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1. Using single fibre vagal afferent recording techniques, we have investigated the longitudinal and circumferential location of slowly adapting stretch receptors in a functionally isolated, in situ segment of the trachea in dogs. 2. We have also studied the depth of these receptors within the airway wall and their response to reflex and drug induced contraction of the airway smooth muscle. 3. Thirty-four per cent of the receptors studied were in the extrathoracic trachea; calculations indicate that about 17-1% of all airway stretch receptors lie outside the thorax. 4. All the receptors were located in the membranous posterior wall of the trachea, and those tested responded more to transverse than to longitudinal stretching of the wall. 5. Receptors in the extrathoracic trachea continued to function after the regional mucosa had been widely resected; subsequent removal of histolocially proven smooth muscle tissue caused the abrupt cessation of receptor discharge. 6. Contraction of airway smooth muscle brought about an increase in receptor discharge frequency. 7. Similar results were found for a smaller number of stretch receptors located in the mainstem and lobar bronchi. 8. These findings procided evidence that stretch receptors are anatomically located within the smooth muscle layer of the airways and are functionally aranged in series with the muscle fibres.

Sedative drugs have been found to depress the respiratory activity of upper airway muscles more than that of the diaphragm. To determine whether CO2 at narcotic levels has a similar action, we recorded phrenic and hypoglossal nerve activities in decerebrate, vagotomized, paralyzed cats. T5 or T6 external intercostal nerve activity was also recorded in some animals. End-tidal CO2 concentration was raised progressively to over 30% or until depression of nerve activity was apparent. Respiratory frequency was reduced by severe hypercapnia in most cats. Hypoglossal nerve activity was consistently decreased more than that of the phrenic nerve. In most cases intercostal nerve activity was also more susceptible than phrenic nerve activity to hypercapnic depression. The results indicate that CO2 at narcotic levels interferes both with the central pattern generator for breathing movements and with the expression of the pattern in specific motor nerves.

Responses of expiratory duration (TE) and laryngeal aperture to small flow resistance loads (2 and 5 cm H2O/LPS) applied to single expirations were measured using repeated applications in four subjects during quiet breathing. All subjects significantly prolonged TE in response to the higher load and 3 of the 4 showed that same response to the lower load, which was not perceived by these subjects. These same 3 subjects showed a narrowed laryngeal aperture in response to loading such that their expiratory impedance must have been greater than the increase provided by the load alone. The effect of such a loading response was to slow the expiratory volume decay so that a small but significant increase in the halftime for volume decay was observed. The prolongation of TE seen with loading could be due to the alteration of volume-related feedback consequent to the increased expiratory impedance. This may serve a role in regulation of expiratory muscle function.

The concentrations of 3 putative neurotransmitters (glutamate, aspartate and gamma-aminobutyrate), 4 related amino acids and 5 non-transmitter-related amino acids have been measured in neurosurgical samples (frontal cortex) from patients with intractable depression and controls. In addition, the glutamate receptor agonist 2-amino-4-sulpho-butanoic acid (homocysteic acid) has been identified in human brain and measured in these samples. There were no changes in the concentrations of amino acids in depressed patients compared to control with the exception of aspartic and homocysteic acids which were elevated in a sub-group of patients with depression compared to control. The Ca2+-dependent release (K+-stimulated) of putative neurotransmitters has been demonstrated for the first time from brain tissue of depressed patients. Glutamate release was unaltered from the control value. Aspartate values showed unexplained variability but it's release and that of gamma-aminobutyrate were elevated in some depressed subjects. These results do not support the hypothesis of reduced amino acid function in depressive illness.

A consequence of the adaptation of pulmonary stretch receptors is that their pattern of discharge depends on both lung volume and its rate of change. For adaptation dependent, flow related information to modify the breathing pattern by a feedback process, appreciable receptor adaptation must take place during a single respiratory cycle. Moreover, for flow related information to have the same significance in all animals, the time course of stretch receptor adaptation would have to vary among species, being more rapid in small animals, with high respiratory frequencies. We recorded single fiber action potentials from 84 pulmonary stretch receptors in six species of mammals, ranging from hamster to dog. The response of the receptors to maintained transpulmonary pressures was similar in the different species,as was the time course of receptor adptation following sudden lung inflations to 5 and 10 cm H2O. These findings show that the behavior of pulmonary stretch receptors is similar in animals with widely differing respiratory frequencies, and that the significance of receptor adaptation for regulation of the breathing pattern must vary interspecifically.

The influence of head position on the respiratory activity of the diaphragm (DIA), posterior cricoarytenoid (PCA) and genioglossus (GG) muscles was studied in conscious cats with chronically implanted electromyographic electrodes. Tracheal pressure was also recorded through a small implanted catheter. Spontaneous or passive downward movements of the head resulted in sustained increases in the respiratory excursions of tracheal pressure and in PCA and GG activities. Conversely, these variables all decreased when the head was raised. Activity of the DIA was little affected. In animals with chronic tracheostomies, which greatly diminished tracheal pressure excursions and their changes with head movements, the postural responses of PCA and GG activities persisted, but were attenuated. The responses also persisted after bilateral superior laryngeal nerve section. These findings demonstrate responses that act to maintain the patency of the upper respiratory tract, probably by reflex mechanisms. Receptors in the upper airway contribute to the responses, but other afferents - possibly from vestibular or joint receptors - are also involved.

Plasma, cerebrospinal fluid and brain tissue amino acid levels were measured in 14 patients with affective illness and generally confirm previous findings. There was no correlation between these values and age, sex, family history and levels of anxiety. GABA levels measured in cortex tissue were negatively correlated with depressive mood (P less than 0.05), supporting a possible involvement of GABA in depressive illness.

This study was undertaken to assess the role of intrapulmonary chemoreceptors in the control of breathing in reptiles. Garter snakes were tracheostomized to remove the influence of upper airway receptors. After recovery from anesthesia, the animals were unidirectionally ventilated or allowed to ventilate normally, but without glottal control of the breath-hold. Breathing movements were recorded by means of a pneumotachograph. When a bidirectionally breathing snake was presented with CO2 at the tracheal tube, inspiratory duration and volume decreased. When CO2 was removed from the inspired air between breaths, inspiratory duration and volume increased. Removing CO2 from the airstream of a unidirectionally ventilated snake during a breath-hold produced apnea, but removing CO2 at the beginning of inspiration caused the duration and volume of the inspiration to increase. This reflex appears to represent a positive feedback mechanism for enhancing inspiration once a breath has been initiated.

Our purpose was to characterize receptors which respond to changes in upper airway pressures. Such changes cause alterations in hypoglossal and phrenic nerve activities. Decerebrate, vagotomized, paralyzed and ventilated cats were prepared so that pressures could be altered within segments of upper airways. Activities of single fibers in the superior laryngeal and glossopharyngeal nerves were monitored. Most superior laryngeal receptors discharged tonically at zero transmural pressure. Discharges of approximately half decreased (A) and the rest increased (B) with pressure reductions of -7 to -28 cm H2O. Pressure increases of +7 to +28 cm H2O caused increases in Group A activities while Group B responses varied. The remaining receptors were silent, being activated by pressure decreases and/or increases. Activities of other silent receptors, similarly activated, were recorded from glossopharyngeal nerve. Tonically active glossopharyngeal receptors increased discharge after both pressure increases and decreases. Most tonically active and silent receptors, having afferents in either nerve, adapted incompletely to sustained pressures. These may have major functions in hypoglossal responses to changes in upper airway pressures.

In decerebrate, vagotomized, paralyzed, and ventilated cats, phrenic and respiratory-related hypoglossal discharges were evident at normocapnic normoxia or hyperoxia. Both increased progressively in hypercapnia or hypoxia. With increasing drive, onset of inspiratory hypoglossal activity began earlier relative to phrenic onset; an early expiratory hypoglossal burst was also observed. Following subanesthetic doses of chloralose, halothane, ketamine, or pentobarbital, hypoglossal activity was depressed much more than phrenic discharge. In moderate hypercapnia or hypoxia, phrenic activity increased more than hypoglossal, whereas, at high drive, the latter rose more sharply in some cats. Electromyograms of the diaphragm and genioglossus were recorded in intact awake cats to determine if their responses and those of decerebrates are comparable. Respiratory-related genioglossal discharge was evident in normocapnia. We conclude that anesthesia suppresses hypoglossal motor activities much more than those of the bulbospinal-phrenic system. Data for decerebrate cats and unanesthetized cats or humans provide no evidence of a differential distribution of chemoreceptor afferents on hypoglossal and bulbospinal-phrenic neurons, as suggested by results in anesthetized animals.

Using a fiberoptic laryngoscope and video equipment, we studied the respiratory movements of the vocal cords during sustained hyperventilation in 4 normal human subjects. The expiratory narrowing of the glottic airway that occurs in quiet breathing was attenuated during hyperventilation in 7 of 8 experiments, and the pattern of vocal cord movements throughout the breathing cycle closely resembled the patterns previously found in exercise and hypercapnia. These responses were similar during normocapnic and hypocapnic hyperventilation. The similarity of laryngeal movements in voluntary and involuntary hyperpneic states suggests that common brain stem mechanisms may be entrained by both 'behavioral' and 'automatic' ventilatory control systems.

Our purpose was to characterize activities of phrenic motoneurons during apneusis. In decerebrate, cerebellectomized, vagotomized, paralyzed and ventilated cats, we recorded activities of phrenic nerve and single phrenic fibers during eupnea and apneusis. Reversible apneusis was obtained by cooling the rostral pons with a fork thermode. Phrenic motoneurons were defined as 'early' or 'late' during eupnea. Early units commenced activity before or during the first 20% of neural inspiration. The onset of discharge of late units extended throughout the rest of inspiration. In apneusis, some late units ceased activity entirely; others commenced activity at the end of the rising phase of phrenic activity or during the apneustic plateau. Early units commenced activities at the same time as in eupnea and generally maintained the same discharge frequency. Hence, the ramp phase of phrenic discharge in apneusis is generated largely by activities of early motoneurons. Our results imply that the level of bulbospinal activity impinging upon the phrenic nucleus is reduced in apneusis. The integration of efferent activity within the phrenic nucleus is discussed.

In an exploratory study of the metabolism of selected intermediates of glycolysis in rbc of patients with schizophrenia and with major depressive disorders, statistically significant decreases in the RSA of 2,3-DPG were found in the rbc of patients with psychotic disorders compared to normal subjects. No statistically significant differences were observed in the RSA of any of the other glycolytic intermediates studied comparing patients to normal subjects.

Between 1979 and 1986 the number of psychosurgical operations carried out in Britain fell from 70 to 15 procedures annually. There are a number of possible reasons for this change of which increased experience with new regimes of psychotropic medication is perhaps the most important. The new Mental Health Act (1983) which brought psychosurgery under the direct jurisdiction of the law was followed by a sudden reduction in the number of patients treated but referals are now increasing. In current psychiatric practice, classification relies largely on description of syndromes, each characterised by a set of core symptoms. Schizophrenia and affective psychoses (endogenous depression, mania and obsessional illness of late onset) are characterised by disturbances of mood, thinking and perception often so profound as to impair the patient's contact with reality. In contrast, neuroses produce symptoms which are quantitatively, rather than qualitatively different from normal experience and psychosurgery has no place in their treatment. Following the introduction of phenothiazines in the early 1950's schizophrenia ceased to be an indication for psychosurgery. For a small group of severely disabled and distressed people suffering from endogenous depressive and obsessional illnesses, when other treatments have failed or ceased to be effective, psychosurgery remains an appropriate treatment. Just over half the patients treated at the Geoffrey Knight Unit are relieved to the extent that they are either free of symptoms or such symptoms that remain do not significantly impair social function. Following operation recovery is slow and progressive and a programme of rehabilitation is usually necessary. Personality which is often severely damaged by the effects of long illness returns towards normal. Neuropsychiatric evaluation has consistently failed to demonstrate adverse cognitive effects. Evaluation and selection of patients for operation should be done by a psychiatrist and neurosurgeon working in partnership. Stereotactic techniques have made it possible to produce precisely located lesions of consistent size, virtually eliminating side effects and reducing the epileptic risk to between two and three percent. The Mental Health Act, contrary to early expectations, has allowed that psychosurgery retains a place in the treatment of a small highly selected group of patients.

The routine air ventriculograms of 66 psychiatric patients, aged from 22 to 73 years, taken during the psychosurgical operation of stereotactic subcaudate tractotomy, were studied. Ventricular size was unrelated to progressive ageing, but a minority of patients over 60 years had abnormally large ventricles, not invariably associated with cognitive impairment on testing. Enlargement was associated with a clinical diagnosis of schizoaffective illness but not with past ECT.

The results of stereotactic subcaudate tractotomy in nine patients with resistant bipolar affective disorder are presented in the form of a single case study with a summary of the other eight cases. Follow-up studies at 2-4 years showed substantial improvement in five patients and amelioration of symptoms in a further four patients, with a tendency for a greater improvement in the manic than in the depressive episodes. These preliminary results suggest that there is a place for this operation in the management of severe bipolar affective disorders which are not responding to any other treatment, although decisive recovery occurs less often than with unipolar depression.

The relationship between neurotransmitter metabolite concentrations and measurements of ventricular size on CAT scans and pneumoencephalographs was investigated in 15 patients with severe affective disorder. An association was identified between reduced levels of plasma free tryptophan and ventricular enlargement, and also between raised ventricular CSF levels of 5 HIAA and ventricular enlargement.

This report describes a young woman with unexplained chronic hypoventilation that was greatly exacerbated during sleep. Treatment with nocturnal O2 during a 2-yr period was associated with stable cardiovascular function but severe morning headaches and lethargy, presumably related to nightly bouts of hypercapnia and acidosis during sleep. A subsequent 2-yr period in which ventilation was assisted during sleep by means of a rocking bed, but supplementary O2 was not used, was associated with disappearance of the headaches and improved psychosocial function, but with the insidious development of signs of pulmonary hypertension and right ventricular hypertrophy. This patient's clinical course demonstrates the separate adverse effects of intermittent hypoxemia and hypercapnia and emphasizes the importance of preventing both hypoxemia and hypercapnia during sleep.

Sleep deprivation appears to increase the severity of obstructive sleep apnea, and inadequate activation of the genioglossus muscle may play an important role in the pathogenesis of obstructive sleep apnea. Therefore, we investigated the effect of sleep deprivation on genioglossal electromyographic (EMG) activity. Eleven men were studied during room air breathing and CO2 rebreathing before sleep deprivation (control), after 1 night of sleep deprivation, and the day after sleep recovery. We measured inspired minute ventilation, tidal volume, respiratory frequency, and peak integrated inspiratory genioglossal EMG activity. After sleep deprivation, no significant changes in inspiratory minute ventilation or tidal volume occurred during room air breathing or CO2 rebreathing, but the breathing frequency during CO2 rebreathing increased significantly after sleep deprivation. Genioglossal EMG activity was diminished during CO2 rebreathing after sleep deprivation, but this was significant only in subjects 30 yr of age and older. The fall in EMG activity was independent of changes in tidal volume. All variables returned towards control levels after sleep recovery. We conclude that sleep deprivation selectively decreases genioglossal EMG activity during CO2 rebreathing in awake older subjects. This influence of sleep deprivation may play a role in the pathogenesis or severity of obstructive sleep apnea.

The aim of this study was to investigate whether psychological abnormalities were present in patients still complaining of low back pain after more than one operation. It was found that these patients were more psychiatrically disturbed and socially disabled than a matched control group whose back pain responded to one operation. These results suggest that patients requiring assessment for a possible second laminectomy should also be psychiatrically examined.

Upper airway obstruction during sleep occurs more commonly in men than in women and has been treated with progestational agents with some success. Alcohol ingestion exacerbates sleep apnea, and recent studies have established that alcohol depresses the respiratory motor activity to upper airway muscles more than that to the diaphragm, a response pattern that favors upper airway obstruction during inspiration. To investigate the possibility that progesterone provides some protection from this action of alcohol, we studied the responses of phrenic and hypoglossal nerve activities to alcohol infusion in decerebrate cats pretreated with medroxyprogesterone acetate (MPA) or with control injections. The results indicate that pretreatment with MPA reduces the alcohol-induced mismatching of hypoglossal and phrenic activities. This action of MPA may contribute to its effectiveness in the treatment of some patients with inspiratory obstruction during sleep.

When lung inflation is temporarily withheld in paralyzed, ventilated cats with intact vagi, the activities of inspiratory motor nerves are greater during the second cycle without inflation than during the first. This response is not easily attributable to increasing drive from chemoreceptors as it is abolished by vagotomy. We examined the hypothesis that the increasing inspiratory activity is the result of decreasing inhibitory feedback from pulmonary stretch receptors (PSRs). Decerebrate, paralyzed cats were ventilated by a servo-respirator in accordance with their own phrenic nerve activity. Afferent activities from individual PSRs were recorded from a few cut fibers of one vagus nerve; the vagi were otherwise intact. When lung inflation was withheld, phrenic and hypoglossal nerve activities and the durations of inspiration and expiration all increased and were significantly greater during the second cycle without inflation than during the first. The frequency of PSR discharge was also greater during the second cycle and thus did not account for the responses recorded from the motor nerves. We conclude that the latter responses probably reflect neural processes within the brain stem, involving a persistent inhibitory influence from lung inflation, which outlasts the inflation itself.

With its head steadied within a form-fitting mask, a macaque was first taught to signal when it detected the application of 0.2-ms electrical pulses at 50 Hz through electrodes chronically implanted within its striate cortex. Stimuli were then applied via a movable microelectrode and the threshold for the animal’s detection determined at intervals of 50-250 micrometers. With permanently implanted 130- 200-micrometers diameter electrodes such thresholds range between 50 and 250 microamperes (and are highly stable), whereas with the microelectrodes sites were encountered, estimated to be primarily within cortical layers V-VI, where the monkey could reliably detect as little as 2-4 microamperes. The threshold at most sites within striate cortex with the microelectrode, however, was 15-25 microamperes. Background unit activity recorded with the microelectrode varied greatly in different laminae and survived the microstimulation, but has so far provided no clear basis for predicting threshold. It is tentatively hypothesized that the relatively rare points where the threshold is as much as 10 times less than that in the surround arise because the giant, solitary cells of Meynert provide the exclusively effective output for the behavioral response. This hypothesis would also explain the singular uniformity of sensation (a "phosphene") evoked in human subjects by such stimuli, and the equivalence of all such stimuli in striate cortex found for the macaque.

The firing frequency of a population of 213 units in striate and circumstriate cortex of the moderately restrained rabbit was studied under the influences of alternating 1-min periods of darkness versus steady, diffuse, featureless illumination. The intent was to determine whether luxotonic responses, so prominent in striate cortex of primates, are indeed absent in rabbits. Such was the case, there being only transient occurrences in three units where the continuing rate of discharge in darkness was double that in the light. There were, however, much more modest differences in rate of continuing discharge in light versus darkness, and for 46% of the units discharging greater than 1/s this difference exceeded 10% and/or 1/s. The rate of discharge in any case did not provide a reliable index as to the characteristics of a unit's receptive field in response to patterned visual stimuli. The nature and function of luxotonic activity in primates still not being understood, it cannot be decided whether its absence in rabbits represents a true qualitative or merely a quantitative difference between species.

The records of 377 patients with head injuries admitted to the South East Thames Regional Neurosurgical Unit in the two years following the introduction of the EMI scanner (computerized tomography) were examined. Each patient was assessed on the reason for transfer, the necessity for transfer, the safety of transfer and whether immediate access to a scanner would have altered management. The results show that the majority of patients were referred because of a possible intracranial haematoma. Thirty per cent of the patients required operation, in 6 per cent transfer was unnecessary and 10 per cent arrived with inadequate resuscitation. It is suggested that with a wider deployment of head-dedicated scanners to some accident centres, the number of patients with head injuries at present being transferred to special units for assessment would be reduced substantially, with improvement of patient care.

Tryptophan and 5-hydroxyindoleacetic acid (precursor and metabolite respectively of 5-hydroxytryptamine) were determined in ventricular CSF of psychiatric patients undergoing stereotactic subcaudate tractotomy. Tyrosine and homovanillic acid (precursor and metabolite respectively of dopamine) were also determined. Results suggest an association between affective state and the above precursor amino acids with lower concentrations in primary depression and higher ones when anxiety or agitation predominate. This leads to lower 5-hydroxyindoleacetic acid concentrations in depression and higher concentrations in anxiety and agitation.

1. Single units in striate cortex were studied in alert macaques while they viewed a ganzfeld. Of the 385 well-isolated units studied for 10 min to 2 h, 24% gave "luxotonic" responses, i.e., their rate of discharge for 1 min or more in diffuse, featureless, wideangle illumination (20-450 cd/m2) was at least double that during a comparable period in darkness, or vice versa, and not attributable to eye movements of blinking. Those discharging faster in the light, "photergic" units, outnumber those responding to darkness, "scotergic" units 1 by 4:1. 2. In the lateral geniculate nucleus, on the other hand, among 46 units studied, 28% were luxotonic, but scotergic units were the more common. Both types were present in both magno- and parvocellular laminae. 3. For striate cortex two-thirds of the luxotonic units were binocular. Some showed highly similar response for either eye alone, and essentially no summation binocularly; others had grossly differing responses from each eye, and complex binocular interaction. 4. Many units of all types at striate cortex showed significant modulation of their activity consequent to saccadic eye movements made in darkness, whereas comparable modulation was not observed at the lateral geniculate nucleus. 5. On the basis of these and other findings it is concluded that luxotonic cortical activity is prominent probably only in alert primates, and that this is a consequence of the fact that all retinal ganglion cells in primates synapse in the lateral geniculate nucleus (Ref. 9). Possible functions range from mere trophic input to providing a veridical image or a scaling factor for maintenance of perceptual constancy in the face of varying levels of general illumination.

We have examined the lungs of eleven species of newborn mammals by quantitative morphometric techniques and related the findings to body weight (BW) and O(2) consumption (Vo2 is found to be proportional to BW(0.88); this exponent is significantly greater than the value of about 0.73, repeatedly found for adult mammals. Lung volume (LV) is essentially proportional to BW, and neonatal alveolar size - as indicated by mean chord length - is nearly constant among species and independent of BW. Thus the respiratory surface area (SA) is not proportional to Vo2, as in adult mammals, but to Vo2(1.23). Neonates of small species have lower SA/Vo2 ratios than adult mammals, possibly owing to constraints of surface forces on alveolar size. Newborn members of larger species have SA/Vo2 values in excess of the adult range. Published data on human newborn lung dimensions suggest that the human infant may have an unexpectedly low SA/Vo2 value in relation to BW. Whether this is a valid finding, or whether it derives from methodological differences between studies cannot be ascertained from the available data.

Electromyographic patterns of the diaphragm and a posterior cricoarytenoid (PCA) muscle were evaluated in anesthetized rabbits with and without reversible blockade of pulmonary stretch receptors by inhalation of 200 ppm sulfur dioxide (SO2). Inspiratory activity of both muscles was increased by hypercapnia and by isocapnic hypoxia, with or without receptor blockade. Expiratory diaphragmatic activity was diminished by these stimuli and was likewise not qualitatively affected by SO2 exposure. Expiratory PCA activity was increased by hypercapnia and hypoxia prior to SO2 exposure, but decreased by these stimuli during stretch receptor blockade. These results are consistent with the previous finding that vagal afferents facilitate expiratory PCA activity, thus maintaining a patent laryngeal airway, even in the face of increased carotid chemoreceptor afferents, which inhibit expiratory activity of the PCA muscle. The results further indicate that some or all of the afferents responsible for this effect are from pulmonary stretch receptors.

We asked to what extent pulmonary innervation influences the postnatal development of the lung. To this end we performed cervical vagotomy and sympathectomy either on the right or on the left side in young rats and rabbits and rats after weaning. One to four weeks later we examined the lungs of the denervated side, the contralateral intact side of the same animal, and sham-operated controls. Dry lung weight, lung volume and the size of subpleural alveoli were not different among the three groups. Lung mechanical properties (static and dynamic lung compliances, lung resistance, frequency dependence of compliance), measured in rabbits, were also not different among groups of lungs, suggesting that neither central nor peripheral airways were markedly affected by the denervation. The breathing pattern, measured in the rats after weaning, was characterized by a larger tidal volume in the denervated animals than in controls, as expected after the partial pulmonary afferent denervation. The absence of major structural and functional changes in the lungs of these animals suggests that an increase in the mechanical stretch to the lung above that normally occurring during resting breathing does not influence the lung structure. We conclude that pulmonary innervation does not play an important role in the postnatal development of the lung.

In decerebrate, paralyzed cats, ventilated by a servo-respirator in accordance with phrenic nerve activity, we examined the influence of lung volume on the activities of the phrenic, hypoglossal and mylohyoid nerves. When lung inflation was briefly withheld, the durations of inspiration (TI) and expiration (TE) and the activities of all three nerves increased. The relative increase in hypoglossal activity greatly exceeded that of phrenic activity and was apparent earlier in the course of inspiration. This hypoglossal response was enhanced by hypercapnia and isocapnic hypoxia. The responses of mylohyoid activity were quite variable: withholding lung inflation augmented inspiratory activity in some cats, but expiratory discharge in others. Sustained increases in end-expiratory lung volume were induced by application of 3-4 cm H2O of positive end-expiratory pressure (PEEP). Steady-state PEEP did not influence nerve activities or the breathing pattern. Bilateral vagotomy increased TI, TE, and the activities of all three nerves. No response to withoholding lung inflation could be discerned after vagal section. The results provide further definition of the influence of vagally mediated, lung volume dependent reflexes on the control of upper airway muscles. These reflexes are well suited to relieve or prevent upper airway obstruction.

Neuronal responses to continuous, diffuse white light or darkness were studied in cortical visual areas 17, 18, 19 and Clare-Bishop of the unanesthetized cat. In contrast to squirrel monkeys and macaques in which about 40 or 25% of the units in striate cortex are luxotonic (response to continuous light or darkness sustained > 2.0 min), all of the visual areas in the cat had fewer than 4.0% of the units exhibiting such luxotonic activity. The functional basis of this difference may be related to differences between the two species in the quantitative balance of antagonistic receptive field properties.

Efferent activities on the phrenic and recurrent laryngeal (RLN) nerves were monitored during eupnea, apneusis, and gasping in decerebrate, paralyzed, and ventilated cats before and after spinal cord transection at the first cervical level. The vagi were sectioned caudal to the RLN being studied and at the midcervical level contralaterally. Before spinal transection, the onset of RLN inspiratory activity preceded that of the phrenic nerve during eupnea and apneusis; in gasping, phrenic activity began before the RLN. These results were the same in normocapnia, hypercapnia, and hypoxia. After spinal transection, no phasic phrenic activity was observed at normoxia or hyperoxia, whereas the RLN exhibited discharge patterns similar to those before transection. Upon end-tidal O2 partial pressure diminutions below 50 Torr, one or more "burst" of phrenic activity were recorded. These bursts were not synchronized with the phasic RLN discharge. It is concluded that automatic ventilatory activity may be generated by inherent brain stem mechanisms. These results further imply the processes underlying gasping neurogenesis may differ fundamentally from those of eupnea or apneusis.

The steady-state ventilatory and end-tidal PCO2 (PETCO2) responses to low-level CO2 inhalation have been studied in four awake cats. Four cats anesthetized with Dial-urethane were also studied before and after vagal section or blockade. Awake cats breathed gas mixtures with FICO2 equal to 0.0015 (control), 0.01 and 0.03 in oxygen or 0.0015, 0.01 and 0.02 in air, while anesthetized cats inhaled FICO2 of 0.0000 (control), 0.005 and 0.01 in oxygen. In order to obtain accurate, unbiased determinations of the respiratory system responses to small increases of FICO2 above control values, we used a protocol in which control conditions preceded and followed each CO2 test. The pairwise response for each variable was calculated from the mean of the two 'bracketing' control values. We found that low-level CO2 inhalation in the cat resulted in consistent and significant increases in PETCO2 (82 of 86 trials) and VT (76 of 86 trials) but inconsistent changes in TTOT. We conclude that low-level CO2 inhalation in the cat results in hypercapnia detectable by a replicated, unbiased experimental design.

Our purpose was to determine the afferent pathways underlying reflexes by which changes in upper airway pressure induced alterations in hypoglossal and phrenic nerve activities. An isolated upper airway was produced in decerebrate, vagotomized, paralyzed and ventilated cats. Efferent activities of the phrenic and hypoglossal nerves were monitored. Hypoglossal activity significantly increased following pressure changes in the upper airway of -4 to -21 cm H2O; phrenic discharge declined in most trials. Similar alterations of neural activities were induced by positive pressures though changes of +14 to +21 cm H2O were required for significant responses. These changes in hypoglossal and phrenic activities were greatly reduced following bilateral sectionings of the superior laryngeal nerves but were augmented after the pharyngeal branches of the glossopharyngeal nerves were sectioned. Additional bilateral destruction of the trigeminal nerves almost entirely eliminated responses to pressure changes. We conclude that upper airway receptors may serve to maintain patency of the upper airways. These receptors may play a crucial role in promoting release from upper airway obstructions, especially in sleep.

The growth and internal partitioning of the lung are increased in young animals exposed to high altitude. Neither the mechanism whereby O2 lack brings this about nor the anatomic site of action of hypoxia is known. To test whether extrapulmonary tissue hypoxia can stimulate lung growth in the prescence of normal alveolar PO2, pulmonary morphology was studied quantitatively in young rats exposed to 208 ppm carbon monoxide for 29-30 days. The results show no effect of this exposure on lung dimensions and thus argue against extrapulmonary tissue hypoxia as the relevant stimulus in the increased lung growth that occurs at high altitude.