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PubMed2006

[Neuromuscular blockades. Agents, monitoring and antagonism].

Currently, the main aims of using neuromuscular blocking agents during general anaesthesia are the improvement of surgical and intubation conditions. Neuromuscular blocking agents themselves are neither analgesic nor anaesthetic. All agents interact with the acetylcholinergic receptor at the neuromuscular junction and induce a blockade either through a continuous activation imitating the effect of acetylcholine or through a competitive antagonism against acetylcholine. Succinylcholine is the only depolarizing muscle relaxant that is in clinical use. Non-depolarizing neuromuscular blockers may be grouped by their chemical structure into benzylisoquinolines or aminosteroids, and cover the complete range from short and intermediate, to long acting agents. Possible adverse drug reactions to the single agents are also related to their mechanism of action. Moreover, pharmacokinetic properties and effects such as histamine liberation could play an important role when choosing a myorelaxant. The depth of a neuromuscular block and recovery from paralysis can be monitored using qualitative and quantitative techniques. Therefore, the monitoring of neuromuscular recovery plays an important role in the prevention of postoperative complications due to residual paralysis. In case of residual paralysis, cholinesterase inhibitors are suitable for reversal.

Anesthesia↗
PubMed1999

[Tryptase, a marker for the activation and localization of mast cells].

The serine protease tryptase (ECNr. 3.4. 21.59), which is almost exclusively expressed in mast cells, is released by mast cell degranulation in an enzymatically active form together with other mediators, e.g. histamine, into the extracellular space and the circulation. The capability of the enzyme to directly stimulate several cell types as well as to cleave polypeptide hormones and to activate pro-enzymes suggests a role for tryptase in inflammatory and tissue-remodeling processes. Therefore, in the skin, a role of tryptase is suggested not only in mastocytosis and immediate type hypersensitivity reactions, but also in other inflammatory diseases, degenerative or neoplastic conditions as well as in wound healing, where an accumulation and/or activation of mast cells is found. Extracellular tryptase may be superior to histamine as a parameter for the onset and course of immediate type reactions and as an indicator for the activation of mast cells in other conditions. Its absence during histamine-liberating reactions may suggest basophil activation. In addition, tryptase has been shown to be a sensitive and specific marker for the localization of mast cells in tissues.

Biomarkers↗
PubMed1996

Influence of low-dose aprotinin on the inflammatory reaction due to cardiopulmonary bypass in children.

BACKGROUND: The serine protease inhibitor aprotinin inhibits trypsin, kallikrein, and plasmin and enhances the complement hemolytic activity of the first complement component C1. We tested whether low-dose aprotinin influences the inflammatory reaction related to cardiopulmonary bypass. METHODS: In an open, randomized study, 25 children undergoing cardiac operations were investigated prospectively. The treated group comprised 11 patients receiving low-dose aprotinin (20,000 kIU/kg [2.8 mg/kg]), and the control group included 14 patients. Complement activation, cytokine production, and leukocyte stimulation were analyzed before, during, and after cardiopulmonary bypass. RESULTS: In all children, significant C3 conversion and C5a generation, interleukin-6 synthesis, and myeloperoxidase, eosinophil cationic protein, and histamine liberation occurred in relation to cardiopulmonary bypass. This was not influenced by aprotinin treatment. In contrast, neutrophil kinetic studies at the end of cardiopulmonary bypass showed a significantly lower increase in the aprotinin as compared with the control group. CONCLUSIONS: Our results suggest that low-dose aprotinin has little influence on the inflammatory reaction induced by cardiopulmonary bypass. Aprotinin affects neutrophil mobilization but not white blood cell degranulation related to cardiopulmonary bypass, and has no influence on complement activation and interleukin-6 synthesis.

Analysis of Variance↗
PubMed1988

Analgesia and plasma beta-endorphin-like immunoactivity in compound 48/80-induced hypovolemia of the rats.

The effects of subcutaneous (s.c.) administration of compound 48/80 (a well known histamine liberator) on latency to thermoalgesic stimulus, hematocrit (Hct) and plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in male rats. The s.c. administration of compound 48/80 in doses ranging from 0.5 to 5.0 mg/kg into the rats produced significant analgesia in the hot plate test and increased Hct in a dose-dependent manner. Concomitant variation was observed between the analgesia and the increase of Hct. This analgesic effect, but not the increase of Hct, was diminished by pretreatment with the opiate receptor antagonist, naloxone (5 mg/kg, s.c.). A significant increase of plasma beta-END-LI was observed by s.c. injection of compound 48/80. Together with a previous finding that compound 48/80 induced-hypovolemia increases the renin release from kidney and then causes water intake in the rats, it is suggested that s.c. administration of compound 48/80 induced analgesia mediated through stimulation of an opioid system, may be closely related to stimulation of the renin-angiotensin system.

Animals↗
PubMed2006

Tissue substance P levels in acute experimental burns.

PURPOSE OF STUDY: To determine the tissue concentrations of substance P (SP) in burns of different depths and to see whether the concentrations of SP relate to the previously reported late increase in tissue histamine concentrations. MATERIALS AND METHODS: Experimental animal study with pigs. Superficial, partial thickness and full thickness burns were created and the microdialysis method used to collect samples for substance P analysis from burned and non-burned control tissue during a 24-h follow-up. RESULTS: Substance P concentrations increase after 4h in the partial and full thickness burns reaching the peak at 18 and 12h, respectively. The increase was later and more modest in the superficial and control sites. At 24h the SP median concentrations in the superficial, partial and full thickness burns were 28%, 85% and 140% higher than in the control site, respectively. There was a peak in the SP concentration in serum at 4h followed by a decrease and stabilization at a level about 15 pg/ml. CONCLUSIONS: The release of substance P in tissue is a possible cause of the late increase in tissue histamine in burns. Medical inhibition of SP is of clinical interest in preventing late histamine liberation in burns.

Acute Disease↗
PubMed1984

The role of ascorbic acid deficiency in human gingivitis--a new hypothesis.

Periodontal disease is one of the most prevalent health problems in the world and is the major cause of tooth loss in the adult population. Its two major subdivisions are gingivitis where disease is confined to the gingiva, and periodontitis where disease is present both in the gingiva and the supporting periodontal tissues. During the first stage there is a vasculitis of vessels subjacent to the junctional epithelium which is followed by exudation of fluid from the gingival sulcus and migration of leukocytes. There is variable expression of this stage throughout the mouth with new areas of involvement appearing in place of healed areas. Mast cells which are present in the gingival connective tissues may participate in this inflammatory response by liberating histamine. Ascorbic acid deficiency has been shown to be a conditioning factor in the development of gingivitis. When humans are placed on ascorbic acid deficient diets there is increased edema, redness and swelling of the gingiva. These changes have been attributed to deficient collagen production by gingival blood vessels. However, this may be due to an antihistamine role of ascorbic acid. This vitamin may act to directly detoxify histamine or effect a change in the level of enzymes responsible for histamine metabolism. This could occur through the influence of ascorbic acid in altering cyclic AMP (c-AMP) levels. Such changes in the level of this regulatory molecule could result in increased histamine-N-methyl transferase and other enzymes responsible for the breakdown of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Pathophysiology of pruritus.

In spite of the research that has been performed, pruritus remains a poorly understood sensation. It is important to remember that the majority of information presented here is derived from observations of human subjects. One can only speculate as to how much of this information can be extrapolated to pruritus in animals. Pruritus is closely intertwined with pain and touch. Pain and pruritus sensations are carried on A delta and C fibers, ascend on the lateral spinothalamic tract, and terminate in various brain centers, including the thalamus and the cortex. The gate control theory of pain and pruritus describes the substantia gelatinosa cells as "swinging gates" to modify peripheral input and result in stimulation of higher centers. Central factors reduce or amplify the perception of these cutaneous sensations. Histamine is the classic mediator of pruritus, although it is still unknown whether a final common mediator of pruritus exists. Numerous other mediators include proteases, peptides, substance P, opiate peptides, prostaglandins, and leukotrienes. These may have pruritic properties directly, or may act as histamine liberators to cause pruritus.

Animals↗
PubMed2006

Contact allergy and respiratory/mucosal complaints from heroin (diacetylmorphine).

After the start of heroin (diacetylmorphine)-assisted treatment to a selected group of chronic treatment-resistant heroin-dependent patients in the Netherlands, we reported about work-related eczema and positive patch tests to heroin in some nurses and nasal and respiratory complaints. To investigate the prevalence of heroin contact allergy, we started a questionnaire-based study with follow-up by allergological examinations. Of 120 questionnaires sent, 101 (84%) was returned: 67 from nurses and 34 from other employees. Of 101 workers, 38 (38%) had reported work-related complaints: 33 of 67 (49%) nurses and 5 of 34 (15%) other employees. Patch tests to heroin were performed in 24 nurses and were positive in 8 (33%). All the 8 had eyelid or facial eczema and, in 6, accompanied by mucosal or respiratory complaints. The prevalence of heroin contact allergy in this study was 8% (8/101) among all employees and 12% (8/67) among nurses. Respiratory and mucosal complaints could not be ascribed to a contact allergy, and in these cases, serum was analysed for specific immunoglobulin E to heroin. A type 1 allergy to heroin could not be shown. These complaints are possibly due to the histamine-liberating effect of heroin, to atopic constitution, to a combination of these factors or - less likely - to other non-allergic factors.

Allergens↗
PubMed1992

Effects of capsaicin, bradykinin and prostaglandin E2 in the human skin.

The actions and interactions of putative mediators of inflammation, such as substance P (SP), histamine, bradykinin and prostaglandins (PGE2) were studied in human skin. In addition, the effects of capsaicin were examined as it is known to release (and to deplete) SP and calcitonin gene-related peptide from C-fibres. The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist). The weal response was not reduced by any of the drugs. The flare evoked by capsaicin was abolished by lignocaine and indomethacin but was unaffected by compound 48/80, mepyramine, atropine and ketanserin. The weal response was reduced by indomethacin. The flare response to bradykinin seems to reflect the activation of C-fibres and associated mast cells, while the flare response to capsaicin seems to reflect the activation of C-fibres only. Repeated injections of capsaicin and bradykinin produced tachyphylaxis (and cross-tachyphylaxis) and greatly reduced the SP-evoked flare. Capsaicin produced tachyphylaxis also after treatment of the skin with a local anaesthetic, suggesting that it develops independently of C-fibre impulse flow. The tachyphylaxis produced by bradykinin and capsaicin seems to reflect the depletion of messenger peptides from the C-fibres. The flare response to SP following capsaicin- or bradykinin-induced desensitization gradually returned to normal after 5-8 weeks. The erythema evoked by PGE2 was reduced by 30% following pretreatment with lignocaine, mepyramine or compound 48/80.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Effect of terbutaline on cutaneous responses in man to rechallenge with allergen and compound 48/80.

Beta-adrenoceptor stimulating agents possess anti-allergic effects in vitro and in vivo. To study the site of action further 15 atopic subjects were pretreated with 1 microgram terbutaline injected intradermally (i.d.) followed by allergen challenge. Other skin sites challenged without such pretreatment served as controls. At different time intervals the skin was rechallenged with the same allergen, dissimilar allergen, or the histamine liberating agent, compound 48/80. In addition terbutaline was injected i.d. alone followed by allergen challenge at different time intervals to determine the duration of the anti-allergic effect. Pretreatment of the skin with 1 microgram terbutaline inhibited skin reactions to subsequently injected allergen with approximately 80% (flare) and 60% (wheal) (P less than 0.001) as compared with control. The inhibitory effect of terbutaline on the wheal and flare response to allergen was found to last up to 8 h (P less than 0.01). Rechallenge with the same allergen or a dissimilar challenging agent resulted in a reduced skin reaction compared with control challenge (P less than 0.01). Skin challenged with allergen in the presence of terbutaline gave a diminished response on rechallenge with the same allergen 24 h later, whereas rechallenge with an unrelated allergen or compound 48/80 produced a response similar to that of the control. The results suggest that allergen challenge in the presence (or absence) of terbutaline desensitizes the mast cells to further challenge with the same allergen and that terbutaline is capable of preventing mediator depletion of skin mast cells.

Adult↗
PubMed1983

Orally administered grass pollen.

In 1900 it was claimed that oral administration of ragweed could be used for the hyposensitization of hay fever patients. Several uncontrolled trials have been published, all showing an effect of oral hyposensitization. Only one study was controlled and showed no effect of oral hyposensitization. It was decided to undertake controlled clinical trials to determine the safety and effectiveness of orally administered enteric-coated grass pollen tablets in patients with hay fever. The actual grass pollen dose in the first trial was 30 times the dose that is normally recommended for preseasonal oral pollen hyposensitization using pollen aqueous solution or pollen powder. The safety study will be described here. Twelve young adults with a history of grass pollen hay fever positive skin prick test and positive nasal provocation test with extracts of timothy grass pollen were randomly allocated to one of the treatment groups with four patients in each group taking enteric-coated Conjuvac Timothy tablets or enteric-coated Whole Timothy pollen tablets or enteric-coated placebo tablets. The study was double blind. Preseasonally, the patients received 342,500 PNU and in total they received 4,500,000 PNU during 6 months. The patients receiving active treatment did not have any side effects. No significant changes were shown in the skin and nasal reactivity to grass pollen during the study. Neither were there any changes in timothy-specific IgE, IgG, total IgE nor histamine liberation from basophils.

Administration, Oral↗
PubMed1984

Inhibition of the late phase reaction to anti-IgE by previous mast cell activation with compound 48/80.

The concept of an obligate association between mast cell activation and development of a late phase reaction (LPR) to various agents in human skin was further elucidated. Skin sites were treated four times at 24 h intervals with non-LPR-inducing doses of the histamine liberator compound 48/80 in 10 volunteers. The previously compound 48/80-challenged sites responded with an approximately 40% attenuated early response (P less than 0.01) and a 70% reduction of the LPR (P less than 0.001) to subsequently injected anti-IgE as compared with simultaneous reactions at control sites. The data suggest that mediators from the cutaneous mast cells are necessary for the final expression of an LPR.

Adult↗
PubMed1957

Analgesic activity of dipipanone hydrochloride in student volunteers.

Dipipanone hydrochloride raised the threshold to ischaemic pain in healthy human volunteers. The lowest dose producing a significant rise in pain threshold was 10.0 mg. The peak effect for all doses was reached after about 2 hr. Side effects, the most common of which were drowsiness, nausea, and vertigo, are described and analysed. The drug was shown to be a histamine liberator and to cause pain and tenderness at injection sites.

Analgesics↗
PubMed1962

On the mechanism of action of Colisan.

Purified Colisan produces instantaneous lysis of paramecia and amoebae, and blebbing of paramecia, rat mast cells and ascites tumour cells. Colisan liberates histamine from mast cells. It also suppresses competitively the bradykinin-provoked contraction of the guinea-pig ileum. Most of these effects are not shared by staphylococcus-haemolysin. The results suggest a rapid change of the permeability of the cell membrane as the mechanism of all the diversified biological actions of Colisan.

Amebicides↗
PubMed1991

Diffuse cutaneous mastocytosis mimicking staphylococcal scalded-skin syndrome: report of three cases.

Three cases of diffuse cutaneous mastocytosis (DCM) were at first incorrectly diagnosed as staphylococcal scalded-skin syndrome. In the first patient, at age 1 day the disease was recognized promptly by simple techniques such as Darier's sign and Tzanck smear. Much delay in making the diagnosis occurred in the other two patients, however: almost 1 year and 15 years, respectively. Bullous manifestations in mastocytosis occur only in the first two or three years. In the first months the disease can be dangerous and life threatening. To distinguish mastocytosis from vesicular and bullous neonatal disorders, one should perform Darier's sign and a Tzanck smear. The diagnosis is confirmed by histopathologic studies. Treatment of the bullous manifestations is symptomatic, with zinc oxide paste and oral antihistamines, which may provide some relief. In addition, cimetidine and sodium cromoglycate may be beneficial. At a later age psoralen plus ultraviolet A therapy may also relieve the symptoms. Particular foods and medicines can liberate histamine and should be restricted as much as possible in extremely affected patients. Special care should be taken when these patients are to undergo anesthesia. The risk of complications during and after anesthesia is also present in other forms of mastocytosis.

Adolescent↗
PubMed1991

Effect of antioxidant therapy on cyclooxygenase-derived eicosanoid release during intestinal ischemia-reperfusion.

Conflicting data have been reported on the relationship between reactive oxygen intermediates and the formation of oxygenase-derived eicosanoids. Plasma levels of prostacyclin (PGI2, measured as the stable metabolite 6-keto-PGF1 alpha) and thromboxane A2 (TxA2, measured as TxB2) in the effluent blood of a canine ileal segment were determined following 1 or 2 h of ischemia. The synthesis of both eicosanoids was significantly stimulated during reperfusion, but extension of the ischemic interval from 60 to 120 min was not followed by a further increase. The role of oxidants potentially involved in the process was investigated by using materials that inactivate the xanthine-oxidase-generated intermediates. Previous studies on the same in vivo animal model had demonstrated the effectiveness of antioxidant therapy in reducing the postischemic histamine release. There was no significant alteration in the amount of eicosanoids synthesized following oral allopurinol, catalase, dimethylsulfoxide, mannitol or desferrioxamine treatment. Intravenously administered allopurinol, however, significantly elevated the postischemic 6-keto-PGF1 alpha/TxB2 ratio. The results suggest that these antioxidants at doses inhibitory to histamine liberation are not effective in influencing the postischemic eicosanoid release. Intravenously administered allopurinol could exert a potentially beneficial effect through a mechanism other than the blockade of xanthine oxidase.

Allopurinol↗
PubMed1993

Skin prick tests with solutions of acid anhydrides in acetone.

Various low molecular acid anhydrides can act as haptens and induce type I allergies. Immunoglobulin E can be detected by radioallergosorbent test (RAST) with the protein conjugates of the respective anhydrides, which are commercially available for some substances. Being almost nonsoluble in water, these species cannot be applied in a skin prick test as a water solution. We will introduce a practicable skin prick test using acetonic solutions of the haptens. 136 persons were tested with acetone for negative control and histamine for positive control. Tests were carried out with 1 and 5% acetonic solutions of phthalic anhydride (PA). The RASTs with conjugates of the PA were performed with 111 subjects who had been exposed to acid anhydrides and with 5 people who possibly had been exposed. In 14 cases, when immediate-type allergy was suspected clinically, a test was performed in addition to the respective anhydride used at the workplace. In order to avoid unspecific histamine liberation, we tested 20 volunteer control persons who had not been occupationally exposed to acid anhydrides. In the prick test performed with acetonic PA solutions, 10 of the occupationally exposed subjects, who had also had a positive result in the RAST with protein conjugates of the PA, showed positive skin reactions, and in 2 further cases, in which the skin reaction was positive, the results of the RAST were just below the limit of a positive evaluation. The skin reaction was positive in 4 cases, in spite of a negative RAST result, while the prick test was reported to be negative in 3 cases although the RAST results were considered to be positive.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMedDate not supplied

Molecular characterization of timothy grass pollen group V allergens.

Phl p V is the dominant allergen of timothy grass (Phleum pratense) with two isoforms having the apparent molecular weights of 38 (Phl p Va) and 32 kD (Phl p Vb) under Western blot conditions. Two-dimensional electrophoresis/immunoblotting reveals that each isoform is split into at least four isoallergens. Structural differences in the isoforms are shown by N-terminal sequencing (only 60% identity), by reaction patterns of monoclonal antibodies and, more convincingly, by enzymic degradation of purified isoforms followed by immunologic fingerprinting. These findings are confirmed by the deduced primary protein structure of cloned Phl p Va and Phl p Vb. Experiments with IgE--affinity-purified by immobilized recombinant allergens or their fragments--reveal identical epitopes and at least one different epitope between the isoforms. Furthermore, on Phl p Va we can localize different IgE-reactive epitopes at the C terminus as well as the N terminus. By probing serum from 11 patients on recombinant C- or N-terminal fragments, an individual reaction pattern was found. Testing the histamine liberation potency of the fragments, we found the N-terminal fragment of Phl p Va to be superior to that of the C-terminal fragment or the whole molecule. These results give insights into the variability of allergens, the individuality of human reaction patterns to epitopes and the alteration of allergenicity to higher or lower levels by fragmentation.

Allergens↗