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Biomedical subjects

M Adler

Publications and source records attributed to M Adler.

At least 253 records · Page 14Linked to original sources
PubMed1976

An analysis of the action of atropine and scopolamine on the end-plate current of frog sartorius muscle.

The effects of atropine sulfate and scopolamine hydrobromide were investigated on the end-plate current (EPC) of frog sartorius muscle by standard voltage-clamp techniques. Both atropine and scopolamine reduced the peak EPC amplitude although scopolamine was only one-third as potent as atropine. The reduction of amplitude became more pronounced with increasing membrane hyperpolarization resulting in nonlinear current-voltage characteristics. Atropine shortened the EPC duration and decreased the voltage-sensitivity of the falling phase; the latter, however, continued to remain a single exponential function of time as in the control. Scopolamine reduced the time to peak, and in addition, converted the falling phase to a double exponential function, consisting of a rapid initial phase followed by a slow terminal phase. Both phases of fall were altered by changes in drug concentration but only the terminal phase responded appreciably to changes in membrane potential. Atropine and scopolamine were without effect on the EPC reversal potential, indicating that the drugs do not exhibit a preference for the ionic species carrying the synaptic current.

Animals↗
PubMed1975

Anatomical specificity as the critical determinant of the interrelationship between raphe lesions and morphine analgesia.

Electrolytic lesions were produced in three separate parts of the raphe mesencephalic area: the nucleus raphe medianus, the nucleus raphe dorsalis and an area between these two nuclei. Seven days after the surgery, the animals were tested for morphine analgesia using the tail compression method and then sacrificed for the estimation of brain serotonin. It was found that the analgesic effect of morphine was significantly reduced in the rats lesioned in the nucleus raphe medianus but not in the animals lesioned either in the nucleus raphe dorsalis or in the 'intermediate raphe area'. Since a decrease of forebrain serotonin was observed in each experimental group, the reduction of morphine analgesia does not involve a simple direct correlation with a decrease of serotonin in the forebrain. The results are discussed in view of the possibility that the reduction of morphine analgesia after lesions of the nucleus raphe medianus is due to a disruption of a specific brain serotonergic system.

Analgesia↗
PubMed1975

[Common categories in the speech of Bert Brechts and the speech of a schizophrenic].

The author demonstrates structural similarities and phenomenal resemblances between the language of Bertolt Brecht and the idiosyncrasies of expression of schizophrenic subjects. He compares some typical modes of expression on the basis of which he draws some general conclusions. What they have in common appears to be a 'disorganization' of the world as we know it which consists of 'things' and 'symbols'. It is only the notion of the more or less conscious use of these means of expression which allows one to distinguish between the 'linguistic world' of Brecht and that of schizophrenic subjects. These findings agree with those of other studies which have revealed affinities between the artistic expression of the mentally deranged and certain trends in art. The author has elaborated a number of heuristic categories which may be employed to understand the various modes of expression and has presented them in table form.

Humans↗
PubMed1969

Plasma and urinary amino acids in primary gout, with special reference to glutamine.

Measurement of the plasma free amino acids by column chromatography (AutoAnalyzer) in 32 patients with primary gout showed statistically significant increases or decreases in several components when compared with the spectrum in 18 control subjects, but the absolute amounts involved were small and the mean total plasma amino acid concentrations in both groups were the same. In the urine all major amino acid components, notably glutamine, serine, threonine, and leucine, were lower in our gouty than in our nongouty subjects, as were also the corresponding renal clearance ratios. These deficits could be reproduced by restricting dietary protein, so appear to be due largely to the some-what reduced mean dietary protein intake of our gouty subjects. However, the low renal clearance of glutamine, the most striking and consistent of the deficits in urinary amino acids noted, could not be accounted for by dietary or other relevant factors, and is interpreted as indicating increased tubular reabsorption of glutamine in primary gout. This interpretation was supported by the results of glutamine loading. The possible compensatory relationship of the abnormality in renal handling of glutamine to the deficiency in renal production of ammonia previously reported is discussed.

Adolescent↗
PubMedDate not supplied

Mechanism of action of sodium cyanide on rat diaphragm muscle.

The effects of sodium cyanide (NaCN) were investigated on the contractile and electrophysiological properties of rat diaphragm muscles in vitro. Sodium cyanide (0.1-1.0 mM) produced an initial potentiation of directly elicited twitch tensions, followed by a slow progressive depression. The potentiation and depression were both dependent on the NaCN concentration and stimulation frequency. Muscles exposed to NaCN exhibited marked reductions of creatine phosphate concentration, but ATP levels were not significantly lowered. Sodium cyanide had no effect on the resting potential, input resistance or action potential, indicating that the toxicity of the metabolic inhibitor is not mediated by alterations of membrane excitability or passive electrical properties. Sodium cyanide reduced the amplitude of contractures elicited by 70 mM K(2)SO(4), suggesting that the actions of NaCN cannot be explained by a failure of action potentials to propagate across the muscle surface or within t-tubular membranes. Sodium cyanide suppressed the first phase of the caffeine contracture, an observation consistent with an impaired release of, or reduced sensitivity to, sarcoplasmic reticular Ca(2+), but did not alter the amplitude of the second phase, which represents rigor following ATP depletion. These results, in conjunction with those of previous studies, suggest that the depression in muscle tension following exposure to NaCN may result from alterations in Ca(2+) homeostasis, intracellular acidosis or from accumulation of one or more products of phosphocreatine breakdown.

Acidosis↗