Blood histamine values

If histamine degradation is a physiological function of vitamin C, it is necessary to delineate the tissue level of ascorbic acid required for this effect. In the rat, which is capable of synthesizing ascorbic acid, serum ascorbic acid rose from 1.10 mg/100 ml to 1.63 mg/100 ml within 30 min of immobilization stress, nearly a 50% increase (Nakano and Suzuki, 1984). Liver ascorbate in these animals fell significantly after 15 min of stress, then rose dramatically to over 60% of the initial value within the next 15 min, indicating elevated hepatic biosynthesis of the vitamin. Adrenal ascorbic acid stores fell to 50% of the initial value following immobilization stress, and these levels remained depressed at 4 hr post-stress. Blood histamine levels rose 80%, from 38 to 68 ng/ml, peaking at about 30 min post-stress (Nakano and Suzuki, 1984). Hence, in the rat, stress induced a rapid rise in serum ascorbate which was fueled by ascorbic acid mobilized from tissue stores and by hepatic synthesis of ascorbate. 

As immediately after the reaction, elevated plasma histamine and serum or plasma tryptase levels of histamine and tryptase have been found [31, 34], an anaphylaxis may be confirmed by blood samples for histamine analysis drawn as soon as possible after the reaction and for tryptase drawn 1-2 h after onset of symptoms [31]. Tryptase values have to be compared to baseline levels. 

Histamine synthesis in the brain is controlled by the availability of L-histidine and the activity of histidine decarboxylase. Although histamine is present in plasma, it does not penetrate the blood-brain barrier, such that histamine concentrations in the brain must be maintained by synthesis. With a value of 0.1 mmol/1 for L-histidine under physiological conditions, HDC is not saturated by histidine concentrations in the brain, an observation that explains the effectiveness of large systemic doses of this amino acid in raising the concentrations of histamine in the brain. The essential amino acid L-histidine is transported into the brain by a saturable, energy-dependent mechanism [5]. Subcellular fractionation studies show HDC to be localized in cytoplasmic fractions of isolated nerve terminals, i.e. synaptosomes. 

Figure 4.4. Plasma histamine levels in response to NT given at t = 0. Rats were anaesthetized and NT (5 nmol/kg) or saline (0-3 ml) given intravenously. Blood was collected at the indicated times. Mean S.E.M. of mean of n values (in parentheses). Horizontal arrow is the histamine level before NT.

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