Leukotrienes
According to the study of Prostaglandins and leukotrienes as inflammatory mediators by John A Salmon and Gerald A Higgs(a), Leukotrienes
is produced in leukocytes as a result of oxidative metabolism of
arachidonic acid by the enzyme arachidonate 5-lipoxygenase, belonging to
the family of eicosanoid inflammatory mediators(a). Its production is
usually accompanied by the production of histamine and prostaglandins.
21. Urinary leukotriene E4 in children with severe atopic eczema/dermatitis syndrome
Leukotrienes are thought to play a role in the pathogenesis of atopic eczema/dermatitis syndrome (AEDS). Urinary leukotriene E4 (U-LTE4) is a marker of whole-body cysteinyl-leukotriene
production. According to the study by the Department of Pediatrics,
Rogaland Central Hospital, in the study to evaluate the role of leukotrienes
in children with AEDS by measuring levels of U-LTE4, and to evaluate
whether levels of U-LTE4 may reflect disease activity and allergic
sensitization in AEDS, indicated that a role for leukotrienes in the pathogenesis of severe AEDS, and may support a role for leukotriene-antagonists
in the treatment of this disorder. Levels of U-LTE4 may reflect the
disease severity and sensitization to allergens in AEDS(21).
22. Leukotriene and eosinophil protein X in children with atopic asthma
In the study to examine the differences in
urinary LTE4 and EPX concentrations between children with stable atopic
asthma and healthy controls and to compare asthmatic children with
different disease severity by evaluating the relationship between
urinary LTE4 and EPX levels and lung function. LTE4 was also measured
(enzyme immunoassay) together with EPX (radioimmunoassay) in urine and
lung function tests were carried out in children with mild asthma
(steroid-naive) (n=49), moderate to severe asthma (using inhaled
steroids) (n=31) and healthy control subjects (n=28), showed that there
were no differences in urinary LTE4 and EPX between the group of mild
and the group of moderate to severe asthmatic children. There were
significant associations between the urinary LTE4 and intrathoracic gas
volume (ITGV), residual volume (RV), forced expiratory volume in one
second (FEV1), forced expiratory capacity (FVC) and maximum expiratory
flow rate at 25% of vital capacity (MEF25). Urinary EPX was only
correlated with maximum expiratory flow rate at 75% of vital capacity
(MEF75)(22).
23. Leukotriene and vasogenic edema
In the study to determine whether tissue leukotriene-like immunoreactivity was increased in intracranial tumors associated with peritumoral edema. 20 patients undergoing craniotomy tissue specimens were immediately frozen after removal and tissue leukotriene C4 levels were determined by radioimmunoassay, indicated that there was a significant correlation between brain edema and tissue leukotriene levels (p less than 0.003). Metastatic tumors (n = 8) had the highest leukotriene C4 level at 13.8 +/- 8.5 pg/mg tissue (mean +/- SE) and the highest index of edema 5.7 +/- 1.8. The mean leukotriene C4 level in the gliomas (n = 5) was 6.2 +/- 2.3 pg/mg tissue and the edema index was 2.1 +/- 0.6(23).
24. Leukotriene D4 in pulmonary edema fluid
In the examination by quantifying the pulmonary edema
fluid concentrations of lipoxygenase and cyclooxygenase products to
detemine the possible contribution of metabolites of arachidonic acid to
the increased permeability of the alveolar-capillary barrier in the
adult respiratory distress syndrome, indicated that The concentration of
leukotriene D4 in pulmonary edema
fluid of 10 patients with the adult respiratory distress syndrome (18.5
+/- 6.8 pmol/ml; mean +/- SD), assessed by specific radioimmunoassay
after isolation of the mediator, was significantly higher (P less than
0.001) than that of five patients with cardiogenic pulmonary edema (4.4 +/- 1.1 pmol/ml). The concentrations of leukotrienes B4 and C4, prostaglandin E2, and thromboxane B2 in edema
fluid were not significantly different in the adult respiratory
distress syndrome patients than in the other subjects with pulmonary edema. The edema fluid concentration of leukotriene D4 correlated with the ratio of edema fluid to plasma concentrations of albumin (r = 0.64). Leukotriene
D4 thus may contribute to the permeability defect which allows an
accumulation of protein-rich alveolar fluid in the adult respiratory
distress syndrome(24).
25. Syndrome of aspirin-exacerbated respiratory disease (AERD)
Chronic rhinosinusitis (CRS) with nasal polyposis (NP) may be associated
with hypersensitivity to nonsteroidal anti-inflammatory drugs,
representing a syndrome of aspirin-exacerbated respiratory disease
(AERD). According to the study by the Jagiellonian University Medical
College, among CRS subjects requiring functional endoscopic sinus
surgery (FESS), as many as 33.3% may have AERD and respond to a small
provocative dose of aspirin with bronchoconstriction and/or mucosal and
skin edema. A simple and inexpensive measurement of uLTE4 (leukotriene
E4) can help diagnose AERD in patients with CRS with sensitivity of
87.5%, but its specificity is limited and depends on the arbitrary
threshold of uLTE4(25).
26. Leukotriene and uterine vascular responses to estrogen
In the study to test hypothesis of that the leukotrienes may be the mediators of the uterine vascular responses to estrogen, by giving FPL 55712, a selective leukotriene
antagonist, to estrogen-primed, nonpregnant rabbits and measured
regional blood flows by the radioactive microsphere technique, indicated
that leukotrienes do not mediate, but rather inhibit, the uterine vascular responses to estrogen(26).
27. Leukotrienes and gastric hyperemia
In the study on anesthetized dogs to determine the role of eicosanoids
in regulation of total, and mucosal gastric blood flow and oxygen
consumption in the stomach damaged by the instillation of 25% ethanol,
showed that The inhibition of prostaglandins generation by indomethacin
caused an ischemia and hypoxia in the stomach. It was an evidence for
their basal generation and tonic influence on circulation in this organ.
OKY--a blocker of thromboxanes synthesis and NDGA--a blocker of
5-lipoxygenase did not alter circulatory and metabolic parameters in the
stomach. Above findings indicate, that thromboxanes and leukotrienes
are not involved in the physiological modulation of blood vessels
activity and oxygen consumption in the stomach. But administration of
25% ethanol on gastric mucosa affected in a rise of total and mucosal
blood flow and oxygen consumption. These effects were significantly
potentiated by OKY and NDGA and suggesting, that damaged gastric mucosa
is able to generate thromboxanes and leukotrienes which cause vasoconstriction. It seems, that endogenous prostaglandins also play an important role, because the gastric hyperemia and the increase in gastric oxygen consumption after alcohol were inhibited by indomethacin.(27).
28. Leukotriene (LT) D4 and coronary constriction
In the study the effects of leukotriene
(LT) D4 (0.5 microgram/min) infusion into the left anterior descending
coronary artery (LAD) of anesthetized pigs, in the absence or presence
of indomethacin (5 mg/kg i.v.), indicated that the coronary constriction
disappeared despite sustained LTD4 infusion and was followed by
reactive hyperemia. Indomethacin did not
affect the coronary flow or hemodynamic responses to LTD4 infusion. The
A-V difference in prostanoids did not change during LTD4 administration.
However, intracoronary bolus injection of LTD4 stimulated prostacyclin
release from the vasculature in a dose-dependent manner causing
significant reactive hyperemia after temporary blood flow cessation. Release of a LTD4-induced(28).
29. Leukotriene D4 (LTD4) and functional impairment
In the Glomerular micropuncture studies to evaluate the glomerular microcirculatory actions of leukotriene
D4 (LTD4) in euvolemic, anesthetized, adult, male Munich-Wistar rats,
indicated that in the preliminary experiments, intrarenal arterial
administration of LTD4 (1 microgram X kg-1 X min-1) was found to cause a
rise in mean systemic arterial pressure, a loss
of plasma volume, and a fall in renal blood flow, effects identical to
those previously reported for LTC4. glomerular microcirculatory dynamics
were assessed during LTD4 infusion while constancy of renal perfusion
pressure and plasma volume were maintained by partial aortic
constriction and isoncotic plasma infusion, respectively, with
saralasin (5 micrograms X kg-1 X min-1 iv) was also given throughout the
study, LTD4 caused a significant increase in efferent arteriolar
resistance in association with a fall in glomerular plasma flow rate
(QA) and a rise in glomerular capillary hydraulic pressure. Despite the
latter, single-nephron filtration rate fell due to combined reductions
in QA and the glomerular ultrafiltration coefficient. These local
glomerular constrictor actions of LTD4 support the possibility that this
eicosanoid might play an important intermediary role in the functional impairment accompanying some forms of inflammatory injury(29).
30. Primary PGs (including prostacyclin), thromboxanes, and leukotrienes during benign or malignant pathological processes
Prostaglandins (PGs) are a family of lipid
compounds synthesized from polyunsaturated fatty acids derived from
phospholipids, and divided into three main classes: primary PGs
(including prostacyclin), thromboxanes, and leukotrienes
and presented in very low quantities under normal or resting condition.
According to the study byRolland PH., Prostaglandins (PGs) showed a
marked increase in levels during benign or malignant pathological
processes as the results from loss of the physiological state of tissue dependence of the cells, which acquire functional autonomy and become endowed with properties which appear to be important in cancer dissemination processes(30).
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Sources
(21) http://www.ncbi.nlm.nih.gov/pubmed/15575936
(22) http://www.ncbi.nlm.nih.gov/pubmed/11106196
(23) http://www.ncbi.nlm.nih.gov/pubmed/3729313
(24) http://www.ncbi.nlm.nih.gov/pubmed/6511865
(25) http://www.ncbi.nlm.nih.gov/pubmed/22814420
(26) http://www.ncbi.nlm.nih.gov/pubmed/6695994
(27) http://www.ncbi.nlm.nih.gov/pubmed/1845317
(28) http://www.ncbi.nlm.nih.gov/pubmed/3568058
(29) http://www.ncbi.nlm.nih.gov/pubmed/3618788
(30) http://www.ncbi.nlm.nih.gov/pubmed/6815214
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