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Biomedical subjects

G K Yim

Publications and source records attributed to G K Yim.

At least 73 records · Page 4Linked to original sources
PubMed1982

Effects of certain hallucinogenic amphetamine analogues on the release of [3H]serotonin from rat brain synaptosomes.

The enantiomers of 3,4-(methylenedioxy)amphetamine (MDA), p-methoxyamphetamine (PMA), and N-Me-MDA (MDMA), along with their alpha, alpha-dimethylated derivatives, were evaluated for an effect on the release of [3H]serotonin from rat whole brain synaptosomes. The amphetamine isomers were all potent in inducing the release of [3H]serotonin at bath concentrations of 1 and 10 micrometers but were inactive at 0.1 micrometers. No significant difference in isomer potency was observed at the 10 micrometers concentration. However, at 1 micrometer the (+) isomer of MDMA was more effective in inducing release than was the (-) isomer. Since it is the (+) isomer which is clinically active, this result suggests that transmitter release may play a role in the biological activity of MDMA. By contrast, the alpha, alpha-dimethyl compounds were not effective in releasing serotonin, even at the highest bath concentration.

Amphetamines↗
PubMed1982

A new, potent, conformationally restricted analogue of amphetamine: 2-amino-1,2-dihydronaphthalene.

A new stimulant compound, 1,2-dihydro-2-naphthalenamine (2-amino-1,2-dihydronaphthalene, 2-ADN), was prepared as an analogue of amphetamine and of 2-aminotetralin. The optical isomers of 2-ADN were obtained by chemical resolution, and the absolute configuration was determined to be R-(+) and S-(-). Preliminary pharmacological evaluation revealed that racemic 2-ADN is approximately one-fourth as potent as (+)-amphetamine as a stimulant in mice. The S-(-) isomer of 2-ADN was found to be solely responsible for the stimulant effects of the racemate. Both reserpine and alpha-methyl-p-tyrosine antagonized the stimulation produced by 2-ADN.

2-Naphthylamine↗
PubMed1981

Reduction of aspirin-induced ulcers by a new imidazoline anti-inflammatory agent.

We have previously described the anti-inflammatory and low ulcerogenic actions of the formamidine pesticide, chlordimeform (CDM). In this study, the related basic compound, CDMI [2-(2-methyl-4-chlorophenylamino)-2-imidazoline], also demonstrated potent anti-edema (vs. carrageenin) and low ulcerogenic activity. A nonulcerogenic i.p. dose of CDMI reduced aspirin (ASA)-induced ulcers [lesion index (L.I.): 25.8 for ASA alond vs. 5.3 for ASA + i.p. CDMI]; prevented stress-induced ulcers in mice; and decreased acid secretion (by 90% in the Shay rat preparation). A mildly ulcerogenic oral dose (0.6 mmol/kg) of CDMI prevented stress ulcers, but did not reduce ASA ulcers. A nonulcerogenic oral dose (0.15 mmol/kg) of CDMI did reduce ASA ulcers (L.I.: 24.5 for ASA alone vs. 14.7 for ASA + oral CDMI). Thus, CDMI is a unique anti-inflammatory agent with additional anti-secretory and ulcer-reducing actions.

Animals↗
PubMed1981

Stereoselective effects of opiate agonists and antagonists on ingestive behavior in rats.

In male Sprague Dawley rats, the (-)-isomer of the opiate antagonist GPA 1843 (beta-9-methyl-5-phenyl-2-allyl-2'-hydroxy-6, 7-benzomorphan) produced dose-related decreases in nocturnal feeding and of hyperphagias induced by 2-deoxy-D-glucose (2-DG; 400 mg/kg) and 24 hr food deprivation (FD). The hyperphagia induced by insulin (10 U/kg) was not significantly decreased by GPA 1843. In contrast, comparable doses of the (+)-stereoisomer, GPA 1847, had no effect on nocturnal, 2-DG or FD hyperphagia. In addition, hyperphagia and hyperdipsia were observed following administration of the opiate agonist levorphanol, but not its stereoisomer, dextrorphan. Thus, the effects of these agents on consummatory behavior are mediated by a stereospecific interaction with opiate receptors, which further indicates that endogenous opiate peptides are involved in the expression of these opiate-related hyperphagias.

Animals↗
PubMed1980

Pharmacological modulation of edema mediated by prostaglandin, serotonin and histamine.

Previous studies demonstrated that the formamidine pesticide chlordimeform (CDM) reversibly inhibited prostaglandin biosynthesis and prevented the late (PG-mediated) phase of carrageenin-induced hind paw edema. This study emphasizes antagonism by CDM of the early (5HT and histamine-mediated) phase of carrageenin edema. CDM and cyproheptadine both antagonized paw edema induced by albumin (5HT and histamine-mediated) and by the direct injection of 5HT and histamine, whereas aspirin and the PG antagonist, SC-19220, were ineffective. As expected, cyproheptadine selectively reduced the early phase, whereas aspirin and SC-19220 selectively reduced the late phase of carrageenin-induced edema. These results are thus consistent with earlier studies demonstrating PG mediation of the late phase of carrageenin edema, and 5HT and histamine mediation of albumin edema and the early phase of carrageenin edema. In addition, they indicate that CDM possesses multiple acute anti-inflammatory actions not exhibited by aspirin, by SC-19220 or by cyproheptadine alone.

Albumins↗
PubMed1980

Dependence of defibrillation threshold upon extracellular/intracellular K+ concentrations.

The effect of increasing extracellular potassium concentration (Ko) upon electrical ventricular defibrillation threshold was investigated in pentobarbital anesthetized dogs treated with intravenous potassium chloride. Defibrillation threshold fell duirng potassium intoxication. The percent decrease in defibrillation threshold was linearly related to the logarithm of Ko and to the potassium equilibrium potential (Ek), calculated from measured extracellular and intracellular potassium concentrations of ventricular muscle. In dogs supported by left ventricular bypass in order to maintain the circulation during potassium intoxication, the values of Ko and Ek required for spontaneous, K+ induced defibrillation (electrical defibrillation threshold = zero) were 16.6 mEq/L and -46 mV compared to the normal values of 3.9 mEq/L and -84 mV. Changes in defibrillation threshold related to changes in Ek may be significant events in digitalis intoxication and in myocardial anoxia during prolonged fibrillation.

Animals↗
PubMed1980

Synthesis and adrenergic blocking effects of 2-(alkylamino)-3,4-dihydroquinazolines.

Based on the known biological activity of a variety of guanidine-containing agents, several N-substituted 3,4-dihydroquinazolines were synthesized. These compounds can be considered to be rigid analogues of phenylguanidines. In anesthetized rats the compounds decreased blood pressure and were antagonists of the pressor response to norepinephrine.

Animals↗
PubMed1979

Elevation of ventricular defibrillation threshold in dogs by antiarrhythmic drugs.

Effects of antiarrhythmic drugs upon the threshold delivered energy (TDE) and threshold peak current (TPC) for electrical ventricular defibrillation by damped sinusoidal shocks were investigated in 25 pentobarbital-anesthetized dogs. TDE and TPC were increased by the three antiarrhytmic drugs tested. Bolus injections produced a transient rise and continuous infusions produced a steady rise in difibrillation threshold. The maximal percent elevations in mean defibrillation threshold during the 60 minutes after intravenous drug treatment in groups of n = 5 dogs were: (formula: see text). Accordingly, individuals receiving antiarrhythmic drugs who nonetheless fibrillate may require greater electric shock strength for defibrillation.

Animals↗
PubMed1979

Reversible depression of electrically-induced contractions of guinea pig longitudinal muscle by a reversible inhibitor of prostaglandin synthetase.

The pesticide chlordimeform (CDM) depressed the electrically-induced twitch responses of the guinea pig longitudinal muscle ED50 = 3 X 10(-5)M). Naloxone reversed twitch depression induced by morphine but not by CDM. Phentolamine reversed twitch depression induced by either norepinephrine or clonidine, but not by CDM. PGE2 completely reversed twitch depression induced by either CDM or indomethacin, but only partially reversed twitch depression induced by lidocaine. The actions of CDM best resemble those of the nonsteroidal anti-inflammatory agents. The reversibility of the CDM depression by washing indicates that the guinea pig ileal preparation is a convenient screen for distinguishing reversible from irreversible inhibitors of prostaglandin biosynthesis.

Amidines↗
PubMed1978

Increased feeding in rats treated with chlordimeform and related formamidines: a new class of appetite stimulants.

Low doses of the formamidine pesticide, chlordimeform (CDM) induce voracious daytime feeding in non-food deprived rats. Following CDM (10 mg/kg), food intakes were five times control intakes after 3 h and 1.1 times control intakes after 24 h. Other selected formamidines, such as the N-demethylated metabolite of CDM, and amitraz, increased 3-h food intake by two and five times control intake, respectively. Anorexia accompanied by excessive CNS stimulation was noted with higher doses of CDM (above 40 mg/kg) and other formamidines. This contrasts with the sedation usually observed with high doses of other structurally diverse appetite stimulants. In addition, hyperphagia was not observed with other CNS stimulants or local anesthetics such as amphetamine, cocaine, and holocaine. Thus the formamidines constitute a new class of appetite stimulants, which should prove to be useful agents for the study of feeding behavior.

Amidines↗