scholarly journals Different Patterns of Mast Cell Activation by Muscle Relaxants in Human Skin

2001 ◽  
Vol 95 (3) ◽  
pp. 659-667 ◽  
Author(s):  
Wolfgang Koppert ◽  
James A. Blunk ◽  
Lars J. Petersen ◽  
Per Skov ◽  
Katharina Rentsch ◽  
...  
Keyword(s):  
Mast Cell ◽  
Side Effects ◽  
Dose Response ◽  
Cell Activation ◽  
Muscle Relaxants ◽  
Mediator Release ◽  
Mast Cell Activation ◽  
Response Curves ◽  
Sensory Effects ◽  
Dose Response Curves

Background Activation of mast cells and systemic release of histamine are major side effects of intravenously administered muscle relaxants. In the current study, dermal microdialysis was used for the investigation of mast cell activation by muscle relaxants. Dermal microdialysis enabled simultaneous assessment of mediator release, vascular reactions, and sensory effects induced by intradermal application of muscle relaxants without systemic side effects. Methods Succinylcholine, the isoquinolines cisatracurium, atracurium, and mivacurium, and the steroids pancuronium, vecuronium, rocuronium, and rapacuronium were tested in human volunteers (n = 6 each). After intradermal insertion of microdialysis capillaries (0.4 mm diameter, cutoff 3,000 kd) and a 60-min equilibration period, the muscle relaxants were delivered via the capillaries for 30 min, followed by a 30-min washout period. Dialysate was sampled at 15-min intervals, and histamine, mast cell tryptase, and protein extravasation were determined. Changes in skin blood flow were measured using a laser Doppler imager. Potency and efficacy were derived from nonlinear fittings of the dose-response curves. Results For succinylcholine and the isoquinolines, dose-response curves for the vascular and sensory effects paralleled the histamine and tryptase release. In contrast, aminosteroids evoked a rapid histamine release that was accompanied by a delayed increase in tryptase. Conclusions Dermal microdialysis has been successfully used to simultaneously assess mediator release, vascular reactions, and sensory effects. The different pattern of tryptase release by isoquinolines and aminosteroids suggests different mechanisms of mast cell activation.

scholarly journals Miltefosine Inhibits Human Mast Cell Activation and Mediator Release Both In Vitro and In Vivo

2009 ◽  
Vol 129 (2) ◽  
pp. 496-498 ◽  
Author(s):  
Karsten Weller ◽  
Metin Artuc ◽  
Gary Jennings ◽  
Tim Friedrichson ◽  
Sven Guhl ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Mediator Release ◽  
Mast Cell Activation ◽  
Human Mast Cell

scholarly journals Mast Cell Activation byMycobacterium tuberculosis: Mediator Release and Role of CD48

2003 ◽  
Vol 170 (11) ◽  
pp. 5590-5596 ◽  
Author(s):  
Samira Muñoz ◽  
Rogelio Hernández-Pando ◽  
Soman N. Abraham ◽  
Jose Antonio Enciso
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Mediator Release ◽  
Mast Cell Activation

scholarly journals Mast Cell Sensitization as a Plausible and Researchable Mechanism for Chemical Intolerance

2021 ◽  
Author(s):  
Claudia S. Miller ◽  
Raymond F Palmer ◽  
Tania T. Dempsey ◽  
Nicholas A. Ashford ◽  
Lawrence B. Afrin
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Disease Process ◽  
Companion Paper ◽  
Mediator Release ◽  
Mast Cell Activation ◽  
Chemical Intolerance ◽  
Stage Disease ◽  
Biological Explanation ◽  
Loss Of Tolerance

Abstract Background Worldwide observations provide evidence for a two-stage disease process called Toxicant-Induced Loss of Tolerance (TILT), described in this journal in the first of two related papers. The disease process is initiated by a major exposure event, or a series of lower level exposures (Stage I, Initiation). Subsequently, affected individuals report that common chemical inhalants, foods, and drugs trigger multisystem symptoms (Stage II, Triggering). Given that foods and drugs also are comprised of chemicals, we refer to these intolerances simply as “chemical intolerance” (CI). In this second, companion paper we propose mast cell sensitization and mediator release as a plausible and researchable biological explanation for TILT. Methods Using the Quick Environmental Exposure and Sensitivity Inventory (QEESI), we compared patients diagnosed with mast cell activation syndrome (MCAS) (n = 147) to individuals who reported chemical intolerances following various exposures (n = 345), and to controls (n = 76). We compared QEESI scores using ANOVA across groups. Clinical scores for the MCAS patient group were used to predict CI status using logistic regression. Results As the likelihood of patients’ having CI increased, their likelihood of having MCAS similarly increased, to a near-perfect correspondence at the high ends of the QEESI and clinical MCAS scores. Symptom patterns were near-identical for CI and MCAS groups. Conclusion The close correspondence between QEESI scores for MCAS and TILT patients supports mast cell sensitization and mediator release as a plausible biological mechanism underlying both conditions, with implications for medicine, environmental health, and regulatory toxicology.

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