Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topical antigen challenge in cheek pouches of immunized hamsters led to an acute inflammatory reaction which was characterized by intravital microscopy. The response consisted of short-lasting arteriolar spasm, followed by leakage of plasma, vasodilation, and accumulation of leucocytes. Several observations indicated that the reaction was due to mast cell activation. Thus, a very similar inflammatory response was seen after challenge with compound 48/80, and both antigen and compound 48/80 degranulated the numerous mast cells present in the cheek pouch. In addition, fluorescein-labelled antigen bound specifically to mast cells in cheek pouches of immunized animals, also suggesting the presence of mast cell-fixed antigen-specific antibodies, possibly immunoglobulin E. However, although antigen and compound 48/80 caused similar microvascular responses, cross-desensitization experiments indicated that the two stimuli activated mast cells via different mechanisms. The histamine antagonist mepyramine, which abolished plasma leakage induced by exogenous histamine, substantially inhibited the increase of microvascular permeability evoked by antigen or compound 48/80, but did not appear to affect the vasospasm and leucocyte accumulation. It is concluded that the hamster cheek pouch may be a most useful tool for investigation of dynamic microvascular events during allergic mast cell-dependent inflammation.
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PMID:An intravital microscopic model for mast cell-dependent inflammation in the hamster cheek pouch. 249 12

To investigate the mechanism of bronchial spasm induced by inhalation of ultrasonically nebulised distilled water (UNDW) ultrasonically nebulised solutions including hypoosmolar (distilled water, 0.3% NaCL) isoosmolar (0.9% NaCL) and hyperosmolar solutions (2.7% NaCL, 3.6% NaCL, 4.6% KCL 22.2% dextrose) were used for challenge test in 12 asthmatic patients and 10 healthy subjects as controls. The dose of solution required to induce a 20% reduction in FEV 1 (FD 20-FEV 1) was recorded. In another 10 asthmatic patients, a challenge with UNDW was conducted after pretreatment with sodium cromoglycate (SC), Ipratropine Bromide (IB) to investigate the protective effect of the two medicines. The results showed that distilled water and three hyperosmolar solutions which were of the same osmotic pressure (3.6% NaCL, 4.6% KCL and 22.2% dextrose) were most potent in inducing bronchoconstriction, and no significant difference in PD 20-FEV 1 was found among them 0.3% and 2.7% NaCL were next and 0.9% NaCL was the least potent. Normal subjects showed no response to the solutions. The SC gave significant protection to nine of the ten patients, and IB gave it to five of the ten. Our results indicate that a change in the osmolarity of the fluid lining the respiratory tract may be an important determinant of the airway response; sodium cromoglycate which inhibits the mediator release of mast cell can reduce the airway response to UNDW.
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PMID:[Effects of nebulized distilled water on tracheal reaction in asthmatic patients]. 253 83

The mast cell is the cellular basis for immediate hypersensitivity reactions. The specificity of the immediate hypersensitivity reaction is attributable to IgE molecules fixed to specific membrane receptors which, when stimulated by specific antigen, initiates the process of degranulation of the mast cell. The granules provide three separate sources of biologic activity: performed or primary mediators, newly generated or secondary mediators, and activities associated with the granular matrix. A number of biologic consequences are generated in response to these mediators and these include: increased vascular permeability, vasodilation, smooth muscle spasm, polymorphonuclear leukocyte chemotaxis, stimulation of adenylate and guanylate cyclase, superoxide radical generation, prostaglandin formation, mucous and gastric acid secretion, hypotension, tissue destruction, and mononuclear leukocyte infiltration. This pharmacopia of activities accounts for the clinical aspects of allergic diseases, suggests that the mast cell granule may be involved in the host's defense against parasitic infections, and is compatible with a suggested role of the mast cell as a widely distributed, monocellular endocrine system.
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PMID:The mast cell. 617 51

The practical importance, prevalence, typical features, physiopathology and therapy of exercise-induced bronchospasm (E.I.B.) are briefly reviewed. The condition is common, especially in children. Prevalence is influenced by the mode, intensity and duration of exercise, the age and possibly the sex of the subjects, the number of test repetitions, and the criterion for presence of spasm. The main site of obstruction is in the large airways. Symptoms appear a few minutes post-effort, peaking 10-15 minutes after exercise. At different times, spasm may arise in the vagal reflex arc, from alterations of sympathetic balance, prostaglandin release, and sensitization of the mast cell. Until recently, the main basis of prophylaxis has been inhalation of sodium cromoglycate (20 mg, 60 minutes prior to competition). Beta agonists have until recently been prohibited in international competitions. However, the use of selective beta agonists such as salbutamol and terbutaline was allowed in the 1978 World Swimming Championship and the 1980 World Cross-Country Championship with a supporting medical letter. The Medical Commission of the International Olympic Committee has also moved recently to sanction the use of salbutamol and terbutaline. Future prophylaxis will thus be based on combinations of selective beta agonists and sodium cromoglycate.
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PMID:Exercise-induced bronchospasm - pathophysiology and treatment. 679 21

In the intestinal mesentery of 40 white rats and 40 mongrel dogs by means of azure-eosin staining, silver impregnation, vital microscopy and certain histological methods, after left-sided cervical vagotomy it has been demonstrated that an increasing functional activity of mast cells is reached by: 1. increasing number of the mast cells; 2. increasing part of degenerating forms; 3. elevating part of the most active forms. As to the microcirculatory bed, a decreasing volume is observed at the expense of opening the arteriolo-venular anastomoses, a certain spasm of the microvessels and loosing of the capillary network. In the intervascular connective tissue, destabilization of the connective tissue elements is observed. Biomicroscopy reveals an accelerated time for the blood elements to get out of the vascular bed. The data obtained demonstrate that the postvagotomic reaction of the microcirculatory bed and its mast cell apparatus is limited with the innervation zone of the vagus nerve.
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PMID:[Microcirculatory bed and mast cells in vagotomy]. 715 12

Problems of arrhythmogenic sudden death (ASD) in athletes have been re-assessed on the clinicopathological plane, encompassing the emerging, unsolved, question of so-called idiopathic ventricular tachycardia, and its debated diagnostics versus arrhythmogenic right ventricular dysplasia-cardiopathy. Ischemic-infarction ASD from coronary artery pathology in young athletes has been seen to present with atherosclerotic "soft" subintimal plaques, rich in newly formed smooth myocytes, often attended by adventitial mast cell, as suspect microscopic markers of spasm, relevant to reperfusion; these features can be found also in precociously intramural arteries, responsible for ASD. Rare congenital abnormalities of the coronary ostia occasionally underlie ASD, together with the acquired aneurysmic coronaritis of chronic Kawasaki disease. Ischemic ASD can also be due to coronary arteriolopathy attending hypertrophic cardiomyopathy, a not uncommon disease in athletes, to be carefully discriminated from training heart hypertrophy. Young South-American sportsmen with Chagas' chronic cardiopathy seem to be at particular risk of ASD. Minor, but specific arrhythmogenic cardiac malformations such as accessory AV pathways have been detected in athletes succumbing to otherwise unexplained ASD, undergone careful post-mortem investigation. The need of more attentive and extended histopathologic control emerges from the hitherto ignored cardiac neuropathological substrates of reflexogenic ASD, which is cogent to problems of ASD in competing athletes. The thorough examination of the cardiac vascular centers in the brain stem, and of the peripheral cardiac innervation, at either abutments of the arc of dive- and/or Bezold-Jarisch cardioinhibitory-vasodepressor reflex, made it possible to suggest novel clinicopathological explanations in controversial cases of athletes' ASD, safeguarding from grave leval misjudgements due to sport's forensic medical mistakes.
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PMID:Structural and non-structural disease underlying high-risk cardiac arrhythmias relevant to sports medicine. 750 Jun 31

A sequential analysis of liver allograft rejection in sensitized rats using immunopathological and ultrastructural microscopy is described. Lewis rats were primed with four ACI skin grafts and challenged with an arterialized ACI orthotopic liver allograft 14 to 17 weeks later. The sensitization resulted in a mix of IgG and IgM lymphocytotoxic antibodies at a titer of 1:512 at the time of transplantation. Specificity analysis of pretransplant immune sera revealed a predominance of IgG anti-class I major histocompatibility complex (RT1) antibodies with a minor IgG fraction showing apparent endothelial cell specificity (non-RT1). This level of sensitization was associated with accelerated graft failure in 3 to 5 days from mixed humoral and cellular rejection. Sequential analysis of serial posttransplant graft biopsies revealed diffuse vascular IgG deposition and platelet thrombi in portal veins and periportal sinusoids within 3 minutes after reperfusion. This was followed by endothelial cell hypertrophy and vacuolization, periportal hepatocyte necrosis, arterial spasm, focal large bile duct necrosis, and hilar mast cell infiltration and degranulation. However, the liver allografts did not fail precipitously and hyperacute rejection was not seen. Kupffer cell phagocytosis of the sinusoidal platelets began as early as 30 minutes posttransplant and by 24 hours, the platelet thrombi had decreased. Cholangioles appeared focally at the edge of the limiting plates by 2 to 3 days, apparently in response to earlier periportal hepatocyte damage. A mononuclear portal and perivenular infiltrate became evident at 3 days, and graft failure was attributed to both antibody and cell-mediated rejection (Furuya et al: Preformed lymphocytotoxic antibodies: Hepatology 1992, 16: 1415-1422). The model described resembles observations in crossmatch positive human liver allograft recipients. The mechanisms of hepatic graft resistance to antibody mediated rejection and the possible long term consequences of early damage to the biliary tree are discussed.
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PMID:Liver allograft rejection in sensitized recipients. Observations in a clinically relevant small animal model. 849 42

The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, cholinergic crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of cholinergic crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.
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PMID:Hypothesis for synergistic toxicity of organophosphorus poisoning-induced cholinergic crisis and anaphylactoid reactions. 882 72

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.
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PMID:[Tryptase levels are elevated during spontaneous ischemic episodes in unstable angina but not after the ergonovine test in variant angina]. 955 75

We report a case of anaphylaxis in which left midventricular hypokinesis was found by echocardiogram performed while the patient was hypotensive shortly after the onset of acute chest pain with S-T segment elevations. Cardiac injury was confirmed by elevation of cardiac enzymes. Repeated echocardiogram 2 days later demonstrated normal ventricular wall function and coronary angiogram demonstrated no angiographically apparent disease. We discuss possible mechanisms for cardiac injury and suggest mast cell-mediated coronary spasm as the most likely.
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PMID:Midventricular hypokinesis as a cardiac manifestation of anaphylaxis: a case report. 1713 42


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