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Biomedical subjects

H Koyuncuoğlu

Publications and source records attributed to H Koyuncuoğlu.

At least 37 records · Page 2Linked to original sources
PubMed1986

Brain asparaginase, ACE activity and plasma cortisol level in morphine dependent rats: effect of aspartic acid and naloxone.

The activities of the brain L-asparaginase and angiotensin converting enzyme (ACE), and the plasma cortisol level were found to be decreased in the rats implanted with morphine (M) containing pellets. Even though 10 mg/kg of naloxone (N) itself showed an inhibitory effect on ACE it abolished the inhibitions seen in the M dependent rats five min following subcutaneous injection. The chronic administration of L-aspartic acid (ASP) during the development of physical dependence or just before the N injection prevented the increase of the plasma cortisol caused by N. It is concluded that in addition to the inhibition of the brain L-asparaginase activity which was previously hypothesized to be the main reason of the development of physical dependence on opiates as a result of the related experimental and clinical data, the inhibition by M of the brain ACE activity may take part in the development of physical dependence. With regard to the plasma cortisol level, the concomitant administration of ASP with M blocks, to a great extent, the development of physical dependence on opiate. The single dose of ASP administration before N injection prevents the effect of N, the manifestation of abstinence syndrome.

Animals↗
PubMed1986

Comparison of the suppressive effects of L-aspartic acid and chlorpromazine + diazepam treatments on opiate abstinence syndrome signs in men.

According to the hypothesis implying that the main reason of physical dependence on opiate is the inhibition of brain L-asparaginase activity and L-aspartic acid gradually decreases compulsory opiate intake so that physical dependence disappears by itself, 31 opiate addicts were given 8 g L-aspartic acid for 7 days after withdrawal from opiate and appearance of abstinence syndrome signs. The attenuations by L-aspartic acid of the abstinence syndrome signs were statistically compared with those obtained from other 12 opiate addicts received daily 50 mg chlorpromazine + 60 mg diazepam which have long been used to suppress abstinence syndrome because of their multiple receptor blocking and sedative effects. The intensity and duration of 13 signs out of 16 ones were found to be significantly more alleviated and shortened in the addicts treated with L-aspartic acid.

Aspartic Acid↗
PubMed1984

Feeding, drinking, urine osmolality in DI Brattleboro rats: changes by morphine, naloxone, D-amino acids, prolyl-leucyl-glycinamide (PLG).

Brattleboro rats placed in metabolism cages were injected with morphine (Mor), naloxone (Nal), D- and L-aspartic acid (D- and L-Asp), D-phenylalanine (D-Phe), D-leucine (D-Leu) and prolyl-leucyl-glycinamide (PLG), alone and in suitable combinations. Food and fluid intake, urine outflow, faeces weight, rectal temperature and urinary osmolality were determined at the end of seven hours period of time. Mor, Nal, D-Asp and PLG alone caused a significant decrease in food and fluid intake, urine volume and faeces weight and a significant increase in urinary osmolality being the osmolality of the Mor, D-Asp and PLG injected groups higher than 300 mOsmol/kg. The combination of Nal with Mor, D-Asp and PLG appeared to intensify the changes induced by Mor, D-Asp and PLG whereas L-Asp antagonized the majority of changes caused by Mor or PLG. The results were discussed in the light of the previous experimental findings.

Amino Acids↗
PubMed1984

Vasopressin release by D-aspartic acid, morphine and prolyl-leucyl-glycinamide (PLG) in DI Brattleboro rats.

The L-asparaginase activities of the brains of the Wistar, heterozygous and homozygous Brattleboro rats divided into three parts namely the anterior, middle and posterior which respectively contained cerebral cortex, hippocampus + midbrain + thalamus + hypothalamus cerebellum + pons + medulla oblongata were estimated. The L-asparaginase activities of all the three parts in the homozygous Brattleboro rats were significantly higher than in the Wistar rats as well as in the heterozygous Brattleboro rats. Twenty min following the injections of 200 mg/kg D-aspartic acid, 20 mg/kg morphine, 200 mg/kg D-aspartic acid + 20 mg/kg morphine, 6 mg/kg prolyl-leucyl-glycinamide (PLG) and 6 mg/kg PLG + 20 mg/kg morphine the L-asparaginase activities of all three parts of the homozygous Brattleboro rat brains were found to be significantly inhibited. After having seen the suppressive effect of the drugs and their combinations used before the homozygous Brattleboro rats were given D-aspartic acid, morphine, D-aspartic acid + morphine, PLG and PLG + morphine for seven days. Then their plasma vasopressin levels were determined by RIA. The treatments applied to the homozygous Brattleboro rats caused the appearance of a significant amount vasopressin in the plasma. The results were interpreted as evidence for the fact that the inhibition of the brain L-asparaginase provides and/or accelerates the biosynthesis and/or release of vasopressin. As morphine has a vasopressin releasing and a brain L-asparaginase inhibiting effect the antidiuretic action of morphine was considered to be linked to its inhibitory effect on the brain L-asparaginase.

Animals↗
PubMed1984

Changes in brain and lung angiotensin converting enzyme activity in various shocks.

The brain and lung angiotensin converting enzyme (ACE) activities of the rats subjected to haemorrhagic, hypovolemic or endotoxic shock and of the mice immunized and then intravenously challenged with bovine serum albumin were determined by means of a spectrophotometric method. The lung ACE activities of all the shock groups were found significantly higher than those of their Control groups whereas only the brain ACE activities of the rats in endotoxic shock and the mice in anaphylactic shock showed a significant increase compared to their own control values. The results were interpreted as supporting evidence for the idea that peripheral and central renin-angiotensin systems may play a deleterious role in shock.

Anaphylaxis↗
PubMed1983

The effect of morphine, naloxone, D- and L-aspartic acid on the brain and lung ACE in mice.

The brain and lung angiotensin converting enzyme (ACE) activities of the mice injected with 10 mg/kg morphine and/or naloxone, 200 mg/kg D- and/or L-aspartic acid were spectrophotometrically determined. Morphine, naloxone, D- and L-aspartic acid alone inhibited both brain and lung ACE activities whereas the combinations of morphine with naloxone, D-aspartic acid with L-aspartic acid and morphine with naloxone + L-aspartic acid showed no inhibitory effect on the brain ACE. While naloxone or L-aspartic acid partly antagonized the suppression of morphine on the lung ACE their combination completely prevented morphine from inhibiting the lung ACE. In the in vivo experiments performed on the brain and lung homogenates of the untreated mice the determination of the ACE activity in the incubating media containing 3.10(-3) M morphine or naloxone, 10(-2) M D- or L-aspartic acid showed a significant decrease in the activity. But no in vitro antagonistic effect was found by using the combinations of the drugs used in the study. The antagonism seen in the in vivo experiments was considered as an indirect one. And the relationship between the inhibitory effect of morphine, naloxone and D-aspartic acid, their suppressive effect on drinking and their beneficial effects in various forms of shock was discussed.

Animals↗
PubMed1982

Effects of L-aspartic acid, L-asparagine and/or L-asparaginase on forced swimming-induced immobility, analgesia, and decrease in rectal temperature in rats.

The effect of L-aspartic acid, L-asparagine and/or L-asparaginase were compared with those of imipramine on immobility, number of defecations, increase of nociceptive threshold, and hypothermia, induced by forced swimming in rats. L-Aspartic acid was found to be as effective as imipramine in reducing the effects of forced swimming, presumable by normalizing the decreased level of endogenous L-aspartic acid, due to the inhibition of L-asparaginase activity and/or by stimulating the inhibited enzyme. The other treatments antagonized the immobility, but not the increased number of defecations. All compounds abolished the elevation of nociceptive threshold and hypothermia.

Analgesia↗
PubMed1982

Effect of D- and/or L-aspartic acids on feeding, drinking, urine outflow and core temperature.

Rats were given D- and/or L-aspartic acids (Asp) in saccharin solution for one week. Body weight gain, daily food and fluid intake, weight of faeces, urine outflow and osmolality, and rectal temperature were compared with those of the pretreatment period. After the rats had been sacrificed the weights of liver, spleen and kidney were estimated and compared with those of the control. The long-term oral administration of D-Asp caused a significant decrease in the weights of total body, liver and kidney, in the daily food and fluid intake, in the weight of faeces and in the volume of urine. The osmolality of urine of the rats administered D-Asp was significantly higher than that of the control. The concomitant oral administration of L-Asp seemed to antagonize the effects of D-Asp.

Animals↗
PubMed1981

The effect of long-term concurrent administration of chlorpromazine and lithium on the striatal and frontal cortical dopamine metabolism in rats.

The effects of lithium and chlorpromazine chronically administered alone and together on the dopamine metabolism in the rat striatum and frontal cortex were investigated by measurement of the levels of dopamine (DA) and its main metabolite, homovanillic acid (HVA). Long-term chlorpromazine administration caused a significant increase in the striatal DA level and a decrease in that of HVA and HVA/DA ratio without any changes in those of the frontal cortex. The prolonged administration of lithium elevated the striatal levels of both HVA and DA, but no change in the frontal cortex was observed. The concurrent administration of chlorpromazine and lithium caused a significant increase in the frontal cortical DA level and a decrease in that of HVA and HVA/DA ratio. The striatal DA and HVA levels increased under the effect of the combined treatment, while the HVA/DA ratio remained unchanged.

Animals↗
PubMed1980

Effect of chronic administration of morphine on primary immune response in mice.

The effect of 3 different doses of chronically-administered morphine on the primary immune response was studied in mice by estimating spleen/body weight ratio and serum hemolysin production against sheep red blood cells (SRBC). It was observed that morphine exerted a dose-dependent inhibitory effect on the immune response which was antagonized by the concomitant administration of naloxone. The findings suggest that the inhibitory effect of morphine is specific.

Animals↗
PubMed1979

The relationship between morphine, aspartic acid and L-asparaginase in rats.

Morphine and aspartic acid were administered separately and in combination to 80 rats divided into 8 groups. Ten and 20 min following the injections, brain, liver and kidney L-asparaginase activity was determined. Morphine decreased brain and liver L-asparaginase activity and increased that of kidney. Aspartic acid completely antagonized the effect of morphine. Additionally 500 IU/kg L-asparaginase and 5 or 10 mg/kg morphine were i.v. injected into 56 rats divided into 5 groups. L-Asparaginase, which, in turn, increased motor activity, antagonized the morphine-induced hypoactivity and analgesia. These results support our previous findings.

Analgesia↗
PubMed1979

The antagonizing effect of aspartic acid on morphine withdrawal and levallorphan-precipitated abstinence syndrome signs and on associated changes in brain levels of free amino acids in the rat.

We have previously demonstrated the antagonizing effect of aspartic acid on some effects of morphine and on the development of physical dependence on, and tolerance to, morphine. In the present study, we have withdrawal from morphine or administration of a morphine antagonist. For this purpose sixty five white rats were given morphine and aspartic acid separately and in combination in a 5% saccharose solution instead of drinking water for 30 days. Some of the dependent rats were then withdrawn and others were injected with levallorphan. Flying, jumping, wet-dog shaking, body weight loss and motor activity were estimated and free amino acid levels in the brain were determined. Aspartic acid was found to prevent or antagonize the behavioural signs and the changes in the free amino acid levels in the brain. The results are discussed in the light of the previous data.

Amino Acids↗