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Biomedical subjects

S B Nelson

Publications and source records attributed to S B Nelson.

46 records · Page 3Linked to original sources
PubMed1989

Transdiaphragmatic twitch pressure. Effects of lung volume and chest wall shape.

The effect of lung volume and thoracoabdominal shape on the transdiaphragmatic twitch pressure (Pdit) amplitude was evaluated in six volunteers during airway occlusion. Twitch stimulation was applied through fine wire electrodes implanted near both phrenic nerves. Stimulations were tolerated with little discomfort and constant phrenic nerve responses were maintained for hours. At FRC the group mean Pdit was 31.4 cm H2O (range, 19 to 36 cm H2O), and its coefficient of variation ranged between 2 and 5% in individual subjects. At 1 L above FRC, the Pdit decreased a mean of 7.8 cm H2O (range, 2.8 to 11.9 cm H2O). This change was caused primarily by a decrease in esophageal pressure amplitude. The shape of the relaxed chest wall was altered by loading the rib cage with a force of 5 to 9 kg. Load and shape had little effect on Pdit independently of lung volume. Our modified technique of phrenic nerve stimulation through small wire electrodes is ideally suited for longitudinal intervention studies in patients. We conclude that the variability of Pdit with shape is small compared with its expected decrease with lung volume.

Action Potentials↗
PubMed1989

Spirometry and flow-volume curves.

Spirometry is the best and most widely used pulmonary function test. Equipment recommendations are made and performance information about different types of spirometers is given. Methods for obtaining clinically applicable spirometric results for use in making diagnostic and treatment decisions are presented. Selection and use of reference or "normal" values and interpretive strategies are discussed.

Forced Expiratory Flow Rates↗
PubMed1985

Topographic organization of the optic radiation of the cat.

Pairs of injections of different neuroanatomical tracers--peroxidase-conjugated wheat-germ agglutinin (WGA) and [3H]proline--were made into the lateral geniculate nucleus (LGN) of the cat, and the course of the labeled fibers in the optic radiation was reconstructed. When the two injections were widely separated in the rostrocaudal dimension of the LGN (i.e., one in the representation of the lower quadrant of the visual field and one in the upper quadrant), the two sets of labeled fibers also remained separated in the long (roughly rostrocaudal) axis of the optic radiation. When the injections were widely separated in the mediolateral dimension of the LGN (i.e., one at the representation of the area centralis and one on the horizontal meridian in the far periphery of the field), the two sets of labeled fibers were separated in the short (mediolateral) dimension of the radiation. Shortly before reaching area 17, however, the medially and laterally placed fibers exchanged positions. This crossing is the basis of the topological inversion in the optic radiation deduced previously by Connolly and Van Essen (J. Comp. Neurol. 226:544-564, '84). The retinotopic organization of fibers in the radiation is less precise (in either dimension) than that of their terminal arborizations in visual cortex, but even injections as close as 1 mm to each other gave rise to spatially distinct fiber distributions. The WGA injections also labeled the corticogeniculate fibers by retrograde transport; these fibers traveled in a separate pathway medial to the optic radiation.

Animals↗
PubMed1985

Clonidine and cortical plasticity: possible evidence for noradrenergic involvement.

In order to test the hypothesis that noradrenergic transmission modulates ocular dominance plasticity in kitten visual cortex, we monocularly deprived kittens while administering the alpha-2 adrenergic agonist clonidine (CLON). To avoid bias in testing the hypothesis, we included, with a single blind technique, saline-treated control kittens in the series. First, using high-pressure liquid chromatography, we demonstrated that CLON treatments resulted in an average decline in cerebrospinal fluid levels of the norepinephrine metabolite, 3-methoxy-4-hydroxy phenylethylene glyolol (MHPG) of 44%. Then, single-unit recording in area 17 revealed the expected ocular dominance (OD) shift in monocularly deprived saline controls, but recording failed to find a significant shift in CLON-treated kittens. Our results support the notion that CLON treatment interferes with ocular dominance plasticity by inhibiting noradrenergic transmission in visual cortex. We discuss side effects of CLON, concluding that CLON's sedative effect may contribute to the lack of OD shift.

Animals↗
PubMed1984

Effects of luminance and flicker on ocular dominance shift in kitten visual cortex.

We raised monocularly deprived kittens in visual environments with low level illumination that was either steady or flickering. With steady scotopic luminance ocular dominance shifted as it does in normal photopic lighting. In flickering light with an average frequency of 2 Hz there was virtually no ocular dominance shift, while in flickering light averaging 0.1 Hz there was a significant shift. Recordings from the 2 Hz flicker-reared were similar to the dark-reared recordings. The flickering illumination was produced in one case by a high contrast-low brightness TV near the cage, and in another case, by a low voltage incandescent bulb driven by a pseudo-random sequence generator. This circuit delivered either a maximum ON time of 1.7 s or a maximum of 40 s, for the 2 Hz and 0.1 Hz respectively. Both the TV and flickering bulb produced average illumination comparable to the dim (0.01 cd/m2) steady scotopic illumination. We conclude that dim flickering light is not a sufficient stimulus for promoting ocular dominance shift in kittens in the critical period unless the flicker rate approaches 0.1 Hz. Furthermore results from the TV rearing suggest that flicker may be capable of preventing an ocular dominance shift expected from a concurrent steady low light level background.

Animals↗
PubMedDate not supplied

Two methods of catecholamine depletion in kitten visual cortex yield different effects on plasticity.

As first clearly demonstrated by the experiments of Wiesel and Hubel, the developing visual cortex is exquisitely sensitive to sensory deprivation. Temporary closure of one eye of a kitten during a critical period that extends from 3 weeks to 3 months of age results in a dramatic cortical reorganization such that most neurones, originally binocularly driven, are dominated exclusively by the open eye. Recently, attention has been directed to chemical factors which may influence the degree of plasticity during the critical period. The work of Kasamatsu and pettigrew suggests that cortical catecholamines, especially noradrenaline (NA), are essential for the normal plastic response to visual deprivation. In an effort to clarify the role of NA in visual cortical plasticity, we have monocularly deprived kittens whose cortex had been depleted of catecholamines by the neurotoxin 6-hydroxydopamine (6-OHDA). We used two strategies to deplete cortical NA: the first, pioneered by Kasamatsu el al., utilized osmotic minipumps to deliver 6-OHDA to visual cortex; the second involved systemic neonatal injections of 6-OHDA, a technique which has proved effective in rodents. We found, using high-pressure liquid chromatography (HPLC), that both techniques produced a substantial reduction in the level of cortical NA. However, single unit recording in area 17 revealed that the plastic response to monocular deprivation (MD) was only diminished in the kittens depleted by minipump.

Animals↗