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V A Patel

Publications and source records attributed to V A Patel.

6 recordsLinked to original sources
PubMed1989

Effects of ethanol on plasma corticosterone and rectal temperature modification by U50488H and WIN 44441-3.

Endogenous opiates are believed to subserve various behaviors and physiological functions. We have examined the effect of U50488H (0-12 mg/kg), a kappa agonist, and WIN 44441-3 (0-4.0 mg/kg), a kappa antagonist, on ethanol (ET)-induced changes in rectal temperature and in plasma corticosterone (CS) levels in rats. The 12 mg/kg dose of U50488H produced marked hypothermia, the other doses either produced hyperthermia comparable to that seen in control animals, or had no effect. The 0.5 mg/kg of WIN44441-3 had a small hypothermic effect while the 4.0 mg/kg produced hyperthermia. U50488H potentiated and the low dose of WIN 44441-3 reversed the hypothermic effect of ethanol. By contrast, neither WIN 44441-3 nor U50488H pretreatments affected the ethanol-induced elevation in plasma CS. These results indicate that kappa agonists increase plasma CS concentration and affect thermoregulatory mechanisms. Furthermore, our data indicate a possible role of endogenous kappa opioids in the hypothermic effect of ethanol, but not in the elevation of plasma CS.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

Interaction of stress and ethanol: effect on beta-endorphin and catecholamines.

To examine the interaction of ethanol (ET) and stress on beta-endorphin and catecholamine (CA) levels, male rats pretreated with ET (3.0 g/kg, i.p.) or saline were immobilized for 30 min and killed 90 min after the initial injection. Stress resulted in (a) an increase in plasma levels of norepinephrine (NE, 243%), epinephrine (E, 175%), beta-endorphin (220%) and corticosterone (CS, 151%) and a decrease in dopamine (DA, 54%); (b) a decrease in hypothalamic NE (15%) and beta-endorphin (33%) levels and an increase E (23%) and DA (58%) levels; (c) a decrease in pituitary beta-endorphin levels in both the neurointermediate (23%) and anterior (131%) lobes. Treatment with ET resulted in: (a) an increase in plasma NE (81%), E (53%), CS (71%), and beta-endorphin (33%) levels and decrease in DA (54%); (b) a decrease in the hypothalamic NE (12%) levels and an increase DA (27%) and beta-endorphin (46%) levels, and (c) a decrease in beta-endorphin (15.5%) in the intermediate lobe of the pituitary. Treatment with ET of stressed animals had only a small effect: (a) in plasma NE, E, CS, and beta-endorphin levels decreased by 30, 31, 14, and 36%, respectively; (b) in the hypothalamus DA levels decreased by 40% and beta-endorphin increased by 71%; (c) in the pituitary beta-endorphin increased in both the intermediate lobe (25%) and anterior (50%) lobes. Thus when the data of the stressed ET-treated group is compared to that of the nonstressed saline injected group, none of the measures differ significantly. These results confirm our earlier work indicating a significant interaction of ET and stress.

Animals↗
PubMed1979

Localization of the nucleolar organizer by computer-aided analysis of a variant no. 21 in a human isolate.

A variant chromosome no. 21 consisting of two stalks and two satellites in tandem was detected during a survey of a human isolate. The variant segregated in three generations of a large kindred. One male had the variant no. 21, a metacentric Y, and a 47,XXY complement; however, no other evidence of chromosomal nondisjunction was found. Computer-aided analysis of sequentially stained variant no. 21 chromosomes indicated that silver-stained material corresponded to the proximal stalk region (as defined by Giemsa), but often covered both the distal stalk and satellite (also as defined by Giemsa). These data support the hypothesis that human nucleolar organizers are localized to the stalks of acrocentric chromosomes.

Azure Stains↗
PubMed1979

Analysis for amniotic fluid crystallization in second-trimester amniocentesis.

A potential complication of second-trimester amniocentesis for genetic indications is inadvertent needle insertion into the maternal bladder, resulting in aspiration of urine rather than amniotic fluid. Amniotic fluid forms a characteristic crystalline arborization pattern when allowed to air dry. We utilized this property of amniotic fluid to distinguish amniotic fluid from maternal urine. In 24 of 25 cases studied in a randomized blind fashion the crystalline arborization test correctly identified amniotic fluid, whereas none of the 25 urine samples showed this pattern. Our study indicates that the crystalline arborization test is reliable in distinguishing amniotic fluid from maternal urine during the second trimester of pregnancy.

Amniocentesis↗
PubMedDate not supplied

Acute and chronic ethanol treatment on beta-endorphin and catecholamine levels.

The effect of acute (2.0 g/kg, intragastrically) and chronic (8.0-11.0 g/kg/day for 10 days, intragastrically) ethanol exposure on beta-endorphin levels in plasma, hypothalamus and pituitary were examined in rats. Hypothalamic and plasma catecholamines and plasma corticosterone were also measured in these animals. Plasma beta-endorphin, norepinephrine (NE) and corticosterone levels were significantly increased and dopamine (DA) was unchanged in acute and chronic ethanol-treated rats. Compared to controls, plasma epinephrine (E) levels were increased in acute ethanol-treated rats but no significant change was observed in chronic ethanol-treated rats. Plasma dopamine were significantly decreased following chronic ethanol treatment while no significant change was observed after acute treatment. In the hypothalamus, beta-endorphin and dopamine contents were increased and norepinephrine levels were reduced in response to ethanol exposure. Beta-endorphin levels were decreased significantly in the anterior pituitary and the neurointermediate lobe of the pituitary in ethanol-treated animals except in the neurointermediate lobe of the chronic ethanol-treated animals. These findings together suggest that there is an interaction between beta-endorphin, catecholamines, corticosterone and ethanol in response to acute and chronic ethanol exposure in rats.

Animals↗