Determination oi 6-keto-prostaglandin Flα in rabbit kidney and urine and its relation to sodium balance

The occurrence of 6-keto-prostaglandin F_lα (6-keto-PGF_1α) was demonstrated in rabbit kidney medulla and cortex by mass-spectrometry. The post-mortem accumulation of 6-keto-PGF_1α was studied by mass-fragmentography in regions of the rabbit kidney using (3,3,4,4,-²H₄) 6-keto-PGF_lα as an internal standard. The cortex contained 1.4 + 0.3 μMg/g, the medulla 2.1 ± 0.6 μg/g and the papilla 3.7 ± 0.7 (S.E.) μg/g. The accumulation of 6-keto-PGF_1α is thus about 5 fold higher in the cortex than reported for PGE₂ and PGF_2α, whereas accumulation of PGE₂ and PGF_2α dominates over 6-keto-PGF_lα in the medulla and the papilla. The occurrence of 6-keto-PGF_lα in rabbit urine was demonstrated by mass-fragmentography. On a low salt diet unanesthetized, female rabbits (n = 6) excreted Na⁺ 0.09 ± 0.01 (S.E.) mmol/day, 6-keto-PGF_lα 11.8 ± 2.2 μg/day and immunoreactive PGF_2α (iPGF_2α) 2.0 ± 0.6 μg/day. Two days treatment with acetylsalicylic acid (30 mg/kgx 2) reduced urinary excretion of 6-keto-PGF_lα and iPGF_2α by 71 and 85%, respectively (both p < 0.05), but sodium excretion was unchanged. On the same diet supplemented with NaCl, the rabbits excreted Na⁺ 27.5 ± 3.4 mmol/day (p < 0,05), 6-keto-PGF_lα 13.3 ± 4.6 μg/day (p > 0.05) and iPGF_2α 0.63 ± 0.10 μg/day (p < 0.05). 6-keto-PGF_lα is a major metabolite of prostacyclin (PGI₂). The occurrence of 6-keto-PGF_lα in kidney and urine indicates a considerable synthesis of PGI₂ in the kidney. The data on urinary PG excretion indicate that intrarenal synthesis of PGI₂, in contrast to PGF_2α, is not influenced by dietary variations in NaCl.     

Different effects of furosemide on urinary excretion of prostaglandin E2 and F2α in rabbits

The effect of a constant infusion of furosemide (130 μg/min i.v. for 60 min, n = 8) was studied on urinary excretion of water, electrolytes and immunoreactive prostaglandin E₂ (iPGE₂) and iPGF_2α in chloralose-urethane anesthetized rabbits. During the furosemide infusion sodium and water excretion increased tenfold and the excretion of potassium and iPGE₂ two to three times. The excretion of iPGF_2α (0.06 ± 0.03 μg/min/100 g kidney weight) was not significantly changed during the furosemide infusion but increased markedly after the infusion and reached a maximum (1.0 ± 0.6 μg/min/100 g) 30 to 45 min later, while the small increase in iPGE₂ excretion at this time could be attributed to cross-reaction with PGF_2α The results indicate that PGE₂ might possibly be involved directly in the action of furosemide, while PGF_2α might participate in sodium and water conserving mechanisms in the rabbit kidney, activated by the drug induced diuresis.     

Comparison of PGE2, 6-keto PGF1α and renin release from dog kidneys

Several renal cell types synthesize prostaglandin E₂ (PGE₂) and prostacyclin (PGI₂). To examine whether the release of these prostaglandins varies in proportion, prostaglandin synthesis was stimulated in anaesthetized dogs by renal arterial constriction, ureteral occlusion, intrarenal angiotensin II infusion and infusion of arachidonic acid, the precursor of PG synthesis. PGI₂ was measured as its stable hydrolysed product, 6-keto PGF_1α. The two former procedures raised PGE₂ release to 13 ± 2 pmol min^-1, 6-keto PGF_1α release to 5 ± 2 pmol min^-1 and renin release to 23 ± 5 μg AI min^-1, Angiotensin II infusion, reducing the renal blood flow by 30%, increased PGE₂ and 6-keto PGF_1α release only half as much as ureteral and renal arterial constriction, and exerted no significant effect on renin release. By increasing the infusion rate of angiotensin II up to 10 times, the renal blood flow remained unaltered in four dogs and fell to 50% of control in two dogs, but PGE₂ and 6-keto PGF_1α release did not increase further in any of the experiments. Arachidonic acid, infused at 40 and 160 μg kg^-1 min^-1, increased prostaglandin release in proportion to the infusion rate. At the highest infusion rate, PGE₂ release averaged 166± 37 pmol min^-1 and 6-keto PGF_1α release 98 ± 28 pmol min^-1. All procedures increased PGE₂ and 6-keto PGF_1α release in a fixed proportion of about 2.5:1, whereas renin release increased only during autoregulatory vasodilation.     

Increased plasma concentrations of vasopressin,oxytocin, cortisol and the prostaglandin F2α metabolite during labour in the dog

Aim: This study investigated if the plasma vasopressin concentration increases during labour in the dog and whether the change in vasopressin correlates with that of oxytocin, 15‐ketodihydro‐PGF_2α and cortisol. Methods: Five beagle dogs each delivered three to seven puppies. Blood samples were taken from a catheter inserted into the cephalic vein during labour and by venepuncture during the other periods. Results: Vasopressin concentration increased from 2 ± 0 pmol L^?1 (anoestrus) to 26 ± 11 pmol L^?1 at the birth of the first puppy, remained high at the birth of the second puppy and then decreased. Oxytocin increased from 63 ± 5 pmol L^?1 (anoestrus) to 166 ± 19 pmol L^?1 at the birth of the first puppy and remained elevated throughout labour. The PGF_2α metabolite concentration increased from 0.2 ± 0.0 nmol L^?1 (anoestrus) to 66 ± 17 nmol L^?1 at the birth of the first puppy and remained elevated 1 h after the completion of parturition. The cortisol concentration increased from 49 ± 9 nmol L^?1 (anoestrus) to 242 ± 35 nmol L^?1 at the birth of the first puppy, remained high during the birth of the second puppy and then declined. Conclusions: The plasma level of vasopressin was strongly correlated with that of cortisol but less with that of the PGF_2α metabolite, and not significantly with the concentration of oxytocin. This indicates that the four hormones play different roles during labour in the dog.     

Gonadotropins Induce the Release of Interleukin-1β, Interleukin-6 and Tumor Necrosis Factor-α from the Human Preovulatory Follicle

PROBLEM; The effects of exogenous gonadotropin administration and steroid levels on the release of various cytokines into the human follicular fluid (FF) were studied. METHOD OF STUDY: Forty patients were included in two groups, those undergoing controlled ovarian hyperstimulation (COH) (n = 33) and natural cycles (n = 7). FF transvaginal aspirations were performed 36 hr after administration of human chorionic gonadotropin or a spontaneous surge of luteinizing hormone, respectively. FF cytokine measurements were performed with sensitive immunoassays. RESULTS: FF cytokine levels were higher after COH [interleukin (IL)-1β, 6.6 ± 0.32 pg/ml; IL-6, 18.7 ± 2.1 pg/ml; and tumor necrosis factor (TNF)-α, 32.5 ± 4.9 pg/ml] than in natural unstimulated cycles (0.52 ± 0.1 pg/ml, P < 0.001; 8.9 ± 1.2 pg/ml, P < 0.01; and 13.2 ± 2.6 pg/ml, P < 0.001, respectively). FF estradiol (E₂) and progesterone levels were not statistically different between groups, despite the higher serum E₂ levels observed in patients after COH. CONCLUSIONS: Gonadotropins might regulate ovarian secretion of cytokines, because FF IL-1β, IL-6, and TNF-α levels after COH were higher than during natural cycles.     

Renal degradation and distribution between urinary and venous output of prostaglandins E2 and I2

Renal degradation and distribution between urinary and venous output of prostaglandins E₂ and I₂ Acta Physiol Scand 130 , 467–474. Received 25 November 1986, accepted 11 February 1987. ISSN 0001–6772. University of Oslo, Institute for Experimental Medical Research, Ullevaal Hospital, Oslo, Norway. To examine renal degradation and distribution between urine and renal venous blood, prostaglandins E₂ and I₂ (PGE₂ and PGI₂), and a metabolite of PGI₂, bketo-PGF_1α, were infused into the suprarenal aorta of anaesthetized dogs after blocking prostaglandin synthesis by indomethacin, 10 mg kg^-1 body wt iv. During one passage through the kidney 80% of PGE, and only 25% of PGI₂ and 6-keto-PGF_1α, were metabolized. Prostaglandin degradation and arterial input were proportional (r > 0.90). To stimulate the intrarenal prostaglandin synthesis in unblocked kidneys, arachidonic acid was infused at rates ranging from 24 to 160 μg min^-1 kg^-1 body wt. During arachidonic acid and PGE₂ infusion the urinary excretion of PGE₂ was about 20% of the renal venous output over a wide range of infusion rates. During arachidonic acid and PGI₂ infusion urinary excretion of bketo-PGF_1α was about 10% of total renal output, but failed to increase further when total renal output exceeded 70 pmol min^-1. Further increase in output occurred only in the renal vein. In contrast, during 6-keto-PGF_1α infusion the urinary excretion and the renal venous output of this metabolite were related as 1:2 over a wide range of infusion rates. Thus, PGI₂ is much less degraded by renal tissue than PGE₂, and the distribution patterns differ. Similar distributions between urine and renal venous blood during aortic infusion and stimulated intrarenal synthesis suggest a pre-glomerular vascular origin of both prostaglandins.     

Treatment of Sheep With Prostaglandin F2α Enhances Production of a Luteal Chemoattractant for Eosinophils

ABSTRACT: Eosinophils were quantitated in sections of luteal tissue obtained from sheep treated with a luteolytic dose of prostaglandin (PG) F₂α. Increased numbers of cells were detected before the onset of either functional (decline in sera or tissue concentrations of progesterone) or morphological regression. Luteal tissue was shown to produce a specific chemoattractant for eosinophils as assessed by a linear under-agarose migration assay. Eosinophils were responsive toward leukotriene B₄, but not toward PGF₂α or a synthetic N-formyl peptide. Because eosinophils are capable of mediating tissue damage in immune/inflammatory conditions, it is suggested that these cells could play a similar role in the mechanics of luteolysis.     

Effects of prostaglandin E1, E2, and F2α on isolated pial arteries of cat

Responses to prostaglandin (PG), E₁, E₂, and F_2α were studied on isolated feline middle cerebral arteries. At resting state PGF_2α produced strong dose-dependent contractions. PGE₂ elicited weak relaxations at low concentrations, followed by powerful contractions at higher doses. PGE₁ had little effect on resting pial vessels. The relative constrictory potency was PGF_2α > PGE₂ > PGE₁. During active tone, induced by administration of either potassium, norepinephrine, or 5-hydroxytryptamine, relaxations induced by PGE₁ were enhanced, whereas PGE₂-induced relaxations were unaffected. PGE₁ induced relaxations were more pronounced when the active tension had been produced by administration of PGF_2α than with either of the vasoactive amines or potassium. This study demonstrates the importance of smooth muscle tone, and by what means this is achieved, when examining the responses of PG's on cerebral blood vessels.     

Duodenal intraepithelial γ/δ T cells and soluble CD8, neopterin,and β2-microglobulin in serum of IgA-deficient subjects with or without IgG subclass deficiency

Expression of the γ/δ T cell receptor (TCR) on CD3⁺ intracpithclial lymphocytes (IELs) was studied by two-colour immunofluorescence in duodenal tissue sections from healthy (n= 6) or infection-prone (n = 7) subjects with selective IgA deficiency (IgAD), and subjects (n= 4) with combined IgAD and IgG subclass deficiency. TCRγ/δ⁺ IEL proportions in selective IgAD subjects (median 6.3%, range 1.0–41%) and in those with combined deficiency (median 4.5%, range 1±2.33%) were well within the range (0.3.38%) for histologically normal controls (n= 11), but the healthy IgAD subgroup tended to show raised TCRγ/δ⁺ IEL proportions (median 13.6%) compared with the other two subgroups. Also the number of TCRγ/δ⁺ IELs per intestinal length unit was relatively high (median 13.9/mm) in the healthy IgAD subjects, and significantly raised (P < 0.03) compared with controls (median 3.2/mm). Paired staining revealed that most TCRγ/δ⁺ IELs in both selective IgAD (98%) and combined deficiency (99%) were CD8, and a large fraction (median 84% and 63%, respectively) expressed the Vδ1/Jδ1-encoded epitope. The total number of CD3’ IELs (mostly CD8⁺) was similar to controls. IgAD subjects, and especially the healthy subgroup, had significantly increased serum concentrations of soluble CD8 (P < 0.0002), neopterin (P < 0.005), and β₂-microglobulin (P < 0.007). which was similar to our previous observations in common variable immunodeficiency, and probably reflected stimulation of cell-mediated immunity. In addition, the increased TCRγ/δ⁺ IELs might reflect a component of compensatory surface protection in the healthy IgAD subgroup.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

The stimulatory effect of α‐melanotropin on progesterone release from rat granulosa cells is inhibited by interleukin‐1β and by tumour necrosis factor‐α

Aim: Several studies have shown that a variety of peptides and cytokines are involved in ovarian regulatory mechanisms; however, their exact function is still unclear. In this work we study whether the administration of peptide α‐melanotropin and the cytokines interleukin‐1β (IL‐1β) and tumour necrosis factor‐α (TNF‐α) on their own modify the release of progesterone in cultured granulosa cells (GC) from pro‐oestrous rats. We also investigate an interaction between these cytokines and α‐melanotropin in the modulation of progesterone secretion. Methods: Granulosa cells were collected from the ovaries of female Wistar rats and cultured for up to 24 h in the presence of different concentrations of α‐melanotropin, cytokines or a combination of both. Progesterone concentration was measured by radioimmunoassay. Results: The addition of α‐melanotropin in a dose of 0.01 and 0.1 mm had no effect on progesterone release, whereas a dose of 1 mm significantly increased progesterone release (P < 0.01) compared with the control culture. Progesterone release was not modified when different concentrations of interleukin‐1β or TNF‐α were added to the cell cultures. However, when interleukin‐1β or TNF‐α were added simultaneously with 1 μm α‐melanotropin, a significant reduction (P < 0.01 for interleukin‐1β and P < 0.05 for TNF‐α) of the steroid release was found with respect to the α‐melanotropin‐treated group. Conclusions: These results lead us to suggest that, although α‐melanotropin stimulates progesterone release in pre‐ovulatory GC, this effect is blocked by the presence of interleukin‐1β or TNF‐α.     

Interleukin-1β (IL-1β) Is Increased in the Follicular Fluids of Patients With Premature Luteinization

PROBLEM : Most, but not all, studies indicate that premature luteinization correlates with poor pregnancy outcome in in-vitro fertilization (IVF) programs. It remains unclear whether cytokines (IL-1β, TNFα), the established immune mediators, play a role in regulation or initiation of an abnormal follicular or embryo development in patients with premature luteinization. METHODS : Levels of cytokines (IL-1β, TNFα), estradiol (E2), progesterone (P4), and androstenedione (Aione) were examined in 18 preovulatory follicular fluid (FF) samples from patients with premature luteinization (group 1) and 37 FF samples from patients without premature luteinization (group 2). The number of oocytes recovered, fertilization rate, and pregnancy outcome were evaluated in these two groups. RESULTS : IL-1β (25.4±11.9 pg/ml, mean ±SD) and TNFα (13.4±10.7 pg/ml) were present in these FF samples. The mean level of IL-1β in group 1 was significantly higher than that in group 2 (37.3±12.3 vs. 20.0±7.6 pg/ml; P<0.00001) and the mean level of E2 was significantly lower in group 1 than that in group 2 (1064±686 vs. 1570±641 ng/ml; P=0.02). The levels of TNFα, P4, and A'ione showed no distinction between these two groups. There was no correlation between the levels of either IL-1β or TNFα and P4, E2 or A'ione. The fertilization rate in group 1 (62/77; 80%) was similar to that in group 2 (124/160;78%). Five of 7 patients in group 1 and seven of 20 patients in group 2 achieved pregnancy following embryo transfer. One of five pregnancies in group 1 aborted. CONCLUSION : The exaggerated levels of IL-1β in patients with premature luteinization may arise from accumulation of this cytokine owing to sustained high LH stimulation, and this may be a protective response to the abnormal LH surge and function to inhibit prematurely increased secretion of P4. These data indicate the important role of LH in the induction of IL-1β secretion and the possible regulatory action of IL-1β in luteinization. According to the diminution of E2 in group 1, there may be a subtle atretic process progressing in follicles primed with prematurely elevated LH. However, the detrimental effect of premature luteinization, if it exists, may work at the stage during or after implantation.     

Cyclic AMP-dependent and independent effects of prostaglandins on the contraction-relaxation cycle of spontaneously beating isolated rat atria

The effects of prostaglandin (PG) F_2α, E₂, E₁ and I₂ on the amplitude, duration of the contraction-relaxation cycle (CRC), the second derivative of developed tension and the cyclic adenosine-3′,5′-monophosphate (cAMP) level and on ⁴⁵Ca uptake were studied in isolated spontaneously beating rat atria. The order of capacity to generate positive inotropic effects was PGF_2α>PGE₂>PGE₁?PGI₂. Only PGI₂ and PGE₁ decreased the duration of CRC. PGF_2α produced an increase during the first 2.5min, whereafter the duration returned to the initial level. PGE₂ had no significant effect on the shape of the CRC. The ratios of the maximum and minimum of the second derivative of the developed tension were reduced by PGI₂ and PGF_2α 2.5 and 5 min after administration, respectively. The ⁴⁵Ca uptake was stimulated equally by all of the tested PGs, but only PGI₂ and PGE₁ could significantly increase the cAMP level. The results do not support the conception that cAMP could mediate the positive inotropic effect of PGs. Rather the contrary, cAMP, increased by PGE₁ or PGI₂, could be responsible for increased relaxation, which might prevent the full development of tension.     

The influence of renal papillary urea concentrations and of plasma vasopressin on the urinary prostaglandins E2 and F2α excretion in conscious rats in steady state of urine formation

Urinary excretion rates of PGE₂ and PGF_2α were measured radioimmunologically in four different groups of unanaesthetized rats: water diuretic rats (I), rats with free access to water (II), water deprived rats (III) and 1.5% saline-loaded rats (IV). The animals were decapitated when steady states of urine formation were ascertained for three to six spontaneously delivered urine portions. Plasma vasopressin was measured radioimmunologically and urea, sodium, potassium concentrations and osmolalities of papillary fluids and of bladder urines were determined. Group means of urinary prostaglandin excretion, papillary urea concentration and logarithmic-transformed plasma vasopressin values vary in parallel for three of the groups (I, II and III) but a dissociation of the effects of papillary urea and vasopressin on the prostaglandin excretion was obtained for group IV. Statistical analyses indicated that the differences in prostaglandin excretion rates between group I and the three other groups are accounted for by the combined effects of vasopressin and papillary urea. The results support the hypothesis that vasopressin stimulates release of arachidonic acid in the papilla and that urea inhibits the trapping of this prostaglandin precursor in cellular lipids. The ratio of urinary PGF_2α to PGE₂ varied greatly between groups but no consistent dependency on the measured parameters was found.     

Glucose stimulates the entry of Ca2+ into the insulin-producing β cells but not into the glucagon-producing α2 cells

Rat pancreatic β and α₂ cells were purified by autofluorescence-activated cell sorting and used for electrophysiological patch clamp studies and measurements of the initial uptake of ⁴⁵Ca. Both β and α₂ cells were electrically active, the action potentials of the latter cells also were detected in the absence of glucose. Furthermore, α₂ cells differed from β cells in lacking a glucose-sensitive K⁺ channel with a single channel conductance of 50–60 pS (in symmetric 140 mm K⁺ solutions). The rate of Ca²⁺ entry into the α₂ cells was slower than that into the β cells, being equivalent to 0.2 mmol, kg^-1 dry wt min^-1. Whereas raising the glucose concentration to 20 mm significantly increased the amount of Ca²⁺entering the β cells, the sugar was without effect on Ca²⁺ entry into the α₂ cells.     

Mechanisms of chorioamnionitis‐associated preterm birth: interleukin‐1β inhibits progesterone receptor expression in decidual cells

In chorioamnionitis (CAM), a major cause of preterm birth (PTB), maternal–fetal inflammation of the decidua and amniochorion cause the release of cytokines that elicit cervical ripening, fetal membrane rupture and myometrial activation. We posit that this inflammatory milieu triggers PTB by inhibiting progesterone receptor (PR) expression and increasing decidual prostaglandin (PG) production. Immunohistochemical staining of decidua detected significantly lower PR levels in decidual cells (DCs) from CAM‐complicated PTB. Incubation of DCs with IL‐1β decreased PR expression and significantly increased PGE₂ and PGF_2α production and COX‐2 expression. The addition of PGF_2α to DC cultures also suppressed PR expression. However, the COX inhibitor, indomethacin, did not reverse IL‐1β suppression of PR expression in DC cultures. Although IL‐1β treatment activated the NF‐K B, ERK1/2 and p38 MAPK signalling cascades in DCs, inhibition of ERK1/2 MAPK signalling alone was sufficient to completely reverse the suppression of PR levels by IL‐1β. These findings suggest that CAM‐associated PTB is induced at least in part by IL‐1β‐mediated functional progesterone withdrawal. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Endotoxin-induced prostaglandin (PGF2α) biosynthesis,fever and miosis in dexamethasonetreated goats

Prostaglandin-releasing, adrenocortical, febrile and miotic responses to endotoxin (ET) (E. coil lipopolysaccharide; 0.25 μg kg^-1) were studied in goats with and without prolonged dexamethasone influence. The i.v. injection of ET induced a three-fold peak elevation in plasma 15-ketodihydro-PGF_2α at 1.5 h post-injection, that is, between the first and second phase of the temperature elevation. During the latter phase, the plasma concentration of this primary PGF_2α metabolite gradually returned to basal level, which implies that the second phase of ET fever is not PG dependent. The PG response exhibited a similar pattern, but was less pronounced in the dexamethasone-ET experiments, where the duration of maximum temperature elevation and of the miosis became shortened by about 20 min, and the typical biphasic pattern of ET fever was no longer seen. The ET-induced rise in plasma aldosterone concentration was completely blocked by dexamethasone. The corresponding rise in plasma cortisol concentration was prevented for 2 h, but was later only partially inhibited in spite of the repeated dexamethasone treatment.     

Quantification of α2A and α2C adrenoceptors in the rat striatum and in different regions of the spinal cord

The α_2C-adrenoceptor preferring radioligand [³H]-MK912 was used for labelling α_2A- and α_2C-adrenoceptors in the rat striatum, in the cervical, thoracic and lumbar parts of the spinal cord, and in the dorsal and ventral halves of the spinal cord. In addition, guanfacine was used as a tool to delineate the α_2A- and α_2C-adrenoceptors. In the striatum the sites were 72% α_2A- and 28% α_2C-adrenoceptors, while in all regions of the spinal cord the proportions of the sites were about 96% α_2A- and 4% α_2C-adrenoceptors. A multi-curve experimental design and computer analysis was used in order to enable the accurate quantification of the α_2A- and α_2C-adrenoceptors in the striatum and spinal cord.     

Amniotic Fluid Thymosin α1 Levels Increase During Gestation

ABSTRACT: Thymosin α₁ is one of several cytokines produced by the thymus that modulates immune function. The presence of elevated serum levels of thymosin α₁ in pregnant women and their newborns has suggested that this peptide may play a role in perinatal immunology. In this investigation, we used a microenzyme-linked immunosorbent assay to assay amniotic fluid for immunoreactive thymosin α₁ and found levels that were remarkably higher than newborn serum levels (P < 10^?4). The increase of thymosin α₁ in amniotic fluid with fetal age was natural logarithmic (r = 0.838, P < 10^?6). Thymosin α₁ in amniotic fluid may account for some of the immunologic properties of this medium.