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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with coronary atherosclerosis in I and III stages content of histamine in blood, excretion of free histamine with urine, activities of serum histidine decarboxylase and diaminooxidase, histaminopexy of blood serum and content of antihistamine factor were studied. In patients with the disease of the I stage during the attacks of stenocardia content of histamine in blood, the activity of diaminooxidase and content of degranulated basophils were increased, but the histidine decarboxylase activity, histaminopexy, content of antihistamine factor and excretion of free histamine with urine were normal. During the stenocardia attacks in patients with coronary atherosclerosis of the III stage content of degranulated basophils, the histidine decarboxylase activity were increased, histaminopexy and titres of antihistamine factor were decreased. Between the content of histamine in blood and the diaminooxidase activity no correlation was observed. This lack of correlation could cause development of hyperhistaminaemia and increased excretion of free histamine with urine. Antihistamine and desensitizing preparations (pipolphen, heparin, amidopyrine and ascorbic acid) increased the therapeutic efficiency of vasodilating drugs, decreased stenocardia attacks, accelerated both clinical improvement and normalization of histamine metabolism.
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PMID:[Metabolism of histamine in patients with coronary atherosclerosis]. 5 86

Effects of partial inhibition of aortic histamine formation on aortic albumin uptake and lipid deposition were examined in male, New Zealand white rabbits maintained on Purina Rabbit Chow containing 0.5% cholesterol for a 2-week period. Aortic histamine synthesis was inhibited by partial inhibition of aortic histidine decarboxylase (HD) through administration of alpha-hydrazinohistidine (alpha-HH, MK785, Regis Chemical Co., 25 mg/kg, i.p. at 12-h intervals). Additional rabbits were maintained on either the cholesterol diet or on Purina Rabbit Chow without cholesterol. Results indicate that administration of alpha-HH for the 2-week period produced a 31% reduction (P less than 0.05) in aortic HD activity in those rabbits maintained on the cholesterol diet, and that concurrently there was a 51% reduction in aorta albumin uptake (P less than 0.025) and a 63% reduction in the extent of oil red O staining. By regression analysis a significant correlation coefficient (r = 0.71, P less than 0.005) was obtained between the aortic albumin uptake and the aortic histamine forming capacity (HFC) in rabbits maintained on this cholesterol diet. These findings indicate that the aortic HD system may be an important enzymatic coupler involved in vascular permeability alterations occurring early in the atherogenic sequence.
Atherosclerosis 1979 Dec
PMID:Relationship between inhibition of aortic histamine formation, aortic albumin permeability and atherosclerosis. 51 43

The histidine decarboxylase (HD) activity of thoracic and abdominal aortic segments obtained from male, Dutch-belted rabbits fed a diet containing 0.5 per cent cholesterol for periods of either 2 or 4 weeks was examined. Mean thoracic aortic HD activities, expressed as histamine-forming capacity (HFC), were 3911 plus or minus 492, 6254 plus or minus 656, and 6215 plus or minus 878 dpm/100 mg benzenesulfonylhistamine (BSH) for the control group and from rabbits fed cholesterol for 2 and 4 weeks, respectively. Both treatment means were significantly higher than the control (P smaller than 0.05). Similar examination of abdominal aortic HD activities yielded mean HFC's of 4029 plus or minus 399, 5694 plus or minus 521, and 4762 plus or minus 902 dpm/100 mg BSH for control animals and those of the 2- and 4-week treatment groups, respectively. The difference between mean HFC's of the control and 2-week treatment group was significant (P smaller than 0.05). All increases occurred in the absence of either aortic structural alterations or any lipid deposition. These results give credence to the concept that the atherogenic process represents, at least in part, a delayed-prolonged inflammatory response phenomenon of the arterial wall.
Atherosclerosis
PMID:Rabbit aortic histamine synthesis following short-term cholesterol feeding. 113 3

Previous work has shown that plasma and tissue concentrations of histamine are elevated in rats with experimental diabetes mellitus and that leucocytes and platelets from patients with peripheral vascular disease have a higher histamine content than those from controls. In the present study, we have measured: (a) plasma histamine concentrations; (b) leucocyte and platelet histidine decarboxylase (the enzyme responsible for the biosynthesis of histamine) in patients with diabetes mellitus (Types I and II) and peripheral vascular disease; and (c) platelet and leucocyte histamine content. Plasma histamine concentration was significantly higher in patients with diabetes and peripheral vascular disease respectively than that in age-matched controls. Leucocyte histidine decarboxylase activity in diabetic and peripheral vascular disease patients was similar to that in controls, while platelets had no histidine decarboxylase activity. The leucocyte and platelet content of histamine were greater in patients with peripheral vascular disease than those in controls, but they were not altered in diabetic patients. There was no correlation between plasma histamine concentration, leucocyte and platelet histamine content, and histidine decarboxylase activity. We conclude that plasma histamine is elevated in diabetics and in patients with peripheral vascular disease and that platelet and leucocyte histamine content is increased in the latter. This increase in platelet and leucocyte histamine content is not due to an increase in histidine decarboxylase activity of these cells. The increase in plasma and cellular histamine content may contribute to the pathogenesis of increased endothelial permeability in diabetes and to the pathogenesis of intimal damage in atherosclerosis.
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PMID:Plasma histamine concentrations are elevated in patients with diabetes mellitus and peripheral vascular disease. 291 44

Oscillatory shear stress applied to the lining of blood vessels causes endothelial cell injury, one of the essential postulated prerequisites to the development of atherosclerosis. The purpose of this investigation was to study effects of shear stress on bovine aortic endothelial cells (BAEC), in vitro, for varying lengths of time (6 h, 12 h, 24 h) on BAEC histamine content (HC) and histidine decarboxylase activity (HD). Low intensity stress (1.6 dynes/cm2) as well as intermediate and high intensity shear stresses (3.5 dynes/cm2 and 7.6 dynes/cm2) resulted in an accelerated HD (281%) and elevated HC (144%). These data indicate that oscillatory shear stress produces increases in histamine metabolism.
Atherosclerosis 1987 Mar
PMID:Cultured bovine aortic endothelial cells show increased histamine metabolism when exposed to oscillatory shear stress. 359 60

We examined the interrelationship between inhibition of aortic histamine synthesis through inhibition of aortic histidine decarboxylase and intra-aortic albumin accumulation in rats made diabetic by a jugular vein injection of 60 mg/kg of streptozotocin under ether anesthesia. Animals were held for 4 weeks following overt manifestation of diabetes. At the end of 3 weeks, at least six animals in each of the diabetic and non-diabetic groups received intra-peritoneal injections of alpha-hydrazinohistidine (25 mg/kg at 12 h) for the last 7 days. Aortic albumin accumulation was measured by quantification of aortic uptake of fluorescein isothiocyanate conjugated to rat serum albumin injected in the jugular vein 1 h before sacrifice. The aortic albumin mass transfer and flux rates of the diabetic group were more than 300% higher than that of the control group; alpha-hydrazinohistidine treated diabetic rats had aortic albumin mass transfer rates equivalent to control values. The aortic albumin content was nearly tenfold higher in untreated diabetic rats, but again treatment with alpha-hydrazinohistidine returned this to control values. These data offer strong support to the premise that accelerated aortic histamine synthesis, which occurs in experimental diabetes, is an important mediator of increased aortic macromolecule uptake, and as such, may be one component of the multitude of factors responsible for increased susceptibility of atherosclerosis among individuals having diabetes mellitus.
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PMID:Inhibition of aortic histamine synthesis by alpha-hydrazinohistidine inhibits increased aortic albumin accumulation in experimental diabetes in the rat. 401 54

We studied histamine metabolism, i.e., histidine decarboxylase (HD)-mediated synthesis and histaminase-mediated catabolism, in relation to intracellular histamine content in both aortic endothelial and subjacent smooth muscle cells of control and diabetic rats. Diabetes was induced by a single jugular vein injection of streptozotocin (55 mg/kg in acidified saline, pH 4.5), and animals were held for either 2 or 4 weeks following overt manifestation of diabetes. An additional 4-week diabetic group received insulin (Iletin NPH, 10 U per 24 hour) during the last week. With respect to control values, the histamine content of aortic endothelial cells increased 138%, HD activity increased 250%, and histaminase activity decreased 50% over the 4-week period. In subjacent smooth muscle cells, the histamine content increased in excess of 150%, HD activity increased more than 300%, and histaminase activity decreased in excess of 30%. Insulin treatment for the last week resulted in complete reversal of all these changes. These results support the concept that a large vessel response similar to the microcirculatory prolonged phase of inflammation occurs in experimental diabetes, a change similar to that occurring in experimental atherosclerosis. They also indicate that both synthetic and catabolic changes occur in histamine metabolism under these conditions, changes that alter arterial wall histamine pools, and suggest that insulin administration under conditions of experimental diabetes may modulate aortic histamine metabolism and the resultant intraaortic histamine pools.
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PMID:Aortic endothelial and smooth muscle histamine metabolism in experimental diabetes. 680 15

We investigated the localization of histidine decarboxylase (HDC), which is the rate-limiting enzyme that generates histamine from histidine, in human aorta/coronary artery. RT-PCR and immunohistochemical staining revealed that the HDC gene was expressed in monocytes/macrophages and T cells in the arterial intima but not in smooth muscle cells in either the arterial intima or the media. A luciferase promoter assay with U937 and Jurkat cells demonstrated that interleukin-4 (IL-4) inhibited the expression of the HDC gene. In contrast, among a scavenger receptor family, IL-4 as well as histamine up-regulated U937 cells to express the LOX-1 gene but not the SR-A gene, which genes encode receptors that scavenge oxidized lipids. These findings suggest that histamine synthesized in the arterial wall participates in the initiation and progression of atherosclerosis and that IL-4 can act as an important inhibitory and/or stimulatory factor in the function of monocytes/macrophages modulated by histamine in relation to the process of atherosclerosis.
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PMID:Effects of histamine and interleukin-4 synthesized in arterial intima on phagocytosis by monocytes/macrophages in relation to atherosclerosis. 1156 79

Chlamydophila (Chlamydia) pneumoniae (C. pneumoniae) is the third most common cause of community-acquired pneumonia and is probably involved in the development of certain chronic inflammatory diseases, including atherosclerosis and adult-onset asthma. Histamine, synthesized by histidine decarboxylase (HDC) from L-histidine, plays an essential role in allergic and inflammatory processes and in cell differentiation. The effect of C. pneumoniae infection on the expression of HDC has not been examined. In the present study, normal Balb/c mice and HDC knockouts, and control mice with a CD1 background were infected intranasally with C. pneumoniae. On days 1, 3, 7, 16 and 31 after infection, the normal Balb/c mice were sacrificed and divided into three groups. In the homogenized lungs of the first group, C. pneumoniae titres were determined and demonstrated peak levels on day 7. HDC production was revealed by a Western blot assay throughout the observation period of 1-16 days, and cytokine concentrations were determined by ELISA. The interleukin-3 (IL-3) and interleukin-6 (IL-6) levels were highest on day 1 and on days 1-3, respectively; the interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) levels reached the maximum on day 7, but the quantity of IL-4 was still three times higher than that in the control group 16 days after infection. The lungs of the mice in the second group were processed for the in situ demonstration of HDC activity, while the lungs in the third group were stained for C. pneumoniae antigen. The HDC activity was increased predominantly in the bronchial epithelial cells, while C. pneumoniae antigens were expressed especially in the interstitial macrophages. The HDC knockout mice exhibited a higher survival rate after C. pneumoniae infection than did the control mice. These results point to a strong association between local histamine production and other inflammatory mediators and are novel in demonstrating the role of histamine in the pathomechanism of C. pneumoniae infections.
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PMID:Chlamydophila (Chlamydia) pneumoniae induces histidine decarboxylase production in the mouse lung. 1455 83

Previously we demonstrated that histidine decarboxylase (HDC), which produces histamine from l-histidine, was detected in monocytes/macrophages located in human atherosclerotic lesions. As monocytic migration is a key event of atherogenesis, we investigated whether histamine induces monocytic expression of monocyte chemoattractant protein (MCP)-1 and its receptors CCR2-A and -B, and also endothelial expression of ICAM-1 and VCAM-1. Furthermore, we studied the effect of interleukin (IL)-4, which inhibits the HDC expression, on the expression of MCP-1 and CCR2. Histamine stimulated monocytes, but not macrophages, to express MCP-1 and CCR2-A and -B. The expression of MCP-1 was inhibited by histamine H2 blocker. In contrast, IL-4 enhanced CCR2 expression but not MCP-1. Histamine stimulated endothelial cells to express ICAM-1 and VCAM-1. These results indicate that histamine and IL-4, which are both synthesized in the arterial intima, chronically participates in the pathogenesis of atherosclerosis via the enhanced expression of monocytic MCP-1, CCR2 and endothelial adhesion molecules.
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PMID:Acute inflammatory reactions caused by histamine via monocytes/macrophages chronically participate in the initiation and progression of atherosclerosis. 1518 99


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