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Biomedical subjects

M L Vargas

Publications and source records attributed to M L Vargas.

At least 37 records · Page 2Linked to original sources
PubMed1991

Pituitary-adrenocortical response to acute and chronic administration of U-50,488H in the rat.

K-opioid substances have been shown to stimulate and/or depress the HPA activity. The objective of this study was to determine the effects of the acute and chronic administration of U-50,488H, a k-opioid receptor agonist, on the pituitary-adrenocortical activity in the rat. The acute administration of U-50,488H (25 mg/kg i.p.) produced a hypothermic effect and an increase in plasma levels of B-END-LI and cortisol, effects which were prevented by naloxone (3 mg/kg s.c.). Chronic administration of U-50,488H twice a day for 4 days resulted in a decrease in basal plasma levels of B-END-LI and cortisol and in the development of tolerance to its neuroendocrine and hypothermic effects. In rats made tolerant to U-50,488H, naloxone precipitated hypothermia (which is an index of opiate dependence in rats), whereas no changes in plasma B-END-LI and cortisol levels were seen. These data suggest that k receptors may be involved in the regulation of pituitary-adrenocortical activity in physiological conditions and during opiate abuse. On the other hand, U-50,488H induced only negligible dependence in rats, which was not morphine-like.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

Influence of stress in the effects of morphine on pituitary-adrenocortical activity in the guinea-pig.

1. Modifications by stress of the effects of morphine on pituitary-adrenocortical activity were examined in the guinea-pig at different lengths of time. 2. An increase in plasma cortisol but not in beta-endorphin levels was obtained in guinea-pigs stressed for 60 min. 3. Morphine (50 mg kg i.p.) enhanced beta-endorphin and cortisol levels 5 min after injection and decreased beta-endorphin concentration 30 and 90 min after its administration. 4. In stressed guinea-pigs plasma beta-endorphin levels were reduced 5 min after morphine injection. 5. These results indicate that stress can alter the effects of morphine on pituitary-adrenal activity in the guinea-pig and that the type of modification may be dependent on the time of the sampling.

Animals↗
PubMed1990

Plasma beta-endorphin and cortisol levels in morphine-tolerant rats and in naloxone-induced withdrawal.

The relationship between morphine tolerance and pituitary-adrenocortical activity was examined. In rats made tolerant to morphine by implantation of morphine-containing pellets, there was a significant reduction in plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI), whereas no significant changes in cortisol levels were seen. Naloxone treatment induced an increase in plasma beta-END-LI and cortisol levels in morphine-tolerant animals. Additionally, acute morphine administration induced an increase in plasma levels of beta-END-LI and cortisol, an effect which was prevented by naloxone. These results are consistent with an increased release of pro-opiomelanocortin-derived peptides after acute morphine and with a decreased release of these peptides in tolerant rats, and suggest that opioid peptides play an important role in the regulation of pituitary-adrenocortical function.

Animals↗
PubMed1990

Stress and morphine mediated changes in pituitary-adrenal axis in guinea-pigs.

1. Changes in plasma levels of B-END and cortisol were investigated in guinea-pigs receiving either stressful stimuli for various lengths of time or i.p. injections of morphine or saline. 2. A decrease in B-END levels occurred when animals were stressed, whereas cortisol was not affected. 3. Morphine (50 mg/kg i.p.) enhanced B-END and cortisol levels 5 min after injection, whereas a decrease in B-END was seen at 30 min. 4. Saline (i.p.) produced a decrease of B-END levels 30 min after injection and an increase in cortisol 5 and 10 min after injection. These findings suggest that in the guinea-pig the response of pituitary-adrenal axis to stress or morphine could change depending upon the time of sampling.

Animals↗
PubMed1990

Detection of immunoregulatory lipid-like factors in human amniotic fluid.

The immunosuppressive activity of amniotic fluid (AF) is extensively documented in the mouse. Although this property is due in part to the presence of alpha-fetoprotein (alpha-FP), other immunosuppressive factors are suspected. In this article, we demonstrate that human amniotic fluid lipid extract (AFLE) is inhibitory of, although not cytotoxic to, PHA-activated human lymphocytes, of mouse bone marrow cells, and of different established cell lines of human and mouse source. This effect is shown to be reversible. Under preparative thin layer chromatography (TLC) using chloroform:methanol:water (60:38:8) as solvents, the activity of AFLE migrates to two peaks of inhibition with Rf values of 0.46-0.62 and 0.84-1, respectively. These lipid-like factors may play a role as a nonspecific immunoregulatory mechanism which prevents maternally mediated immune rejection of the conceptus.

Amniotic Fluid↗
PubMed1989

Decreased levels of circulating CD4+ T lymphocytes during normal human pregnancy.

Peripheral blood mononuclear cell (PBMC) populations during human pregnancy have been investigated by many authors, although the different results obtained, principally in relation to T cells, are very discrepant. In this study we aimed to exclude all the possible causes of these discrepancies: small sample size; diurnal rhythm of CD4+ T cells; smoking habits; haemodilution which occurs during pregnancy and inappropriate statistical analysis; in order to determine whether gestation has a definite effect on PBMC populations. We found that the percentage of CD4+ T lymphocytes decreases in the first and second trimesters, returns to the non-pregnant level in the third trimester and remains there in the postpartum period. The percentages of CD3+ T lymphocytes run parallel to those of CD4+ while CD8+ T lymphocytes do not vary. The proportion of CD16+ cells, which include mature NK cells, diminishes in the second trimester and this reduction is maintained in the third trimester and the puerperium. No variation was found in the other PBMC studied (CD20+ lymphocytes, CD14+ monocytes and D/DR+ cells). When parity was considered no difference was seen between primiparous and multiparous women in any of the cell populations tested.

Adult↗
PubMed1989

Antinociceptive effects of azepexole (BHT 933) in mice.

Subcutaneous (s.c.) administration of azepexole (BHT 933) at doses between 4 and 40 mg/kg produced dose-dependent antinociceptive effects in mice as assessed by tail-immersion, tail-pinch and acetic acid writhing tests. The ED16s were 5.6 +/- 0.4, 6.7 +/- 1.2 and 2.96 +/- 0.2 mg/kg respectively. Similarly, morphine produced analgesia in the same tests with ED16s of 0.87 +/- 0.03, 0.47 +/- 0.1 and 0.45 +/- 0.01 mg/kg respectively. In all instances naloxone (0.1 mg/kg s.c.) shifted the dose-response curves to morphine to the right in a parallel manner. Naloxone (0.1 and 1 mg/kg s.c.) partially antagonized the effect of azepexole in the tail-immersion and tail-pinch tests but significantly decreased the slope of the dose-response curve suggesting that a competitive interaction at the level of the opioid receptors did not occur. Naloxone had no effect on the antinociceptive action of azepexole in the acetic acid writhing test.

Analgesics↗
PubMed1989

Influence of dopaminergic and noradrenergic systems on the release of opioid peptides in guinea-pig ileum.

Neuroleptic drugs increase the biosynthesis and release of opioid peptides from the myenteric plexus of guinea-pig ileum. In the present work, the involvement of dopamine receptors or alpha-adrenoceptors in the release of opioids from the myenteric plexus of guinea-pig was investigated. Acute or chronic treatment with prazosin, an alpha 1-blocking drug, produced no changes in the release of these peptides. Release was also unchanged after acute or chronic treatment with the alpha 2-blocking drug yohimbine. However, treatment with domperidone, a selective dopamine receptor antagonist, resulted in an increase in the release of opioids, as did treatment with (-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine ((-)-3-PPP), a dopamine autoreceptor stimulant. It is concluded that the effect of neuroleptics on the release of opioids from myenteric plexus is due to the blockade of dopamine receptors, and that interruption of dopaminergic transmission produces an increase in opioid release at this level.

Adrenergic alpha-Antagonists↗
PubMed1987

Naloxone elicits an excitatory response in the morphine-tolerant mouse vas deferens.

The effects of naloxone on the electrically stimulated vas deferens from mice implanted with morphine (tolerant) or placebo (naive) pellets were studied. In tolerant vas deferens, naloxone produced an 86.6% increase of the twitch contractions when the preparations were stimulated with 15 V, while only a 12% increase was observed with supramaximal voltage (40 V). Naloxone had no effect at either voltage in preparations from naive animals. The effect of morphine in naive vas deferens stimulated with 15 V, was reversed by naloxone without further increase over baseline contractions. The results suggest that opioid receptors other than those located in the neuronal soma and/or coupled to adenylate cyclase may be involved in the development of dependence.

Animals↗
PubMed1987

Effects of droperidol on the biosynthesis and release of endogenous opioid peptides in guinea-pig ileum.

Acute administration of droperidol 2 or 5 mg kg-1 induced an increase in the inhibitory response obtained by stimulation at 10 Hz of the myenteric plexus longitudinal muscle preparation of the guinea-pig ileum. The increase in the response induced by droperidol was markedly reduced by naloxone which suggests that it is mediated by endogenous opioid release. Cycloheximide treatment significantly reduced the increase of the inhibitory response induced by droperidol, indicating that the biosynthesis and the release of endogenous opioid are increased by droperidol.

Animals↗
PubMed1987

Effect of selective monoamine oxidase inhibitors on the morphine-induced hypothermia in restrained rats.

Morphine (30 mg/kg i.p.) produced a hypothermic effect in restrained rats which was antagonized by naloxone pretreatment (10 mg/kg s.c.). This hypothermia was inhibited by deprenyl pretreatment (5 mg/kg i.p.) and by beta-phenylethylamine treatment (25 mg/kg i.p.). However, the effect of morphine was partially potentiated when a higher dose of deprenyl (10 mg/kg i.p.) was administered. Pretreatment with clorgyline (1 mg/kg i.p.) potentiated the morphine-induced hypothermia. In contrast, the effect of morphine was antagonized when a higher dose of clorgyline was used (5 mg/kg i.p.). Based on these results, a possible role of brain serotonin and dopamine in the thermoregulatory effects of morphine is proposed in this paper.

Animals↗
PubMed1987

[Interaction of opioid peptides and the dopaminergic system in the myenteric plexus of the guniea pig ileum].

The effects of treatment with dopamine agonists and 6-hydroxydopamine on the release of opioid peptides from the myenteric plexus of guinea-pig ileum were examined. Apomorphine or bromocriptine treatment at doses that act on dopamine autoreceptors to inhibit dopamine release resulted in a significant elevation of the release of opioid peptides. 6-hydroxydopamine treatment, which produces a lesion of catecholaminergic nerve terminals also resulted in an increase in opioid peptide release. These findings indicate that interruption of dopaminergic transmission in the myenteric plexus produces an increase in the release of opioid peptides and suggest an inhibitory modulation of opioid peptidergic neurons by dopamine systems in the myenteric plexus of the guinea-pig ileum.

Animals↗
PubMed1986

Pharmacological evidence for the existence of interactions between dopaminergic and opioid peptidergic systems in guinea-pig ileum myenteric plexus.

Apomorphine or bromocriptine treatment at doses that act on dopamine autoreceptors resulted in a significant elevation of the release of opioid peptides from the myenteric plexus of guinea-pig, since these drugs produced an increase of the inhibitory response which was reversed by naloxone. 6-Hydroxydopamine treatment also resulted in an increase in opioid peptide release. These findings would indicate that the interruption of dopaminergic transmission in the myenteric plexus produces an increase in the release of opioid peptides and suggest an inhibitory modulation of opioid peptidergic neurons by dopamine systems at this level.

Animals↗
PubMed1986

Effect of ACTH-like peptides on morphine-induced hypothermia in unrestrained guinea pigs.

Peripheral treatment with adrenocorticotropin (1-24) (ACTH1-24), at different doses and sequences, consistently antagonized the decrease in body temperature produced by morphine in the freely moving guinea pig, whereas adrenocorticotropin (4-10) (ACTH4-10), which lacks corticotrophic activity, was partially effective only when it was administered in a high dose 24 h prior to morphine. Centrally administered ACTH1-24 completely prevented the hypothermic effect of intracerebroventricularly (i.c.v.)-injected morphine. Likewise, the i.c.v. administration of ACTH4-10 was equally effective in blocking the i.c.v. morphine-induced hypothermia. Neither ACTH1-24 nor ACTH4-10 did produce changes in body temperature. These results suggest that peripherally administered ACTH1-24 antagonizes indirectly the actions of morphine through the release of adrenal corticosteroids, whereas centrally injected ACTH1-24 or ACTH4-10 act as direct antagonists of morphine effects through opioid receptors.

Adrenocorticotropic Hormone↗
PubMed1985

Mechanism of action of B-HT 933 (azepexole) in rat vas deferens and guinea-pig ileum.

The mechanism of action of B-HT 933 (azepexole) was studied on the rat vas deferens and myenteric plexus-longitudinal muscle (MP-LM) of the guinea-pig ileum. The drug caused a concentration-dependent inhibition of the twitch response in both preparations. The maximal inhibition in both preparations was 80-90%. B-HT 933 did not affect the cumulative dose-response curves of the vas deferens and of MP-LM to noradrenaline (NA) and acetylcholine (Ach) respectively. Yohimbine antagonized in a competitive way the twitch inhibitory effect of B-HT 933 on vas deferens and on MP-LM; the pA2 values were 8.62 and 8.5, respectively. The twitch inhibitory effects of B-HT 933 were not antagonized by propranolol. The results suggest that the action of B-HT 933 is mediated by stimulation of presynaptic alpha 2-receptors.

Acetylcholine↗
PubMed1985

Effects of chronic treatment with atypical neuroleptics on the biosynthesis and release of opioid peptides in guinea-pig ileum.

The guinea-pig ileum myenteric plexus is known to contain opioid peptides, which can be released by electric stimulation at high frequency. Haloperidol, a classic neuroleptic drug, increases the biosynthesis and release of endogenous opioid peptides from the myenteric plexus. In the present work we have examined the effects of chronic treatment with sulpiride and clozapine, two atypical neuroleptics, on the release of these peptides in the myenteric plexus of guinea-pig ileum. Both neuroleptics, administered over a period of 7 days, produced an increase of the inhibitory response obtained by electrical stimulation at 10 Hz of the ileum myenteric plexus-longitudinal muscle preparation. The inhibitory response was reversed by the specific opioid antagonist naloxone, which suggest that the increase in the inhibitory response produced by blocking the dopaminergic receptors is mediated by an increase in the release of opioid peptides. When sulpiride- or clozapine-treated guinea-pigs received cycloheximide (an inhibitor of peptide biosynthesis) there was a significant decrease of the inhibitory response, which indicates that neuroleptics produced an increase of the synthesis of opioid peptides in the ileum myenteric plexus. These results reveal a possible influence of the dopaminergic system on the biological turnover of these peptides.

Animals↗
PubMed1984

Haloperidol treatment increases the biosynthesis and release of endorphins in guinea-pig ileum.

Guinea-pigs treated acutely (5 mg kg-1 i.p.) and chronically (2 or 5 mg kg-1 day-1 for 4 days) with haloperidol, show an increase of the inhibitory response produced by electrical stimulation at 10 Hz of the ileum myenteric plexus-longitudinal muscle (MPLM) preparation. The response can be reversed by the specific narcotic antagonist naloxone (5 X 10(-7) M), which suggests that the increase in the response produced by haloperidol is mediated by release of endorphins. When haloperidol-treated guinea-pigs received cycloheximide (24 and 12 h before death), there was a substantial decrease in the response indicating that the biosynthesis and release of endorphins are increased by haloperidol.

Animals↗