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Bordetella pertussis does not induce beta-adrenergic blockade.

机译:百日咳博德特氏菌不引起β-肾上腺素能阻滞。

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摘要

Bordetella pertussis organisms induce histamine sensitivity and diminish the normal hyperglycemic response to epinephrine in experimental animals. These effects have been attributed to beta-adrenergic blockade. However, under conditions in which the decrease in epinephrine-induced hyperglycemia after B. pertussis administration was demonstrable, there was no change in rat reticulocyte beta-adrenergic receptor number or affinity measured by iodohydroxybenzylpindolol binding or in isoproterenol-stimulated adenylate cyclase activity. Therefore, there was no generalized beta-adrenergic blockade induced by B. pertussis. The observed effects can be explained by the hypersecretion of insulin resulting from B. pertussis administration.
机译:百日咳博德特氏菌生物体诱导组胺敏感性,并减少实验动物对肾上腺素的正常高血糖反应。这些作用归因于β-肾上腺素能阻滞。但是,在证实百日咳博德特氏菌给药后肾上腺素引起的高血糖减少的情况下,大鼠网织红细胞β-肾上腺素能受体数量或亲和力没有改变,这是通过碘羟苄基松多醇结合或异丙肾上腺素刺激的腺苷酸环化酶活性测得的。因此,没有百日咳博德特氏菌引起的全身性β-肾上腺素能阻滞。观察到的效果可以通过百日咳博德特氏菌施用引起的胰岛素过度分泌来解释。

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