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Biomedical subjects

R A Levy

Publications and source records attributed to R A Levy.

At least 91 records · Page 5Linked to original sources
PubMed1979

Student pilots referred to the neuropsychiatry branch, USAFSAM 1968-78: implications for selection.

The case records of 76 student aviators referred to the Neuropsychiatry Branch of the USAF School of Aerospace Medicine during the period 1968-78 are reviewed. Demographic and diagnostic data are provided including source of recruitment, age, marital status, aircraft flown, flying hours, and diagnostic categories. Psychophysiological categories are particularly scrutinized and cameo case histories provided. Implications for pilot selection are discussed.

Adult↗
PubMed1978

Delimitation of neuronal substrates necessary for the analgesic action of baclofen and morphine.

The loci of neuronal substrates necessary for the analgesic action of baclofen and of morphine were determined by systematic transection of the rat cerebrospinal axis. Severe reduction in the analgesic capacity of both drugs, assessed with the tail flick test, occurred after section of the thoracic spinal cord, indicating that necessary substrates are located rostral to this level. These data also suggest that baclofen-induced analgesia does not primarily result from a pharmacological blockade of nociceptive information at the first sensory synapse in the spinal cord. Neither baclofen- nor morphine-induced analgesia was altered by transection of the brain stem between the superior and inferior colliculi, but the action of both drugs was greatly reduced following section of the medulla 3 mm rostral to the obex. Thus, the rostral margin of neuronal substrates mediating the effects of both drugs lies somewhere in the pons or anterior third of the medulla. This observation is compatible with the notion that analgesia induced by baclofen and morphine involves, at least in part, common neuronal substrates.

Aminobutyrates↗
PubMed1977

Lignocaine: a new technique for intravenous administration.

Current practices of intravenous lignocaine administration may result in a significant drop in blood level between the peak serum level from the initial bolus and the subsequent steady state from the constant infusion. This can cause a significant interval when plasma lignocaine levels are less than therapeutic, and ventricular ectopy may occur. To eliminate this subtherapeutic interval, a new therapeutic approach was devised. Seven patients were studied who had no evidence of congestive heart failure or liver disease. Lignocaine was infused at a rate of 25 mg/min; infusion dosages were selected by patient weight. The above therapeutic regimen eliminated the subtherapeutic hiatus and did not result in clinical toxicity. Therefore, this new infusion technique has significant clinical advantages in patients who require therapy with intravenous lignocaine.

Adult↗
PubMed1977

The analgesic action of baclofen [beta-(4-chlorophenyl)-gamma-aminobutyric acid].

When administered to mice, baclofen induced dose-related antinocisponsive activity in the stretch, hot plate and tail-flick tests. Although high doses also impaired motor coordination, as measured by the rotating rod test, the following observations suggest that the pronounced antinocisponsive effect of higher doses did not reflect a reduced capacity to respond to perceived pain: motor impairment, having shorter onset of action, was fully developed before the appearance of any analgesic action; mice made completely tolerant to the motor effect were still analgesic; and other agents which severely impaired rotating rod performance did not necessarily show antinocisponsive activity in the hot plate test. The mechanism of action of baclofen is not similar to that of morphine since naloxone did not antagonize the analgesic effect of baclofen, and cross-tolerance between morphine- and baclofen-induced analgesia could not be demonstrated.

Aminobutyrates↗
PubMed1975

The effect of intravenously administered gamma-aminobutyric acid on afferent fiber polarization.

(1) The effect of intravenously administered gamma-aminobutyric acid (GABA) on afferent fiber polarization in the feline spinal cord was ascertained from fluctuations induced in the DC level of dorsal root filaments. (2) A dose-related depolarization of the filament, with a concomitant reduction in the magnitude of the dorsal root potential, was observed after 50 and 100 mg/kg GABA. (3) GABA also depolarized filaments of preparations in which interneuronal activity was suppressed by pretreatment with tetrodotoxin. Since the magnitude of the depolarization induced in these preparations was equal to that observed in nonpretreated animals, it is likely that the depolarization in the latter preparations reflects a direct effect on afferent terminals or fibers rather than an action on interneurons. (4) GABA failed to depolarize filaments in animals pretreated with bicuculline. This suggests that intravenously administered GABA interacted with receptors that are identical with or similar to those involved in neurally evoked primary afferent depolarization (PAD). (5) The direct depolarization of afferent fibers by intravenous GABA and the blockade thereof by bicuculline are characteristics compatible with those of the endogenous axo-axonic transmitter operating in pathways mediating neurally evoked PAD. These data, therefore, support the involvement of GABA at this synapse in the mammalian spinal cord.

Aminobutyrates↗