Role of the cardiopulmonary blood volume in changes in left ventricular output during stimulation of somatic afferent nerve fibers

1986 ◽  
Vol 101 (5) ◽  
pp. 564-567
Author(s):  
L. I. Osadchii ◽  
T. V. Balueva ◽  
I. V. Sergeev
Neurosurgery ◽  
1984 ◽  
Vol 15 (6) ◽  
pp. 917-920 ◽  
Author(s):  
Ilmar Jurna

Abstract The intrathecal (i.t.) administration of morphine inhibits nociceptive motor responses and activity in ascending axons evoked by stimulation of nociceptive afferent nerve fibers (nociceptive sensory response) in the rat. The i.t. administration of cholecystokinin octapeptide and ceruletide inhibits nociceptive motor responses, but does not affect ascending nociceptive activity. This shows that drug-induced depression of nociceptive motor responses is not always associated with depression of the nociceptive sensory response of the spinal cord. The microiontophoretic application of substance P excites single dorsal horn neurons that respond to noxious stimulation, whereas the i.t. administration of substance P inhibits both nociceptive motor and sensory responses. Thus, the results obtained from the i.t. administration of a drug may differ from those obtained from its application to single spinal neurons. Diazepam inhibits spinal reflexes and may reduce pain sensation in humans. To assess whether a spinal action is involved in the pain-relieving effect of diazepam, experiments were carried out on spinalized rats in which activity evoked by the stimulation of nociceptive and nonnociceptive afferent nerve fibers of the sural nerve was recorded from single ascending axons below the site of spinal cord transection. Diazepam, 20 ųg i.t., reduced activity evoked by afferent A delta and C fiber stimulation and by stimulation of afferent A beta fibers. The depressant effect caused by diazepam, 2 mg/kg i.v., on C fiber-evoked ascending activity was reduced by the i.t. injection of the benzodiazepine antagonist, Ro 15-1788 (40 ųg), an imidazodiazepine. It is concluded that the depression by diazepam of C fiber-evoked ascending activity contributes to pain relief caused by the drug.


1976 ◽  
Vol 230 (4) ◽  
pp. 1003-1007 ◽  
Author(s):  
Y Uchida

The role of afferent cardiac sympathetic nerve fibers in the regulation of respiration has been examined. Application of potassium chloride or lactic acid solutions to the left ventricular surface of anesthetized vagotomized dogs resulted in a decrease in the manimum firing rate and shortening in period duration of firing of phrenic nerves. Also, application of the agents caused a decrease in amplitude and an increase in rate of respiratory thoracic movements. The same changes in phrenic nerve activity and respiratory movements were produced by coronary artery occlusion and centrifugal electrical stimulation of the left inferior cardiac nerves. The results indicate tachypnea that can be produced by excitation of afferent cardiac sympathetic nerve fibers.


1973 ◽  
Vol 82 (4) ◽  
pp. 464-472 ◽  
Author(s):  
Merle Lawrence ◽  
Lars-Göran Johnsson

An analysis of the contribution to hearing made by the presence of a normal organ of Corti as compared to direct electric stimulation of the nerve leads to the following conclusions: The portion of the basal turn of the cochlea which can be stimulated contains activity regions primarily limited to frequencies above 5000 Hz. Electrical stimulation of sensory afferent nerve fibers gives rise to sensations of very limited dynamic range compared to normal adequate stimulation through the organ of Corti. Following destruction of the organ of Corti, the speed of nerve degeneration in man is not known, but appears to be slow. Some ganglion cells almost always persist but it is doubtful that these are excitable. The severe nerve degeneration known to be present in most cases of human deafness raises critical questions about the feasibility and logic of a direct stimulation of the auditory nerve in these patients. The unavoidable damage to the capillaries and endosteum of the walls of the scala tympani by insertion of a wire is certain to produce further degeneration and new bone formation.


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