PubMed · 3157042
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C E Graham. 1985-04-15. Chemonucleolysis for sciatica and low back pain.. https://doi.org/10.5694/j.1326-5377.1985.tb113453.x
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The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.
BACKGROUND: Natural rubber latex (NRL) has become an important occupational health concern in recent years, particularly among health care workers. It has been suggested in some reports that the prevalence of latex sensitization among occupationally exposed groups is not different from that in the general population. METHODS: The findings of prevalence studies conducted among occupationally-exposed and general population groups were reviewed to determine whether there is evidence to support this suggestion. RESULTS: Numerous surveys of HCWs have demonstrated that the prevalence of sensitization to latex ranged in most studies from 5 to 12%; sensitization of HCWs may produce clinical effects including urticaria, rhinoconjunctivitis, occupational asthma, and potentially life-threatening anaphylactic shock. More than a decade ago, data from Finland indicated that the prevalence of latex allergy in the general population was less than 1%. Recent reports from Finland have confirmed this, with observations that 0.7-1.1% of large series of patients were NRL-allergic, while among 804 unselected patients, the prevalence of latex skin prick test (SPT) positivity was 0.12%. In contrast, other studies have suggested that from 4 to 6.4% of individuals tested were positive for serum latex-specific IgE antibodies. However, the specificity of these assays has been reported to be low. In three recent studies based on SPTs, published in 1997, the prevalence of positive reactions to latex was about 1% or less. The prevalence was 0.7% (95% CI 0.3-1.4) among 758 apprentices in Quebec, Canada; and 1.1% among more than 3,000 children tested in Finland (1.0% confirmed on latex use test). There were no first- and second-year dental students with positive latex SPTs in Ontario, Canada. CONCLUSIONS: These recent investigations provide further evidence consistent with earlier studies based on skin testing that the prevalence of latex sensitization in occupationally-unexposed groups is quite low (< 1%). The marked differences in the findings based on serological assays may relate to the nonspecificity of these assays and deserve further investigation.
Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell-deficient WBB6F1- W/Wv (W/Wv) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/Wv mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/Wv mice. Administration of monoclonal anti-IL-4 antibody completely prevented the fatal reactions, and the effect of anti-IL-4 was associated with its suppressive activity on Pen V-specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/Wv mice, high levels of PAF in the circulation after challenge in both +/+ and W/Wv mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.