability to decrease histamine uptake. It is evident from the ratio between histamine and serotonin liberation on one side, to the uptake of both amines in mast cells on the other side, that with the exception of Kö 1124, all investigated BAB drugs possesses higher inhibition of extracellular amine uptake in comparison with histamine and serotonin liberation. Such an effect might be a result of a primary interaction of BAB drugs with mast cells at the plasma membrane.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of exogenous and endogenous histamine on the respiratory system.

There is a statistically strong correlation between the increase of the histamine concentration in the arterial plasma and the increase of airway resistance. The histamine causes a reflex bronchoconstriction on the sensory receptors. Histamine in low concentration increases the unspecific reaction in the bronchial system. This can also be achieved using low concentrations of allergen aerosols. Patients with chronic obstructive bronchitis show high concentrations of histamine in the sputum. The bronchoconstrictive potency of this histamine was found to be not always active. Higher concentrations of histamine can be liberated by washing the inner surface of the bronchial tree. Histamine injected in similar concentrations as that measured in the sputum causes bronchoconstriction. There should be high concentrations of histamine receptors as well as mast cells near the surface of the mucosa of the bronchial wall. There are many questions remaining open, which will be discussed.

Airway Resistance↗
PubMed1983

Compound 48/80 and substance P induced release of histamine and serotonin from rat peritoneal mast cells.

The effect of substance P and compound 48/80 on histamine and serotonin release from not isolated and isolated mast cells have been compared in experiments in vitro. The response of not isolated and isolated mast cells were virtually identical. The release of both amines, in response to 48/80 and substance P, was dose-dependent. The percentage of histamine released by 48/80 was significantly higher than the percentage of serotonin, the difference being higher at lower concentrations of compound 48/80 after 15 min of incubation. Substance P also showed a tendency to higher efficiency for histamine than for serotonin release. In contrast to 48/80, the dose-response curves for histamine and serotonin release were parallel. These results support the view that the ratio between histamine and serotonin release depends on the liberator used. They also showed that this ratio can depend on the concentration of the agent inducing secretion. The results indicate that substance P as well as 48/80 act rather selectively as histamine liberators and that there is some difference in releasing properties of 48/80 and substance P.

Animals↗
PubMed1983

Release of intestinal diamine oxidase by histamine in rats.

Diamine oxidase activity was measured in the intestinal mucosa, lymph, and in the serum of rats, to determine whether histamine, a substrate of diamine oxidase, liberates this enzyme from its mucosal storage site(s). Histamine induced a sharp rise in intestinal lymph flow, lymph protein, and lymph diamine oxidase, lasting less than 1 h after the histamine injection. The rise in lymph diamine oxidase activity was dose dependent over a narrow concentration range (0.05-0.2 mmol/kg, i.v. and 0.15-0.6 mmol/kg i.d.). It did not correlate with the dose dependent increase in lymph flow or lymph protein. A single maximal intraduodenal dose of histamine caused a 41.6-fold increase in the lymph diamine oxidase activity and a 2.4-fold increase in the serum enzyme level temporarily. A second injection of histamine, 2 h after the first, resulted in a comparatively smaller increase in the lymph enzyme. The extent of the reduction was dependent on the magnitude of the first injection. The results suggest that histamine causes a limited liberation of diamine oxidase from the intestinal mucosa. The function of this enzyme release may be a protective response by the mucosa to reduce toxic levels of free histamine, either liberated by the mucosal tissue or absorbed from the intestinal lumen.

Amine Oxidase (Copper-Containing)↗
PubMed1997

Investigations into the role of nitric oxide and the large intracranial arteries in migraine headache.

Previous studies suggest that nitric oxide (NO) is involved in headaches induced by i.v. infusion of the vasodilator and NO donor glyceryl trinitrate (GTN) in healthy subjects. Extending these studies to sufferers of migraine without aura, it was found that migraineurs experienced a stronger headache than non-migraineurs. In addition, most migraineurs experienced a delayed migraine attack at variable times (mean 5.5 h) after GTN provocation. This biphasic headache response in migraineurs may be linked to hypersensitivity in the NO-cGMP pathway. Thus, compared to controls, migraineurs were found to be more sensitive to GTN-induced intracranial arterial dilatation, which is known to be mediated via liberation of NO and subsequent synthesis of cGMP Furthermore, histamine infusions in migraineurs induced headache responses and intracranial arterial responses resembling those induced by GTN in migraineurs. Histamine is known to liberate NO from the endothelium via stimulation of the H1 receptor, which is present in the large intracranial arteries in man. Because both immediate histamine-induced headache and intracranial arterial dilatation and delayed histamine-induced migraine are blocked by H1-receptor blockade, a likely common pathway for GTN and histamine-induced headaches/migraines and intracranial arterial responses may be via activation of the NO-cGMP pathway. The delay in the development of these experimental migraines may reflect activation of multiple physiological processes. The intracranial arteries of migraineurs were found supersensitive to the vasodilating effect of GTN (exogenous NO). This relates to clinical findings suggesting dilatation of the large intracranial arteries on the headache side during spontaneous migraine attacks. The function of arterial regulatory mechanisms involving NO in migraine was therefore studied. In peripheral arteries, no endothelial dysfunction of NO was found and cardiovascular and intracranial arterial sympathetic function was normal. A mild parasympathetic dysfunction may be involved and may, via denervation supersensitivity, be responsible for the observed supersensitivity to NO. Another possibility is that NO initiates a perivascular neurogenic inflammation with liberation of vasoactive peptides. NO also mediates a variety of other physiological phenomena. One of these, the pain-modulating effect observed in animals, was evaluated in a human study using GTN infusion and measurements of pain thresholds. No definite effects of GTN were demonstrated. The precise mechanisms involved in NO-triggered migraines and which part of the NO-activated cascade that is involved remain to be determined. The possibilities for pharmacological stimulation and/or inhibition of several steps of the NO-activated cascade increase rapidly and soon may be available for human studies.

Cerebral Arteries↗
PubMed1998

Increased histamine content in Ca2+-ionophore A23187-activated human blood platelets.

Stimulation of human blood platelets with Ca2+-ionophore A23187 at the concentrations of 0.5, 1, 2 and 3 micromol/ litre increased the total platelet histamine content from 25 ng (resting platelets) to 35, 40, 42 and 47 ng/10(8) platelets, respectively. The maximum rise was 90% , while in the presence of thrombin (0.01-1 NIH U/ml) or phorbol 12-myristate 13-acetate (PMA) (10-100 nmol/l) histamine content rose maximally by 40%. Ionophore induced a histamine increase in the same concentration range as that needed to induce platelet aggregation and liberation of [3H]-arachidonic acid. Decrease of temperature from 37 to 0 degrees C or inhibitors of platelet functions, such as acetylsalicylic acid (1 mmol/litre) or [H1]-histamine receptor antagonist Dithiaden (0.1 mmol/litre), 1 inhibited histamine liberation from A23187- stimulated platelets, but did not affect the total rise in histamine content. The presented results indicate that, similarly as with other stimuli, Ca2+-ionophore A23187 activation of human blood platelets is accompanied by histamine synthesis.

Journal Article↗
PubMed1982

The effect of hydrocortisone and intal on histamine release from isolated target cells.

The effect of hydrocortisone on cell degranulation and histamine release in the presence of specific and non-specific liberators as compared with that of intal was investigated. Experiments were carried out on isolated rat most cells and human basophils. It was found that the stabilizing effect of drugs investigated depends on their concentration, the kind and concentration of histamine liberators and type of the target cells used in experiments.

Animals↗
PubMed1988

[The effect of aprotinin on intra- and postoperative histamine release and hemostasis. A clinical study].

Histamine, a biogenic amine normally stored in basophilic granulocytes and tissue mast cells, can be liberated in pathological concentrations during inflammation, tissue damage, and hypoxemic cell injury. After the addition of aprotinin to banked blood, complete inhibition of histamine liberation from stored blood cells could be observed. In the present clinical trial, in which 40 consecutive patients underwent hysterectomy, a similar effect was achieved. Following administration of 2, 3.5, and 5 million KIU of aprotinin, the intraoperative increase of histamine concentration from 0.3 to up to 1.28 ng/ml could be almost completely inhibited. In addition, the aprotinin-treated patients showed higher numbers of intact thrombocytes and less disturbance of the clotting, fibrinolytic, and inhibitor systems compared to the control patients.

Adult↗
PubMed2003

Histamine releasing peptide (HRP) has proinflammatory effects and is present at sites of inflammation.

Albumin, the most abundant plasma protein, readily enters sites of inflammation during the period of increased vascular permeability. There it encounters proteases released from mast cells and invading leukocytes which earlier work has shown can act on albumin to liberate the peptide, histamine releasing peptide (HRP), first identified and named by its ability to stimulate histamine release from isolated mast cells. In this report we show that HRP releases histamine from cutaneous mast cells in vivo resulting in increased vascular permeability and persistent edema while in vitro, HRP promotes chemotaxis of leukocytes and enhances macrophage phagocytosis. Moreover, we show that the level of HRP is increased with the induction of an acute cutaneous inflammatory response in rats, that HRP is present at sites of acute and chronic inflammation in humans and that HRP is rapidly degraded by proteases thereby limiting its action to the area of its generation. We suggest that HRP is a pro-inflammatory peptide that helps amplify and perpetuate the inflammatory response. Inhibitors of inflammatory proteases or antagonists that block the action of peptides like HRP may, therefore, be useful in breaking the cycle of inflammation.

Animals↗
PubMed2000

Chloroquine: a multipotent inhibitor of human platelets in vitro.

Chloroquine inhibited human platelet aggregation in vitro both at receptor- and nonreceptor-operated stimuli. The inhibition was dose-dependent, recorded on isolated platelets as well as in platelet-rich plasma, and followed the rank order of stimuli: adrenaline (second phase)>phorbol 12-myristate 13 acetate>adenosine diphosphate>adrenaline (first phase)>thrombin>calcium ionophore A23187. In thrombin-activated platelets, chloroquine decreased in a dose-dependent manner phospholipase A(2)-induced arachidonic acid liberation from membrane phospholipids, malondialdehyde formation (a marker of membrane phospholipid peroxidation), and thromboxane generation, considered the most potent autoaggregatory agent. Chloroquine only slightly altered the arachidonic acid cascade of platelets stimulated with A23187 and phorbol 12-myristate 13 acetate. Histamine formation and liberation induced with thrombin and A23187 were not affected by chloroquine. On the other hand, thrombin-stimulated serotonin secretion was significantly decreased with chloroquine in the concentration of 10 micromol/L. This indicated that chloroquine might interfere with stimulated secretion from platelets. The results suggest that chloroquine inhibited activated platelets: first, intracellularly; second, in a close relationship to the intraplatelet Ca(2+) mobile pool; and third, most probably at the site of platelet phospholipase A(2) activation.

Adult↗