Biomedical subjects
Publications and source records attributed to N Tremblay.
A patient is presented in whom a pulmonary artery catheter (PAC) formed a knot which was fixed in the region of the tricuspid valve chordea. The PAC was successfully and nonsurgically freed from its attachment and removed. A guide wire was introduced by the distal port of the PAC and under fluoroscopy the PAC was manipulated free and then extracted easily.
The use of blood products in 1480 consecutive cases of adult cardiac surgical procedures over a period of 15 mth was studied retrospectively using the database of the Department of Anaesthesia of the Institut de Cardiologie de Montréal. Use of blood products was compared in patients having (1) coronary artery bypass grafting, (2) valvular surgery, (3) or a combination of 1 and 2. First operations were compared with reoperations. Overall, the use of homologous blood products was greatest in patients of Group 3, intermediate in patients of Group 2, and smallest in patients of Group 1. Reoperations were associated with an increase in intraoperative transfusion of packed red blood cells, but postoperative chest drainage was similar to first operations. When all blood products (packed red blood cells, fresh frozen plasma and platelets) were taken into consideration, patients undergoing primary CABG or valve surgery were the least exposed to homologous blood donors (five and six units transfused respectively). Repeat CABG was associated with an intermediate exposure to homologous blood products (eight units). Finally, primary and repeat combined procedures, and repeat valve surgery were associated with the greatest exposure to foreign blood products (10, 13 and 10 units respectively). The data presented in this study provide a rational basis for stratification of procedures according to the expected use of blood products, particularly in view of future studies which may be planned to examine the efficiency of blood conservation strategies.
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One method for the treatment of chronic musculoskeletal pain involves stimulation of the peripheral or central nervous system. Such stimulation includes transcutaneous electrical nerve stimulation, dorsal column stimulation, and deep brain stimulation. This review discusses the clinical use of electrical stimulation for the relief of musculoskeletal pain, and describes the results of studies conducted in our laboratory suggesting that such stimulation reduces pain transmission along sensory-discriminative pathways.
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1. Microelectrodes attached to iontophoretic pipettes were used to isolate 410 single neurons in the primary somatosensory cortex of halothane-anesthetized cats. Basal forebrain (BF) stimulation, when paired with pulses of iontophoretically administered glutamate, affected the responsiveness in 24 (54%) of 39 neurons; 17 were facilitated, and seven were inhibited. Five minutes after BF stimulation the average response for a sample of 20 cells was enhanced by 45% (+/- 19). All but one of the effects lasted as long as the cell was studied, often greater than 1 h. 2. When atropine was administered while the BF was stimulated during glutamate excitation, 7 of 16 cells were enhanced, but the average increase was only 16% (+/- 15) for a sample of 15 cells. After the atropine had dissipated, four cells were enhanced by the BF stimulus. In three of these the enhancement had been blocked previously by atropine. 3. BF stimulation had effects similar to iontophoretically administered acetylcholine (ACh), but the effects appeared more frequently with BF stimulation than they had with acetylcholine administration. 4. We propose that the enhanced neuronal responsiveness is due to the release of acetylcholine by cortical terminals of cholinergic neurons located in the BF. The BF stimulus may be more effective than acetylcholine administration because corticopetal cholinergic fibers may end in the immediate vicinity of receptors responsible for long-term changes in membrane permeability.
1. Of the sample of 322 neurons located in somatosensory cortex and tested for their responsiveness to somatic stimulation, 91 (28%) responded to stimuli applied to the skin. The majority were located in the middle cortical layers. Each of the cells subjected to tests with glutamate and acetylcholine (ACh) was rapidly adapting to cutaneous stimuli, giving a response at the onset of skin indentation and sometimes after the stimulus withdrawal. 2. Of the 30 cells tested by pairing basal forebrain (BF) stimulation with cutaneous stimulation. 18 (60%) displayed enhanced responses to the same cutaneous stimulus after the pairing. These effects lasted for greater than 5 min in 17 cases, persisting for as long as the cell was studied, sometimes greater than 1 h. 3. The enhanced responsiveness to cutaneous stimuli could not be reversed by atropine, but in each of the 11 cells where atropine was administered while the BF stimulus was paired with the skin stimulus, the pairing produced no enhancement. 4. We conclude that pairing a BF stimulus with a cutaneous stimulus leads to long-term facilitation of the responsiveness of the cortical neuron subjected to this treatment and that this effect is mediated by the release of acetylcholine from BF cholinergic neurons that act on muscarinic receptors found on neurons in the somatosensory cortex.
Somatosensory cortex reorganizes following restricted deafferentation so that deprived neurons acquire new receptive fields. Electrophysiological data suggest that a decrease in inhibition might be one of the mechanisms contributing to these changes. This hypothesis was tested by evaluating quantitatively glutamic acid decarboxylase (GAD) immunoreactivity and cytochrome oxidase (CO) activity in normal and partially deafferented rat hindlimb somatosensory cortex. In normal animals, there were laminar differences in the frequencies of GAD+ cells that correlated with the levels of CO activity. Two weeks after transection of the sciatic nerve, CO levels were reduced in all layers of the hindlimb somatosensory cortex contralateral to the nerve transection whereas the frequencies of GAD+ cells were unchanged except in layer IV where a 16% decrease was observed. This observation is consistent with the hypothesis that the expression of GAD in layer IV is partially controlled by the amount of afferent input. The ability of novel inputs to develop stable patterns of excitation in deafferented somatosensory cortex may depend upon the reduction of GABAergic inhibition which follows deafferentation.
In area 3b of primary somatosensory cortex, neurons may be classified as either rapidly adapting or slowly adapting to sustained stimuli and may be differentiated further by the presence or absence of a receptive field and by their threshold of activation. It is also possible to use the rate of adaptation of the background activity to a sustained stimulus to divide the cortex into slowly adapting regions or rapidly adapting regions. By blocking GABA-mediated inhibition with iontophoretically administered bicuculline methiodide, others have observed an increase in receptive field size in rapidly adapting regions but not in slowly adapting regions. The present study was designed to look for a different inhibitory transmitter which might control receptive field size in slowly adapting regions. Iontophoretically delivered strychnine was employed as an antagonist because it interferes with glycine-like inhibitory transmitters such as glycine, taurine and beta-alanine. Pharmacological tests were performed on 157 neurons in two series of experiments. In the first series three effects were documented. (i) In rapidly adapting regions, the size of the receptive field increased in 11 out of 25 cases whereas none of the 20 receptive fields tested in slowly adapting regions enlarged. (ii) In 13 of 24 cases a receptive field was revealed for previously unresponsive neurons in rapidly adapting regions whereas only 5 of 22 unresponsive cells tested in slowly adapting regions developed a receptive field. (iii) In 15 of 25 cells with receptive fields tested in rapidly adapting zones, strychnine reduced the threshold for somatic stimuli but only 8 of 20 cells isolated in slowly adapting zones showed this effect. In a second series of experiments, the effect of beta-alanine, glycine and taurine was examined on neurons of the rapidly adapting regions. beta-Alanine and taurine reduced the excitability of all neurons tested. Glycine inhibited most neurons. However, strychnine only antagonized the inhibitory effects of beta-alanine on responses to peripheral stimuli (9 of 11 cases). When neurons could not be driven by peripheral stimuli, the inhibition of spontaneous or glutamate-induced activity could not be blocked by strychnine (0 of 18 cases). We suggest that glycine-like amino acids contribute to the control of receptive field size and the control of neuronal excitability in rapidly adapting regions but not in slowly adapting regions. Our data suggest that strychnine-sensitive synapses are limited only to a subset of cortical neurons driven by somatic inputs.
1. Two-hundred thirty-three single neurons were isolated and studied in somatosensory cortex of cats anesthetized with pentobarbital sodium or urethane. Two-hundred and three were studied during iontophoretic administration of acetylcholine (ACh), 173 during administration of glutamate, and 24 during administration of atropine. 2. Fifty-six percent of the 218 neurons tested responded to somatic stimuli. Another 21% did so during glutamate administration. In 11 cases ACh iontophoresis uncovered a receptive field in a previously unresponsive cell. 3. Forty-six percent of the 160 cells tested responded to thalamic stimulation. Another 17% did so in the presence of glutamate, but 19 cells responded to neither cutaneous nor thalamic stimuli. 4. Sixteen percent of the 203 cells tested were overtly excited by ACh and the responses to somatic stimulation of 29% were modulated by administration of ACh. Cells displaying overt excitation and/or modulation of responses were said to be cholinoceptive and made up 39% of the sample. These cells were located in all cortical layers. 5. Cholinoceptive neurons were more likely than noncholinoceptive cells to be driven by thalamic stimulation. 6. The changes observed during ACh administration tended to be facilitatory: an enhanced responsiveness to somatic stimuli, an increased firing rate, or an increased receptive-field size. However, in 10 of the 203 cases tested one or more of these variables decreased. 7. The enhanced responsiveness during ACh administration was a robust phenomenon; responses were often increased by as much as 200% and the discharge pattern was altered so that bursts of impulses following stimulation were more common. 8. ACh tended to enhance one attribute of a cell selectively rather than to act as a general excitant. 9. ACh is a powerful neuromodulatory agent in somatosensory cortex that, when released in specific behavioral states, should enhance the responsiveness of cortical neurons.
1. Two-hundred and seven neurons were examined for changes in their responsiveness during the iontophoretic administration of acetylcholine (ACh) in barbiturate-anesthetized cats. 2. The laminar locations of 78 cells were determined. Cholinoceptive neurons were found in all cortical layers and ranged from 50% of the cells tested in layer I to 78% in layer VI. 3. When the responsiveness of a neuron was measured by the magnitude of the discharge generated by a fixed dose of glutamate, 30 of 47 cases (64%) were potentiated, and 4 (8%) were depressed when ACh was administered during glutamate-induced excitation. 4. ACh administered during glutamate excitation was significantly more effective in altering neuronal responsiveness than was ACh administered alone (P less than 0.001). 5. When the responsiveness of a neuron was measured by the magnitude of the discharge generated by a standard somatic stimulus applied to the receptive field, 42 of 52 cases (81%) were potentiated during ACh application. This was again different from ACh treatment alone where only 4 of 27 tests (15%) resulted in subsequent enhancement of the response to somatic stimuli. 6. ACh generally increased the responsiveness of neurons with peripheral receptive fields and caused the appearance of a receptive field in some cells lacking one. 7. In many cases the changes in excitability, as measured by responses either to glutamate or to somatic stimulation, remained for prolonged time periods. When glutamate was used to test excitability, 34% (16 of 47) of the enhancements lasted more than 5 min. When somatic stimuli were used 29% (15 of 52) lasted more than 5 min. With both measures some neurons still displayed enhanced responses more than 1 h after the treatment with ACh. 8. ACh appears to act as a permissive agent that allows modification of the effectiveness with which previously existing afferent inputs drive somatosensory cortical neurons. 9. This mechanism to alter neuronal responsiveness has many of the characteristics necessary to account for the reorganization observed in somatosensory cortex following alterations in its afferent drive and may be related to some forms of learning and memory.
Acetylcholine (ACh) was administered iontophoretically to single neurons in cat somatosensory cortex. Using extracellular recording techniques, neuronal responsiveness was determined at regular intervals from the number of action potentials produced either by iontophoretically applied glutamate or by tactile stimulation of the cutaneous receptive field. The responses were altered in only 21% (13/61) of the neurons following the application of ACh alone. In contrast, 75% (66/88) of the neurons displayed altered responses during administration of ACh simultaneously with either iontophoretically administered glutamate or with tactile stimulation of the receptive field. Forty-seven percent (29/62) of the responses potentiated in the presence of ACh remained enhanced for periods lasting from 8 min to over 1 h. The responsiveness of cortical neurons to afferent inputs changes during the reorganization of somatotopic maps that occurs after deafferentation, and perhaps during some forms of learning. As ACh has been implicated in some of these processes, it may be that the changes in responsiveness observed here following iontophoretically applied ACh are similar to those which facilitate the acquisition of neuronal responses to altered or novel afferent inputs.
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