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Biomedical subjects

B Bishop

Publications and source records attributed to B Bishop.

At least 73 records · Page 4Linked to original sources

Vagal control of diaphragm timing in cat while breathing at elevated lung volumes.

This paper proposes and tests an hypothesis to account for the roles of the volume and rate components of vagal feedback in determining the steady-state pattern of breathing during continuous positive pressure breathing (PPB) and expiratory threshold loading (ETL) in Dial anesthetized cats. During PPB the duration of diaphragm activity (Tdi) is shortened; the duration of its expiratory pause (Tep) is lengthened with little or no change in cycle duration (Tt); with onset of inspiration, flow (dV/dt) is increased; as inspiration proceeds, flow decelerates (d2V/dt2). During ETL Tdi, Tep and Tt are all prolonged; dV/dt is decreased at onset of inspiration, with either no change or an acceleration in flow as inspiration proceeds. PPB and ETL cause similar increases in resting lung volume and Tep, and high negative correlations between Tdi and flow. These relationship suggest that the 'volume component' of vagal feedback is one important factor controlling Tep whereas the 'rate component' contributes to the restraint of Tdi.

Animals↗

Spasticity: its physiology and management. Part I. Neurophysiology of spasticity: classical concepts.

Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.

Animals↗

Spasticity: its physiology and management. Part II. Neurophysiology of spasticity: current concepts.

A review is presented of current information about the structural and functional details of the muscle spindle, denervation supersensitivity, neurotrophism, regenerative capabilities of the peripheral and central nervous systems, CNS plasticity as revealed by recovery of function following brain lesions, and the secondary functional consequences of long-term spasticity. If this recent basic information is to have any practical impact, it must ultimately be incorporated into our concepts of spasticity and applied to our clinical evaluation and treatment procedures.

Brain↗

Spasticity: its physiology and management. Part III. Identifying and assessing the mechanisms underlying spasticity.

Patients with spasticity may have similar motor signs and yet have completely different underlying neural mechanisms. This paper reviews some experimental tests which have been developed to detect and analyze excitatory excesses and inhibitory deficits giving rise to the abnormal motor signs of spasticity. Although at the present time these tests may not lend themselves to routine clinical application, their results are creating a body of knowledge which will become the foundation for diagnosis and treatment of spasticity in the future.

Brain↗

Spasticity: its physiology and management. Part IV. Current and projected treatment procedures for spasticity.

Today's prescriptions for treating spasticity may include pharmacological, surgical, or physical procedures. All derive their rationale from the classical concepts of decerebrate rigidity and of brain organization as discussed in Part I. This paper describes the advantages and disadvantages of these current treatment procedures and proposes that recent discoveries about the "recovery" capabilities of the central nervous system may influence the means for managing spasticity in the future.

Forecasting↗

Vagal afferents essential for abdominal muscle activity during lung inflation in cats.

Maintained inflation of the lung evokes abdominal muscle activity in anesthetized cats only if the vagus nerves are intact, indicating the importance of vagal receptors. The location of these receptors was determined in 14 anesthetized cats by comparing prevagotomy inflation responses of the abdominal muscles and diaphragm to the responses obtained after section of the thoracic vagi at one of three different levels. The abdominal muscle and diaphragm responses to maintained lung inflation persisted following vagotomy below the roots of the lung or denervation of the heart and great vessels. Denervation at the root of the lung, however, abolished the abdominal muscle response and the Hering-Breuer inflation reflex of the diaphragm. It is concluded that pulmonary receptors are essential for the abdominal expiratory activity, but vagal receptors in the abdomen, esophagus, trachea, heart and great vessels are not.

Abdominal Muscles↗

Vibratory stimulation. Part II. Vibratory stimulation as an evaluation tool.

Phasic neural mechanisms are heavily involved in volitional movements, where as tonic mechanisms support postural adjustments. Yet, the two systems are so intimately related that any disturbance in one will exert profound effects on the other. Whether one system or the other is involved preferentially in different neural disorders is not known; hence, tests are needed to evaluate phasic and tonic functions independently. In this article, the classical applications of the tendon jerk reflex and H-response for assessing phasic mechanisms are first reviewed. Following this review, the tonic stretch reflex and tonic vibration reflex (TVR) are analyzed and compared. The effects of experimentally ablating or stimulating precise brain regions are described as a means of revealing the role of supraspinal mechanisms in the TVR. Finally, the responses to vibratory stimulation in specific motor disorders are examined and discussed as to their usefulness in prognosis and diagnosis.

Cerebellar Diseases↗

Vibratory stimulation. Part III. Possible applications of vibration in treatment of motor dysfunctions.

Vibratory stimulation holds promise of becoming a useful therapeutic tool in the treatment of motor disorders. The benefits of vibratory treatment are predictable on the basis of current knowledge about the neurophysiological mechanisms underlying the motor effects of vibration. Actual results of vibratory treatment are described for patients with a wide variety of motor disorders. The importance of attending to practical details such as the proper selection of both stimulus parameters and patients is stressed. Specific recommendations are offered for learning to use vibratory stimulation effectively safely, and intelligently.

Cerebral Palsy↗

Effects of increased ambient pressure and nitrogen on man's monosynaptic reflexes.

Neurological signs during dives may result from altered excitability of central neurons. The present study assesses the effect of an increase in pressure from 1 to 3 ATA on the excitability of muscle spindles and alpha motoneurons by comparing the EMG amplitudes of the mechanically and electrically elicited monosynaptic reflexes of the gastrocnemius-soleus muscle in 10 normal adults breathing a normoxic oxygen-nitrogen gas mixture. At the surface the amplitude of the electrically elicited H response was matched to that of the mechanically elicited Achilles tendon reflex (ATR), but at depth these amplitudes became significantly different. In every subject the amplitude of the ATR, which depends upon the excitability of both muscle spindles and the alpha motoneurons, was reduced on an average of 38% (with a range of 12-75%). The H response bypasses the muscle spindles and hence, depends primarily upon alpha motoneuron excitability. Its amplitude was unaltered in four, reduced in three, and increased in three subjects. Since the ATR was always depressed despite the direction of change in the H response, we have concluded that an increase in ambient pressure (i.e., pressure per se, or nitrogen, or both) must have decreased the responsiveness of muscle spindles to the tendon tap via a reduction in fusimotor activity.

Achilles Tendon↗

Hematology and blood chemistry in saturation diving: I. Antiplatelet drugs, aspirin, and VK744.

Blood chemistry and cellular parameters were studied before, during, and after saturation (2.4 ATA) dives in the HYDRO-LAB habitat on two separate occasions. In both, platelet count fell greater than 20% 12-24 hours after surfacing and moderate (5%) reductions in hemoglobin, red-cell count, and packed-cell volume were observed. Plasma cholesterol and triglyceride levels were depressed postdive as were most plasma enzymes (GOT, GPT, CPK, LDH, ALP). The latter changes were very slight. In the first study, the incidental ingestion of aspirin by some divers did not prevent the loss of platelets even though the platelet-release reaction in response to ADP was inhibited. In the second study the platelet-suppressive drug VK744 was administered, on a double-blind randomized basis, to six divers, six others taking a placebo capsule. Dosage of VK744 was 300 mg TID for 2 days before, 5 days during, 3 days after saturation dive. The drug inhibited the postdive loss of circulatory platelets and in fact the treated group showed a rebound in platelet count above control values, 48-72 hours postdive. Megathrombocyte counts indicated the production of new platelets in both groups at this point. The treated group also showed a marked and significant reduction in plasma cholesterol and triglycerides, suggesting an antilipidemic effect of the drug. Theses results confirm previous observations and indicate that postdecompression loss of platelets may be related to sequestering of reactive platelets, possibly by microbubbles, and that the phenomenon can be inhibited by some antiplatelet drugs.

Adult↗

Comparative influence of proprioceptors and chemoreceptors in the control of respiratory muscles.

Previously we have demonstrated that continuous positive pressure breathing (PB) depresses diaphragm activity and excites expiratory activity in the abdominal muscle (AMR) via vagal proprioceptive impulses. During prolonged PB the AMR persists at a constant level whereas inhibition of the diaphragm wanes, possibly as a result of CO2 retention. This study measures CO2 retention during PB and compares the responses of the abdominal muscle and diaphragm to chemostimulation alone and to chemostimulation and PB in combination. Continuous recordings of minute ventilation, integrated EMGs of the diaphragm and abdominal muscle, and mass spectrometer analysis of airway gases were obtained during PB on air, 5.25 percent CO2 and 12.4 percent O2 in eight Dial-anaesthetized cats. Between 0 and 15 cm H2O the steady-state end-tidal CO2 rises about 0.6 mm Hg/km H2O, diaphragm activity decreases and AMR increases exponentially with each increment in PB. When 5.25 percent CO2 is inspired, diaphragm activity is augmented at every pressure suggesting algebraic summation of proprioceptive and chemoreceptive effects at the respiratory centre. In contrast, the AMR is not significantly altered by hypercapnia. The absence of all abdominal muscle expiratory activity after bilateral vagotomy suggests that the role of active expiration is to regulate thoracic-lung volume, not blood gases.

Abdominal Muscles↗