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Biomedical subjects

C von Euler

Publications and source records attributed to C von Euler.

At least 37 records · Page 2Linked to original sources
PubMed1982

Bilateral reflex effects on phrenic nerve activity in response to single-shock vagal stimulation.

The bilateral reflex actions of vagus nerve afferent signals on phrenic efferent activity have been tested by unilateral graded single shock electrical stimulation. An early excitation (latency 3-5 msec) was more prominent in the phrenic nerve contralateral to the stimulated vagus. Spinal cord hemisection at C3 eliminated both contralateral and ipsilateral responses: thus, both were mediated via descending tracts in the contralateral cord. A bilaterally symmetrical early inhibition (latency 8-12 msec) followed the early excitation. The electrical thresholds for evoking the early responses and the temperature for blocking these responses during graded vagal cooling were closely similar to the threshold and blocking temperature for pulmonary stretch receptor afferents. Higher stimulus strengths evoked a strong, bilaterally similar, late excitation (latency 12-20 msec) followed by a late inhibition. At very high stimulus strengths a third excitation (latency 25-30 msec) could appear. Sometimes these responses were followed by lowered phrenic activity for the remainder of inspiration. Single shock stimulation of the intact vagus nerve or of the peripheral end of the cut recurrent laryngeal nerve provoked, by the contraction of laryngeal muscles, a strong, short latency (12 msec) inhibition of phrenic activity mediated by superior laryngeal nerve afferents. The implications of these results with respect to the reflex pathways of the different responses and their possible integration in the central respiratory control mechanisms are discussed.

Afferent Pathways↗
PubMed1982

Intra-operative variations in carotid artery blood flow and cardiac output: the effects of changes in blood volume and carbon dioxide during surgery under neurolept anesthesia.

Seven patients were operated on for stenosis of the internal carotid artery (ICA) with endarterectomy under neurolept anesthesia. The ICA blood flow was found to be unchanged after reconstruction following an operative blood loss of one fifth of the patient's blood volume despite variations in cardiac output. The relationship between carbon dioxide tension and cerebral blood flow remained unchanged during hypovolemia. It is concluded that the autoregulation of the cerebral blood flow is maintained under neurolept anesthesia.

Aged↗
PubMed1981

Central haemodynamics during halothane and enflurane anaesthesia in vascular surgery.

Central haemodynamics were studied before and during reconstructive vascular surgery in 18 patients receiving halothane or enflurane anaesthesia (nine patients in each group). In both groups cardiac output (CO), stroke volume (SV), oxygen uptake (VO2) and arterial blood pressure fell significantly after induction of anaesthesia, whereas the arterio-venous oxygen difference (AVD) and the total peripheral resistance (TPR) remained unchanged. In spite of an average intraoperative blood loss of 600 ml, which had not been substituted for, surgery brought about an increase in CO, SV and VO2, while the AVD and TPR remained unchanged. Following transfusion of 900 ml of blood, CO and SV showed a further significant increase in both groups, whereas VO2 was unchanged and the AVD and TPR fell significantly. The pulmonary capillary venous pressure (PPCV) was stable during induction of anaesthesia and surgery but increased after blood transfusion. The changes in SV and PPCV were analyzed in relation to the concept of ventricular function curves. It is concluded that there were no fundamental differences in central haemodynamics between halothane and enflurane anaesthesia either before or during surgery. In both groups the changes in CO and SV were due mainly to a reduced demand of oxygen transport and expected changes in sympatho-adrenergic tone rather than to myocardial depression.

Aged↗
PubMed1981

Characteristics and rate of occurrence of spontaneous and provoked augmented breaths.

The tidal volume and corresponding efferent phrenic activity of spontaneously occurring and provoked "augmented" breaths, AB, and the subsequent post-augmented breaths were studied in cats anesthetized with pentobarbitone during hypercapnia and hypoxia. The augmentation phase (phase II) begins at, or close to, the crest of what appears as a "normal" inspiration (phase I). The amplitude and duration of phase II remained fairly constant whereas the amplitude and the duration of phase I changed with chemical drive just as in control breaths. The smaller amplitude and shorter duration of post-augmented breaths as compared to control breaths seems to be due to both a lower-than-normal inspiratory "off-switch" threshold following the AB and an increased rate of rise of inspiratory activity. With increasing hypercapnia and hypoxia both the time interval between AB and the refractory period following an AB during which a new AB cannot be provoked were reduced. Following bilateral vagotomy AB was temporarily abolished but reappeared after 1-2 h. The relatively low rates of occurrence after vagotomy still showed the same type of dependence on chemical stimuli. The refractory period was not abolished although usually decreased by gallamine paralysis or high thoracic spinalization.

Animals↗
PubMed1981

Positive feedback facilitation of external intercostal and phrenic inspiratory activity by pulmonary stretch receptors.

Both in lightly pentobarbitone anesthetized and decerebrate cats increments in lung volume (V) during inspiration caused facilitation of inspiratory activity both in phrenic (Phr) and external intercostal (EI) motoneurons. This effect had low volume threshold, well below eupnoeic tidal volumes. It was readily reduced or abolished by small additional doses of pentobarbitone. This facilitatory effect appeared with considerably greater magnitude in EI than in Phr. The response magnitude was linearly related to the corresponding increments in V but not to increments in airflow (V). Sustained elevation of V at zero V caused sustained facilitation of EI and Phr. This positive feedback facilitation which was similarly obtained in spontaneously breathing and paralysed cats occurred continuously with great regularity in every breath. It was abolished by bilateral vagotomy but could then be elicited by electrical stimulation of the central end of the vagus nerve at the same threshold strengths required to elicit a just detectable shortening of inspiratory duration. The results indicate that the slowly adapting pulmonary stretch receptors are responsible for this positive feedback facilitation prior to the negative feedback effect on the inspiratory 'off-switch' elicited by the same receptors. Clear distinctions are described between the reflex characteristics of this 'low-threshold' volume dependent facilitatory reflex and the 'high-threshold' transient excitatory reflex effects provoked by large and rapid inflations.

Animals↗
PubMed1981

The contribution of sensory inputs to the pattern generation of breathing.

Current concepts of the basic neural control system and its modulation by afferent inputs are reviewed. It is emphasized that, in analogy with locomotion, the central pattern generator (CPG) for automatic metabolic respiration does not depend on any afferent feedback from receptors sensitive to the movements of the "pump," or the streams of pumped air, for its production of a rhythmic motor output provides the CPG receives some "drive" inputs above threshold and adequate bias. The operation for a variety of reflexes and feedback loops is of fundamental importance, however, for adapting the breathing pattern to the varying requirements for gas exchange to the many behavioural, nonmetabolic demands on the breathing apparatus which are competing with its primary metabolic control functions. The presentation is focussed also on available evidence that the respiratory CPG exerts powerful modulations on the transmission in these reflex pathways controlling the pattern of breathing and adjusting it to the various metabolic and behavioural demands. Mechanisms for "gating," "phasic gain changes," and "phase-dependent reflex reversal" are exemplified.

Adult↗
PubMed1981

Leg haemodynamics during different forms of anaesthesia in patients undergoing reconstructive vascular surgery.

In the present study the effects of three different anaesthetics (halothane, n = 9, enflurane, n = 9, and neurolept, n = 11) on leg circulation were studied during vascular reconstruction with a reversed femoropopliteal saphenous vein bypass graft. Leg vascular resistance showed significant differences between the three anaesthetic groups. Thus, during the pretransfusion period, leg resistance in the neurolept group was significantly higher than in the halothane and enflurane groups, although the blood volume did not differ significantly between the groups. Though leg resistance after blood transfusion decreased significantly more in the neurolept group compared with the two other groups, the resistance after transfusion was still significantly higher in the neurolept group. Inducing pharmacological vasodilatation caused significant increases in common femoral arterial and bypass blood flows in all groups, but the increases were significantly more pronounced in the neurolept group. It is concluded that leg haemodynamics are influenced in different ways according to the anaesthetic agents used. This, in turn, might contribute to a better understanding and a more correct interpretation of the results of intraoperative flow and pressure measurements, and, consequently, to improvement of the reconstructive procedure.

Aged↗
PubMed1980

Ventilatory studies in two older infants with prolonged apnea.

Two infants, both born before term, were found apneic, cyanotic and limp at home when they were 9 weeks and 2 weeks old, respectively. Their respiration was monitored in the hospital and found to be remarkably periodic during sleep, and was in one case accompanied by pronounced bradycardia. The periodic breathing and apnea seemed to be caused by a decreased oxygen tension which can induce an instability of the central respiratory control mechanisms.

Apnea↗
PubMed1979

Experimentally induced Cheyne-Stokes breathing.

We have studied the propensity for periodic breathing to occur in cats anaesthetized with pentobarbitone breathing either spontaneously or with the aid of a 'servo-respirator' governed continuously by the efferent phrenic nerve activity. Sustained periodic breathing could be induced increasing 'controller gain', either by increasing the gain of the respirator, or by lung deflation, which reflexly increased controller responses to both hypoxia and hypercapnia. Periodic breathing was potentiated both by hypoxia and by diminishing the central (CO2, H+)-drive by focal cooling at the ventral surface of the medulla, two procedures which increase the relative influence of hypoxic drive. Less hypoxia was needed to produce periodic breathing at high rather than low controller gains. Reducing controller gain to zero by constant artificial respiration always abolished periodic breathing. Periodic breathing was also eradicated when the relative importance of CO2 drive was enhanced by breathing the cats with CO2-enriched gas mixtures or with 100% O2. The results are consistent with theoretical predictions for the occurrence of oscillations in the mechanisms for the chemical control of breathing and indicate that increasing controller gas can produce periodic breathing. The results further emphasize the importance of the (CO2, H+)-drive in preserving ventilatory stability.

Animals↗
PubMed1979

Graded changes in central chemoceptor input by local temperature changes on the ventral surface of medulla.

1. In cats under pentobarbitone anaesthesia the effects of focal temperature changes of the ;chemoceptive' areas on the ventral surface of medulla, described by Loeschcke and his associates, were studied with respect to tidal volume, V(T), tidal variation in efferent phrenic activity, Phr(T), and respiratory rate. The cats were either paralysed and ventilated at various constant P(A,CO2) and P(a,O2) levels, or breathing spontaneously.2. It was confirmed that focal bilateral cooling of the intermediate, ;I((S))', areas caused rapid depression of respiration even at constant artificial ventilation. In normocapnic and normoxic conditions apnoea usually ensued at brain surface temperatures of 20-22 degrees C.3. The effects were graded along continuous temperature-response curves with enhancements of ventilation above and depression below normal body temperature.4. The strongest effects on V(T) and Phr(T) were obtained from the I((S)) areas with no or only small effects on inspiratory or expiratory timing in the vagotomized animal. The Hering-Breuer inflation reflex and its effects on timing and amplitudes were not affected by cooling this area.5. Focal cooling of the caudal or the rostral ;chemoceptive' areas, ;C((L))' and ;R((M))' areas, caused smaller effects on V(T) and Phr(T) but produced significant effects on respiratory rate even after vagotomy.6. The effects of focal cooling of these areas could be mimicked by topical application of procaine solution which has been shown not to penetrate deeper than 100 mum from the surface.7. Moderate focal cooling of area I((S)) to temperatures above 28-30 degrees C caused a parallel shift in the CO(2)-response (V(T), Phr(T)) curves to the right with little change in slope. The P(CO2) thresholds for apnoea were correspondingly raised. These focal temperature effects could be compensated by changes in P(CO2) with, on the average, 2.7 torr/ degrees C. Focal temperatures below 28 degrees C usually caused some decrease in slope of the CO(2)-response curves in addition to further shifts.8. Added hypoxic stimulus or electrical stimulation of the carotid sinus nerves caused an almost parallel increase of Phr(T) at all P(CO2) levels and all focal temperatures suggesting an additive type of interaction between the input from the peripheral chemoreceptors and that from the central (CO(2), H(+)) sensing structures whether the latter was altered by changing P(CO2) or by focal temperature changes on the I((S)) areas.9. In contrast to these effects of hypoxia and stimulation of the carotid sinus nerves the reflex increase of inspiratory activity caused by lung deflation or by electrical stimulation of the glossopharyngeal nerve distal to the carotid sinus nerves was CO(2) dependent. These reflex effects decreased with focal cooling of the I((S)) areas as with hypocapnia, suggesting a mainly multiplicative or ;gain-changing' type of interaction with the central chemoceptive drive.10. The close similarities in effect of focal cooling and of hypocapnia on the different respiratory parameters even during constant artificial ventilation indicate that focal temperature changes of the I((S)) areas intervene effectively with the normal ventilatory response to CO(2) without changing the chemical or physical environment of those neural structures in the brain stem which set respiratory pattern.

Animals↗
PubMed1977

The functional organization of the respiratory phase-switching mechanisms.

Recent results support the view that inspiration gets inhibited and terminated when a centrally generated inspiratory activity (CIA) combined with afferent activity from pulmonary stretch receptors has grown to a critical threshold. CO2 acts both to increase the rate of rise of CIA and to raise the 'off-switch' threshold. Body temperature affects only the growth rate of CIA but not the threshold. Once switched off, inspiration is kept inhibited for the subsequent expiration with a decaying power that can be strongly modulated by different reflexes. The rostral pontine "pneumotaxic" structures provide the 'off-switch' mechanism with a threshold lowering input but do not seem to form part of the oscillating network. Thus, it appears that the basic network for respiratory rhythmicity depends on excitation and inhibition between the two basic neural mechanisms: the CIA-generator, and the 'off-switch mechanism. The necessary non-linearities are provided for by the threshold function of the 'off-switch' and the decay of the inhibition, which keep inspiration turned off during expiration.

Afferent Pathways↗
PubMed1976

Effects of lesions in the parabrachial nucleus on the mechanisms for central and reflex termination of inspiration in the cat.

The effects of PCO2 and body temperature on the time course and peak amplitude of the central inspiratory activity (CIA) and the inspiratory "off-switch" threshold was studied in apneustic and non-apneustic cats. Apneusis resulted from lesions of the inspiratory inhibiting structures of the medial parabrachial nucleus (NPBM) and by interrupting vagal volume feedback. The cats were paralyzed and ventilated either proportionally to their phrenic output or at predetermined rate and volume. The dependence of the rate of rise and maximal amplitude of phrenic activity on PCO2 and body temperature were comparable in apneustic and non-lesioned animals. The Hering-Breuer volume threshold for inspiratory termination was increased following the rostral pontine lesions. Both hyperthermia and hypercapnia caused augmentation of the absolute rate of rise of inspiratory activity but hypercapnia, in contrast to hyperthermia, caused virtually no change in the fractional increment per unit time. With hypercapnia the inspiratory "off-switch" threshold was raised in the apneustic animals in intact ones, whereas hyperthermia did not seem to influence this threshold. In apneustic conditions expiratory duration remained constant, independent of the large variations in the inspiratory durations. Our results suggest that the NPBM merely provides an excitatory, threshold-lowering input to the inspiratory "off-switch" mechanism.

Animals↗