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Biomedical subjects

S Mousa

Publications and source records attributed to S Mousa.

34 records · Page 2Linked to original sources
PubMed1985

Decreased enkephalinase activity following postnatal treatment with phenobarbital.

The effect of postnatal administration of phenobarbital on enzymes degrading enkephalin was examined. Daily subcutaneous injections (45 mg/kg) of phenobarbital were given to male and female rats from postnatal day 1 to 19. Brains from rats treated with saline and phenobarbital were used to prepare aminopeptidases (high speed supernatant) and enkephalinase A (synaptosomal membrane preparation). Incubation of methionine enkephaline (ME) with aminopeptidases from rat brain liberated tyrosine (T), while incubating with enkephalinase A resulted in the formation of tyrosylglycylglycin (TGG). Separation and quantification of tyrosine, tyrosylglycylglycin and methionine enkephalin was performed using a high performance liquid chromatograph, coupled to electrochemical and ultraviolet detectors in series. The treatment of the rats with phenobarbital resulted in a significant inhibition of enkephalinase A when measured in vitro, using methionine enkephalin as substrate. Preliminary studies with secobarbital show similar results to those obtained with phenobarbital.

Aminopeptidases↗
PubMed1984

Prenatal alcohol exposure alters enkephalin levels, without affecting ethanol preference.

Pregnant dams were pair-fed a liquid diet containing 35% ethanol derived calories or isocaloric sucrose during the last two trimesters of pregnancy. No differences were observed in adult ethanol preference between fetal alcohol exposed (FAE) animals and pair-fed controls. However, Met- and Leu-enkephalin levels were significantly elevated in globus pallidus of adult FAE animals. Pituitary levels were unaffected.

Alcohol Drinking↗
PubMed1983

Analysis of enkephalins, beta-endorphins and small peptides in their sequences by highly sensitive high-performance liquid chromatography with electrochemical detection: implications in opioid peptide metabolism.

Sensitivity in the 10-100 pg range for enkephalins, beta-endorphin, tyrosine (T), 12 tyrosylglycine (T-G) and tyrosylglycylglycine (T-G-G) was attained by using a high-performance liquid chromatographic (HPLC) method with electrochemical detection which is at least 100 times more sensitive than HPLC with UV detection. The chromatographic conditions on a reversed-phase C18 silica column were 50 mM sodium phosphate buffer (pH 2.1) (A) in acetonitrile-methanol (1:1) (B), isocratic mixture, flow-rate 0.6-1 ml/min, UV detection at 205 nm, electrochemical oxidation potential + 1.25 V. The separation of T, T-G and T-G-G was obtained by using 10% B while the separation of the pentapeptide, enkephalins required 40% B. Separation of enkephalins from beta-endorphin was attained at a shorter retention times did not exceed 15 min. This method can be used to determine tissue levels and pharmacodynamics of enkephalins and beta-endorphin. A highly specific measurement of the different enzymes involved in the metabolism of enkephalin has been achieved.

Adrenal Cortex Hormones↗
PubMed1983

Prolonged intermittent footshock stress decreases Met and Leu enkephalin levels in brain with concomitant decreases in pain threshold.

The influence of a 21 day intermittent footshock regimen upon enkephalin levels in brain and adrenals was examined in the rat. Changes in pain sensitivity as well as analgesic and hyperthermic responsiveness to morphine (7.5 mg/kg) were also monitored. Following the stress regimen, Met and Leu enkephalin levels were decreased by 40 to 50% in brain, but were unchanged in adrenals. Post-stress pain thresholds were markedly decreased in stressed animals while the analgesic properties of morphine were enhanced. Core body temperature of stressed animals was significantly raised, but the hyperthermic response to morphine was unchanged.

Animals↗
PubMed1983

Dexamethasone and stress-induced analgesia.

Analgesia induced in rats by cold-water swim stress and measured by the tail-flick and hot-plate methods was significantly antagonized after IP pretreatment for 3 days with 8 mg/kg dexamethasone. The analgesia developed by the cold-water swim stressor was also attenuated by 1 mg/kg naloxone. These results suggest that the corticosteroids may have a role in modulating stress-induced analgesia and that the adrenal-pituitary axis modulates the endogenous opiate system. These conclusions are based on recent reports that indicate the release of the opiate-like peptide beta-endorphin and adrenocorticotropin (ACTH) from the pituitary are increased by acute stress and inhibited by administration of the synthetic glucocorticoid dexamethasone.

Animals↗
PubMed1981

Corticosteroid modulation and stress-induced analgesia in rats.

Early evidence has indicated the presence and involvement of specific neural systems which can inhibit the responses to painful stimuli. More recently, further advances suggest that the opiate system may interact with other systems to modulate the analgesia produced by the opiates or various stressors. Since corticosteroids were found to be elevated under the conditions of different stress-induced analgesia (SIA), there may be interactions between the pain-inhibiting systems and the corticosteroids. Recently it was reported that acute stress or long-term adrenalectomy can result in release of beta-endorphin (beta E) and ACTH from the pituitary gland, which can be blocked by dexamethasone. In our early studies we have shown partial antagonism of the SIA by dexamethasone and complete antagonism after naloxone. In this report it was found that chronic treatment of the rats with 0.02% metyrapone in drinking water for 8 weeks resulted in minor hyperalgesia. The chronic pretreatment with metyrapone resulted in a significant potentiation of the analgesia induced via the cold swim stress model, which was reversed by 1 mg/kg (IP) naloxone. Also, hyperalgesia was noted 18 days after the bilateral adrenalectomy of the rats as measured in our laboratory by the hot plate method and as reported by Heybach and Vernikos-Danellis in 1978. These results suggest that the corticosteroid modulation (pituitary-adrenal axis) may have a role in regulating the SIA, and this may implicate the interactions of the corticosteroids with pain-inhibiting systems.

Adrenal Cortex Hormones↗
PubMed1981

Allosteric properties of rat lung phosphofructokinase.

Rat lung phosphofructokinase is purified 250-fold to a specific activity of about 10 by using ATP-sepharose affinity chromatography. The enzyme is activated by cyclic AMP, 5'-AMP, ADP, Pi, NH4+ and K+ ions. Depending upon the concentration of these effectors, the enzyme can exist in several interconvertible forms, differing widely in their affinity for fructose-6-P. These activators also overcome the inhibition of the enzyme by ATP and citrate, thus increasing the glycolytic rate in lung during hypoxia. Unlike the enzyme from other sources, the lung phosphofructokinase is not inhibited by cyclic GMP or phosphoenolpyruvate. The enzyme is very sensitive to inactivation by trypsin and this inactivation is completely reversed by assaying the proteolyzed enzyme in presence of its activators.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects in humans of intravenously administered endotoxin on soluble cell-adhesion molecule and inflammatory markers: a model of human diseases.

1. Endotoxin, a component of the cell wall of Gram-negative bacteria, could be a predisposing mediator of many pathological disorders. The present study was undertaken to determine the effects and time-course of acute endotoxin challenge on inflammatory and cell-adhesion molecule markers shedding in the plasma as potential surrogates. 2. Six normal male subjects per group (age range 21-35 years) were injected with 4 ng/kg, i.v., reference standard Escherichia coli (0113:h10:k) endotoxin or physiological saline. 3. Plasma inflammatory markers (tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and TNF-receptor I (RI)) and cell-adhesion molecule markers (soluble L-selectin, soluble P-selectin, soluble vascular cell adhesion molecule (VCAM)-1) were determined using sensitive and specific ELISA. 4. Tumour necrosis factor-alpha increased from a basal level of 2.8 pg/mL to approximately 800 pg/mL at 90 min after endotoxin. Similarly, IL-6 peaked 2-3 h after endotoxin injection, with a rapid decline by 6-8 h, and levels returned to basal values by 24 h. 5. In contrast, TNF-RI peaked at 2 h (increasing from basal levels of 900-3300 pg/mL) with a much slower decline and without return to basal levels at 24 h (1400 pg/mL). 6. Endotoxin resulted in a rapid rise in soluble L-selectin within 1 h, which increased from a basal of 150-425 ng/mL. This rapid rise in soluble L-selectin was sustained for up to 2.5 h and then rapidly declined to basal levels by 3.5 h. 7. In contrast, plasma soluble P-selectin levels showed a delayed and progressive increase up to 8 h (increasing from a basal level of 50-95 ng/mL), with a partial decline at 24 h (80 ng/mL). 8. Similarly, soluble VCAM-1 levels showed a progressive rise up to 24 h (increasing from basal values of 600-1000 ng/mL). 9. This acute human model of endotoxin exposure demonstrated an upregulation of inflammatory stimuli leading to a short-term hyperactivation of leucocytes and a more sustained activation of platelets and endothelium. 10. This model provides a non-invasive method for studying the complex effects of endotoxin-like pathogens on different cellular events using soluble plasma surrogate markers.

Adult↗
PubMedDate not supplied

Evaluation of sympathetic blockade after intrathecal and epidural lidocaine in rats by laser Doppler perfusion imaging.

The widespread use of neuraxial anaesthesia increases the need for animal models to evaluate therapeutic prospects, mechanisms and risks of this technique. As a methodological prerequisite, we characterised the sympathetic blockade after different modes of neuraxial anaesthesia with regard to segments supplying the splanchnic region. Under haemodynamic monitoring, lidocaine 2% or saline were infused via intrathecal (10 microl), lumbar epidural (10 and 30 microl) or thoracic epidural (10 and 30 microl) catheters. Segmental spread of neuraxially infused local anaesthetic was assessed using methylene blue. Mean arterial blood pressure decreased more severely after neuraxial lidocaine in thoracic epidural (10 and 30 microl) compared to high-volume (30 microl anaesthesia animals. Determination of the sympathetic blockade by means of laser Doppler perfusion imaging was restricted to the paws due to a higher density of subcutaneous blood vessels as compared to the abdominal wall (mean +/- SD: 3.93 +/- 0.06 vs. 1.35 +/- 0.05/384 mm(2), p < 0.05). Only high-volume (30 microl) lumbar and thoracic epidural anaesthesia (10 and 30 microl) increased skin perfusion in both hind and front paws. This extensive sympathetic blockade was demonstrated to include splanchnic segments using thermography. Segmental spread of methylene blue did not closely correspond to laser Doppler findings and should be interpreted as minimum rather than exact epidural spread of local anaesthetic.

Anesthetics, Local↗
PubMedDate not supplied

Intestinal mucosal changes in thalassaemia major.

Ten infants and children suffering from Thalassaemia major, proven by clinical, hematological and biochemical criteria, were subjected to intestinal biopsy. Specimens were studied for histological and histochemical patterns. The histological picture showed shortening and fusion of villi with cellular infiltration. Reduced mucopolysaccharides and relatively normal alkaline phosphatase activity were demonstrated. The degree of histological and histochemical changes correlates with the degree of anemia. The effects of these changes on the iron absorption and the tissue hemosiderosis are aroused. The possibility of these changes, being non-specific and secondary to anemia and tissue hypoxia is also postulated.

Child↗