PubMed · 2264757
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M S Poliak. 1990. [Errors in antibiotic therapy].. https://pubmed.ncbi.nlm.nih.gov/2264757/
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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.
Intestinal anaphylaxis triggers neuronal activation in the nucleus tractus solitarius (nTS) of the rat brain stem. Stress may modulate reflex circuitry in the brain stem and facilitate intestinal inflammatory responses. We hypothesized that stress would modulate central neuronal activation during intestinal anaphylaxis. NTS neurons were activated following intestinal antigen challenge in sensitized Hooded Lister rats but not in negative controls (P < 0.05). The number of Fos-positive neurons following intestinal anaphylaxis decreased in animals exposed to water-avoidance stress (P < 0.05), although serum levels of rat mast cell protease II were not different in stressed and unstressed animals, indicating a similar degree of mast cell degranulation. Stress seems to inhibit neuronal activation in the rat brain stem during intestinal inflammation without modulation of the inflammatory response itself. This may have implications for a potential efferent neuronal modulation of inflammatory responses in the gut.
This study was undertaken to examine whether glucocorticoids could be implicated in the hyporesponsiveness of diabetic rats to systemic anaphylaxis. Rats were actively sensitized with a mixture of Al(OH)(3) plus ovalbumin and challenged i.v. with ovalbumin 14 days later. Diabetes was induced by alloxan-injected i.v. either before or after sensitization. Elevation of total and specific serum immunoglobulin E (IgE) was abolished in rats turned diabetic and then sensitised, but not in those first sensitised and then turned diabetic. In both conditions, increased serum corticosterone levels occurred in parallel with protection of diabetic animals against fatal shock, intestinal haemorrhage and elevation in plasma histamine levels evoked by antigen challenge. The resistance of diabetic rats to fatal shock was no longer significantly different from that of non-diabetic rats following treatment with the glucocorticoid receptor antagonist RU 486 (mifepristone). These findings indicate that endogenous glucocorticoid plays a pivotal role in the phenomenon of hyporeactivity to systemic anaphylaxis in alloxan-diabetic rats.