TY - JOUR
T1 - Changes in plasma histamine concentration in the streptozotocin-diabetic rat
AU - Hollis, Theodore M.
AU - Kern, John A.
AU - Enea, Ned A.
AU - Cosgarea, Andrew J.
N1 - Funding Information:
’ Supported by NIH Grant HL 20460 and the Coronary Heart Disease Research Project, of the American Health Assistance Foundation. * To whom reprint requests should be addressed.
PY - 1985/8
Y1 - 1985/8
N2 - Plasma histamine concentrations were measured in rats made diabetic via jugular vein injection of streptozotocin and held 4 weeks following diabetes diagnosis. At least 15 diabetic animals received insulin (6-8 U/day) or α-hydrazinohistidine (α-HH) for the last week of the holding period. α-HH is a specific inhibitor of histidine decarboxylase (HD), the principle histamine-forming enzyme in mammals. Plasma histamine concentrations, expressed as means and mean standard errors (ng/ml) were as follows: control, 25.5 ± 2.4; diabetic, 47.1 ± 5.2; diabetic-insulin, 34.6 ± 2.9; diabetic-α-HH, 28.1 ± 2.1. These data indicate that in experimental diabetes there is an expansion of the nascent, or inducible histamine pool, an increase which is reflected by increased circulating plasma histamine. This may be one component mediating altered microvessel as well as large vessel permeability characteristics, an underlying component of both diabetic microangiopathy and macroangiopathy.
AB - Plasma histamine concentrations were measured in rats made diabetic via jugular vein injection of streptozotocin and held 4 weeks following diabetes diagnosis. At least 15 diabetic animals received insulin (6-8 U/day) or α-hydrazinohistidine (α-HH) for the last week of the holding period. α-HH is a specific inhibitor of histidine decarboxylase (HD), the principle histamine-forming enzyme in mammals. Plasma histamine concentrations, expressed as means and mean standard errors (ng/ml) were as follows: control, 25.5 ± 2.4; diabetic, 47.1 ± 5.2; diabetic-insulin, 34.6 ± 2.9; diabetic-α-HH, 28.1 ± 2.1. These data indicate that in experimental diabetes there is an expansion of the nascent, or inducible histamine pool, an increase which is reflected by increased circulating plasma histamine. This may be one component mediating altered microvessel as well as large vessel permeability characteristics, an underlying component of both diabetic microangiopathy and macroangiopathy.
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U2 - 10.1016/0014-4800(85)90058-9
DO - 10.1016/0014-4800(85)90058-9
M3 - Article
C2 - 3159596
AN - SCOPUS:0021969039
SN - 0014-4800
VL - 43
SP - 90
EP - 96
JO - Experimental and Molecular Pathology
JF - Experimental and Molecular Pathology
IS - 1
ER -