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Biomedical subjects

A Goldstein

Publications and source records attributed to A Goldstein.

At least 289 records · Page 16Linked to original sources
PubMed1975

A routine procedure for monitoring clinical ultrasound equipment.

A procedure has been devised for monitoring many critical performance characteristics of clinical ultrasound systems. It is easy to use in a clinical environment and is sufficiently precise to check system consistency or reproducibility. The procedure permits monitoring the system as a whole with enough specificity to locate malfunctioning components. The range response of the system with the beam normal to a planar reflector in distilled water at room temperature is obtained in a single Polaroid image for various control settings. System performance, excluding B mode velocity calibration, display linearity, and position registration, may be routinely monitored with a minimum of measurements. A feasibility test confirmed the method's precision, reproducibility (2%), and ease of performance.

Quality Control↗
PubMed1975

Failure of the opiate antagonist naloxone to modify hypnotic analgesia.

Hypnotic analgesia in some respects resembles opiate analgesia. We tested the hypothesis that some features of hypnotic analgesia are mediated through neuronal pathways activating specific opiate receptors in brain. The opiate antagonist naloxone had no effect on hypnotic analgesia in three subjects. Thus, the hypothesis was not confirmed.

Female↗
PubMed1974

Partial purification of an opiate receptor from mouse brain.

A proteolipid isolated from a lipid extract of mouse brain demonstrates stereospecific binding properties for levorphanol. It is present only in neuronal tissue and most abundant in the rhombencephalon. One component saturates at a concentration corresponding to maximum pharmacologic effect in vivo. The estimated mass is 60,000 daltons per bound opiate molecule.

Animals↗
PubMed1973

Cellular and metabolic tolerance to an opioid narcotic in mouse brain.

1. Running activity and brain levorphanol concentration were measured in nontolerant and tolerant mice given various doses of (3)H-levorphanol.2. The principal factor responsible for tolerance in the mouse is a loss of sensitivity to the narcotic drug at the cellular level in brain; despite adequate brain concentrations, the pharmacological effects are diminished or absent.3. There is also metabolic tolerance; a given dose establishes a lower brain concentration in tolerant than in non-tolerant animals.4. The two kinds of tolerance are distinguished here and the contribution of each is assessed.

Animals↗
PubMed1973

Morphine-tolerant longitudinal muscle strip from guinea-pig ileum.

1. Implantation of morphine pellets in guinea-pigs produced a high degree of tolerance and dependence within 3 days.2. The contractions of the longitudinal muscle induced by electrical stimulation of the myenteric plexus-longitudinal muscle preparations obtained from tolerant animals were less depressed by morphine than the contractions evoked in preparations from non-tolerant animals.3. Naloxone did not alter the size of the evoked twitch but antagonized the depressant action of morphine in tolerant and in non-tolerant animals. When given to tolerant guinea-pigs, naloxone caused an increase in intestinal activity in vivo.4. The contractile response of the longitudinal muscle to acetylcholine was the same in preparations obtained from tolerant and non-tolerant animals. Electrically evoked contractions of the myenteric plexus-longitudinal muscle preparations from tolerant animals showed reduced sensitivity to the depressant effects of adrenaline, isoprenaline, and particularly, dopamine.

Animals↗
PubMed1973

Lethality of the morphinan isomers levorphanol and dextrorphan.

Significantly different (P<0.05) LD(50) values were found in Swiss-Webster mice for levorphanol (73 mg/kg, i.p.) and dextrorphan (120 mg/kg, i.p.). A subcutaneous injection of naloxone 15 min before challenge prevented the lethal effect of an LD(98) of levorphanol, with ED(50) value of 1.36 mg/kg. Naloxone, in doses from 2 to 100 mg/kg, did not prevent death caused by 150 mg/kg of either dextrorphan or levorphanol. Levorphanol was lethal for mice pretreated with 10 mg/kg of naloxone, a dose sufficient to block opiate-specific lethal effects, but the LD(50) value was 109 mg/kg, in contrast to 73 mg/kg in the absence of naloxone. By the criteria of stereospecificity and naloxone blockade, levorphanol-induced mortality in mice is a typical opiate effect in the lower of the two dose ranges studied. At higher doses of levorphanol a non-specific effect supervenes, with an LD(50) value virtually the same as that of dextrorphan.

Animals↗