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Biomedical subjects

J N Davis

Publications and source records attributed to J N Davis.

At least 163 records · Page 9Linked to original sources
PubMed1970

The proprioceptive reflex control of the intercostal muscles during their voluntary activation.

1. A quantitative study has been made of the reflex effects of sudden changes in mechanical load on contracting human intercostal muscles during willed breathing movements involving the chest wall. Averaging techniques were applied to recordings of electromyogram (EMG) and lung volume, and to other parameters of breathing.2. Load changes were effected for brief periods (10-150 msec) at any predetermined lung volume by sudden connexion of the airway to a pressure source variable between +/- 80 cm H(2)O so that respiratory movement could be either assisted or opposed. In some experiments airway resistance was suddenly reduced by porting from a high to a low resistance external airway.3. Contracting inspiratory and expiratory intercostal muscles showed a ;silent period' with unloading which is attributed to the sudden withdrawal from intercostal motoneurones of monosynaptic excitation of muscle spindle origin.4. For both inspiratory and expiratory intercostal muscles the typical immediate effect of an increase in load was an inhibitory response (IR) with a latency of about 22 msec followed by an excitatory response (ER) with a latency of 50-60 msec.5. It was established using brief duration stimuli (< 40 msec) that the IR depended on mechanical events associated with the onset of stimulation, whereas stimuli greater than 40 msec in duration were required to evoke the ER.6. For constant expiratory flow rate and a constant load, the ER of expiratory intercostal muscles increased as lung volume decreased within the limits set by maximal activation of the motoneurone pool as residual volume was approached.7. The ER to a constant load increased directly with the expiratory flow rate at which the load applied, also within limits set by maximal activation of the motoneurone pool.8. For a given load, the ER during phonation was greater than that occurring at a similar expiratory flow rate without phonation when the resistance of the phonating larynx was mimicked by an external airway resistance.9. It is argued that the IR is due to autogenetic inhibition arising from tendon organs and that the ER is due to autogenetic excitation arising from intercostal muscle spindles.10. The initial dominance of inhibition in this dual proprioceptive reflex control was not predicted by the servo theory. It is proposed that the reflex pathways subserving autogenetic inhibition are under a centrifugal control which determines in relation to previous experience (learning) the conditions under which autogenetic facilitation is allowed.

Airway Resistance↗
PubMedDate not supplied

Persistence of sympathetic ingrowth fibers in aged rat hippocampus.

Sympathetic fibers appear in the rat hippocampus following interruption of the septal-hippocampal pathway. The current study examined the relative ability of young (3 month) and old (24 month) rats to produce sympathetic ingrowth fibers. Sympathetic ingrowth was present in the hippocampus of young adult rats 2 months after fimbria/fornix transection. The aged rats either lacked, or had very limited, hippocampal ingrowth two months after fimbria/fornix transections. In contrast, aged rats which had fimbria/fornix transections as young adults had extensive hippocampal ingrowth fibers. The topographical distribution of ingrowth fibers in the hippocampal formation was similar in young 3-month-old rats and rats which were lesioned young and sacrificed when aged. Counts of sympathetic fibers found similar numbers of hippocampal ingrowth fibers at both of the post-operative ages. Thus, although aged animals were acutely impaired in their ability to initiate the ingrowth response, the sympathetic fibers which were established at a young age persisted into senescence.

Aging↗
PubMedDate not supplied

Ultrastructure of the muscle spindle in dystrophia myotonica. I. The intrafusal muscle fibres.

The abnormal intrafusal muscle fibres of four spindles located in extensor indicis biopsies from two patients with dystrophia myotonica have been examined by electron microscopy. In all cases, the fibres had undergone severe longitudinal fragmentation in their equatorial, proximal-polar and mid-polar zones. It was not possible to differentiate the fibres into nuclear bag and nuclear chain types. Many of the fragments were arranged in clusters, each cluster being bounded by a single basement membrane. Numerous partially divided fibres were seen in mid-polar sections, and a morphological picture of the fragmentation process has been presented. The ultrastructural appearance of individual fibre fragments ranged from normality through to severe atrophy. Intrafusal satellite cells showed an increase in numbers, presumably in response to the pathological processes affecting the muscle fibres. The nature of this response is discussed.

Cell Division↗
PubMedDate not supplied

Ultrastructure of the muscle spindle in dystrophia myotonica. II. The sensory and motor nerve terminals.

The normal pattern of innervation was lost in the four dystrophia myotonica muscle spindles examined. There had been a proliferation of both sensory and motor nerve terminals, and many endings showed varying degrees of structural abnormality. The changes seen in the sensory nerve endings were an incomplete contact relationship between the terminal and the muscle fibre, the association of Schwann cell processes with the nerve ending, abnormal shape of the terminal, multiple sensory endings, and changes in the ultrastructural organization of the terminal axoplasm. Remnants of degenerated sensory terminals, and isolated sensory endings were also seen. Motor nerve terminals varied in size and shape. In general, they contained a normal complement of vesicles and mitochondria. Junctional folding was often absent or simplified, and sarcoplasmic specialization was, at the most, rudimentary. The relationship between these changes and intrafusal muscle fibre fragmentation is discussed.

Humans↗
PubMedDate not supplied

Naloxone administration to patients with acute stroke.

Naloxone, an opiate antagonist, has recently been reported to temporarily reverse neurologic deficits associated with subarachnoid hemorrhage. To determine if this unexpected effect of naloxone might also occur in other forms of cerebrovascular diseases, 13 patients who presented with acute neurologic deficits were administered intravenous naloxone. In 3 of these patients, coincidental improvement in neurologic status was seen. In one patient the improvement was permanent. Ten of the 11 patients with non fatal neurologic damage improved later in their hospital course--7 of them to their pre-admission state. The only side effect noted was the temporally related onset of a single focal seizure in an ethanol intoxicated patient with an intracerebral hemorrhage.

Acute Disease↗