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Biomedical subjects

S A Saeed

Publications and source records attributed to S A Saeed.

At least 73 records · Page 4Linked to original sources
PubMed1988

GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

Animals↗
PubMed1988

Differential effects of dimethyl sulfoxide on human platelet aggregation and arachidonic acid metabolism.

DMSO inhibited human platelet aggregation induced by ADP, AA, PAF, or collagen in a concentration-related manner, in vitro. DMSO was a more effective inhibitor for aggregation induced by ADP and collagen than PAF or AA. However, in vivo experiments on rabbits showed that DMSO did not protect rabbits against death from pulmonary platelet thrombosis induced by AA. On the other hand, DMSO (1-30% v/v) had no effect on thromboxane production by platelets incubated with [14C]AA. Moreover, DMSO stimulated PGE2 production by bovine seminal vesicle PG synthase. DMSO also stimulated the production of 12-HETE but inhibited the production of tri-HETE produced via lipoxygenase pathway. Since lipoxygenase products play an important role in inflammation, our data suggest that the anti-inflammatory effects of DMSO are probably not mediated via its action on AA metabolism.

Animals↗
PubMed1987

Ability of human plasma to inhibit prostaglandin F2 alpha in asthma.

Human plasma has been reported to inhibit the conversion of arachidonic acid into prostaglandin (PG) E2 and PGF2 alpha. In the present study the plasma inhibitory activity was determined in three groups (16 each) of plasma obtained from normal healthy volunteers, treated asthmatics and untreated asthmatic patients. The result showed that plasma from all three groups were equally effective in inhibiting the biosynthesis of PGE2. Plasma of normal volunteers and treated asthmatics also inhibited PGF2 alpha biosynthesis. In contrast the plasma obtained from untreated asthmatics was considerably less active in inhibiting the biosynthesis of PGF2 alpha than plasma from the other two groups.

Asthma↗
PubMed1985

Endogenous stimulant of prostaglandin endoperoxide synthase activity in human amniotic fluid.

In this study we describe the discovery and characterization of a substance in human amniotic fluid that stimulates prostaglandin biosynthesis by a microsome-enriched preparation of bovine seminal vesicles. The stimulatory activity is not retained substantially upon anisotropic ultrafiltration through a filter with a molecular weight exclusion limit of 500. Stimulation of prostaglandin biosynthesis by this substance is time- and concentration-dependent; maximal stimulation of approx. 200% being observed within 20 min of commencing incubation with 1 ml-equivalent of stimulant fraction. Stimulatory activity is demonstrable both in the presence of reduced glutathione (1.3 mM) and L-tryptophan (20 mM), either separately or combined, and in the presence of exogenous arachidonic acid (5-120 microM). In the absence of added cofactors, the stimulatory substance increases the rates of biosynthesis of prostaglandin E2 and prostaglandin F2 alpha to equal extents. The amount of stimulatory substance added to incubations is correlated positively with increased oxygen consumption during incubations. The stimulatory substance is stable to heating at 100 degrees C for 10 min but is inactivated substantially (to less than 20% of original activity) by treatment with pronase. It is concluded that human amniotic fluid contains a substance of relatively low molecular weight, which is proteinaceous in character, that stimulates prostaglandin endoperoxide synthase activity.

Amniotic Fluid↗
PubMed1984

Prostaglandin synthase inhibitory activity in plasma of women with dysmenorrhea.

Prostaglandins have been implicated in the etiology of dysmenorrhea, and plasma levels of prostaglandin F metabolite are increased in women during dysmenorrhea episodes. We determined the prostaglandin synthase inhibitory activity of plasma obtained from the blood of women who experience moderate to severe dysmenorrhea. Blood was obtained at the onset of dysmenorrhea ("symptomatic") and during the late follicular phase of the ovarian cycle ("asymptomatic"). Prostaglandin synthase inhibitory activity in all samples was comparable to that previously found in adult women, and we found no difference in activity between the paired plasma samples, those obtained during symptomatic and asymptomatic times. Protein denaturation of the plasma by boiling also did not produce differences in prostaglandin synthase inhibition.

Adult↗
PubMed1983

Stimulation of prostaglandin biosynthesis by urine of the human fetus may serve as a trigger for parturition.

Urine of the human fetus stimulated prostaglandin biosynthesis in vitro by increasing the conversion of arachidonic acid into prostaglandins. The stimulatory activity in urine from fetuses delivered at term after labor of spontaneous onset was greater than that in urine from fetuses delivered by cesarean section at term before the onset of labor. Such stimulation of prostaglandin biosynthesis by the fetal membranes, by way of a substance released into the urine and thence into amniotic fluid, could serve as a signal for the initiation of parturition.

Adult↗
PubMed1983

Conversion of arachidonic acid to lipoxygenase products by human fetal tissues.

[14C]Arachidonic acid was converted to several lipoxygenase products by homogenates of human fetal tissues as determined by thin-layer chromatography. The net conversions of [14C]arachidonic acid to radiolabeled lipoxygenase products were high (greater than or equal to 5%) in the case of fetal liver and brain, and low (less than or equal to 2%) in the case of fetal adrenal, heart, and kidney.

Arachidonic Acid↗
PubMed1983

Lipoxygenase activity in human uterine and intrauterine tissues: new prospects for control of prostacyclin production in pre-eclampsia.

The formation of lipoxygenase metabolites by human uterine and intrauterine tissues was evaluated using [1-14C]arachidonic acid (AA) as substrate. The major lipoxygenase product synthesized by human amnion, decidua vera and placenta was identified as 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE); smaller amounts of 5-HETE and 5-HETE (lactone form) were also formed. In chorion laeve only a trace amount of 12-HETE was detected. Human myometrium and cervical tissue converted [1-14C]AA to 5-HETE and 12-HETE in almost equal amounts. The formation of lipoxygenase products in all tissues was markedly inhibited by nordihydroguaiaretic acid (NDGA) an inhibitor of lipoxygenase activity and slightly stimulated or inhibited by indomethacin, an inhibitor of cyclooxygenase activity. These results are indicative that uterine and intrauterine tissues are probably potential sources of lipoxygenase products during pregnancy and parturition. Since 12-hydroperoxy-eicosatetraenoic acid (12-HPETE), the labile precursor of 12-HETE potently inhibits prostacyclin biosynthesis, our findings are suggestive of the possibility that aberrant lipoxygenase activities may contribute to the complications of pre-eclampsia.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Stimulants of prostaglandin biosynthesis in human fetal membranes, uterine decidua vera and placenta.

Modulation of prostaglandin (PG) biosynthesis by cytosolic fractions derived from homogenates of human amnion, chorion laeve, decidua vera and placenta was examined. PGF2 alpha and 6-oxo-PGF1 alpha synthesis by bovine seminal vesicle (BSV) PG synthase was stimulated by the cytosolic fractions of each tissue in a dose-dependent manner. The cytosols from decidua vera and placenta were the most effective in stimulating synthesis and also stimulated PGE2 biosynthesis. Reduced glutathione (GSH) acted to increase the biosynthesis of PGE2 at the expense of other PGs both in the presence and absence of various cytosols. These data are indicative that the mode of action of cytosolic fractions on the stimulation of PG biosynthesis is unlike that of GSH. Indomethacin and aspirin, inhibitors of fatty acid cyclo-oxygenase activity, strongly inhibited the cytosol-induced stimulation of BSV PG synthase. The cytosolic factors that stimulated PG biosynthesis exhibited differential behavior towards boiling and dialysis. The stimulatory effect of all cytosolic fractions was sensitive to boiling except in the the chorion laeve effects toward 6-oxo-PGF1 alpha production. In dialysis studies we found that the cytosolic components that stimulated the production of PGF2 alpha were not removed by dialysis except in the case of cytosol of placenta whereas the stimulatory effects of various cytosols toward the biosynthesis of PGE2 and 6-oxo-PGF1 alpha were removed by dialysis. These results are indicative of the presence of endogenous factors in human intrauterine tissues that preferentially stimulate the biosynthesis of PGF2 alpha and 6-oxo-PGF1 alpha and are further suggestive that PG biosynthesis in intrauterine tissues is, at least in part, regulated by cytosolic factors.

Animals↗