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Biomedical subjects

S Jennett

Publications and source records attributed to S Jennett.

At least 19 recordsLinked to original sources

Changes in ventilation related to changes in electromyograph activity during repetitive bouts of isometric exercise in simulated sailing.

This study examined the control of ventilation during repetitive bouts of isometric exercise in simulated sailing. Eight male sailors completed four successive 3-min bouts of similar isometric effort on a dinghy simulator; bouts were separated by 15-s rest intervals. Quadriceps muscle integrated electromyograph activity (iEMG) was recorded during each bout and expressed as a percentage of activity during maximal voluntary contraction (%iEMGmax). From the first to the fourth bout, the 3-min mean averages for ventilation and for %iEMGmax increased from 19.8 (SEM 1.1) to 37.5 (SEM 3.0) l.min-1 and from 31 (SEM 4) to 39 (SEM 4)% respectively; also, ventilation and %iEMGmax over each minute throughout the four bouts were significantly correlated (r = 0.85; P < 0.05). Progressive hyperventilation reduced the mean end-tidal partial pressure of carbon dioxide from 5.0 (SEM 0.3) kPa during bout 1 to 4.3 (SEM 0.4) kPa during bout 4 [37.7 (SEM 2.0) to 32.4 (SEM 3.0) mmHg]. From the first to the fourth bout the end-of-bout blood lactate concentration did not increase significantly although the concentration from the third bout onwards was significantly greater than at rest. The results suggested that the development of muscle fatigue, which was enhanced by the insufficiency of recovery during the 15-s intervals and mirrored in the progressive increase in iEMG, was linked with stimuli causing progressive hyperventilation. Though these changes in ventilation and iEMG could not be associated with changes in blood lactate concentration, they could both have been related to accumulating metabolites within the muscles themselves.

Adult↗

Sudden large and periodic changes in heart rate in healthy young men after short periods of exercise.

The instantaneous heart rate and respiratory pattern were recorded immediately after brief periods of exercise in 41 healthy male students. Recordings were taken with the subjects both supine and standing. More than half of these subjects showed oscillatory heart changes when recovering supine but not when standing. During these oscillations the heart rate slowed suddenly by more than 30 beats/min; the oscillations had a period of 4 to 8 seconds, and they continued for half to two minutes. The P waves of the electrocardiogram were decreased during the slowing, consistent with increased vagal activity. When these oscillations occurred they each followed the start of an inspiration with the same latency as in respiratory sinus arrhythmia; unlike respiratory sinus arrhythmia, however, they did not occur after every inspiration but varied from 1:1 to 1:3 oscillations:breaths. They were not usually stopped by breath holding but were reduced or abolished by procedures which reduced venous return. This pattern of oscillations--"vagushalt"--seems to be different from respiratory sinus arrhythmias, and central venous pressure may contribute to the phenomenon. Although it is not widely recognised, vagushalt is probably very common and possibly its occurrence may change in disease.

Adolescent↗

Pial arterial response to systemic hypoxia in anaesthetised cats.

Pial arterial responses to reduction in arterial oxygen tension were studied in anaesthetised cats. In 12 cats under chloralose, dilatation occurred in vessels of all sizes between 20 and 200 micrometers, at variable levels of PaO2, and to a very variable extent. At PaO2 25-35 mm Hg, dilatation ranged from negligible to 175% above initial diameter. The variations in response were largely dependent on associated blood pressure (BP) changes. Increase in BP counteracted dilatation; dilatation was greater during hypoxia when the BP change was prevented. At the induction of hypoxia, the first response of the vessels was a constriction, which occurred about 5 s after the chemoreflex increase in BP. Dilatation was delayed a further 30-90 s, and this delay was similar when BP was prevented from rising. Vessels of all sizes responded in the appropriate manner when only BP was transiently changed within the autoregulatory range. In 3 cats in which similar procedures were compared under pentobarbitone anaesthesia, there were smaller and less consistent changes in responses to BP changes alone and to hypoxia and its associated BP changes. The findings were compatible with a local effect of lowered PO2. From the time course of the changes there was no indication of a chemoreflex component in the responses of these vessels at the induction of hypoxia.

Animals↗

Rapid cerebral vasodilatation in brief hypoxia in anaesthetized animals.

In anaesthetized dogs, cats and rabbits, intracranial pressure was measured continuously during brief or transient hypoxia, induced by (a) lowering inspired O2 to 9--10% for 2--3 min, or (b) giving 2--3 breaths of nitrogen. In almost all instances there was an increase in i.c.p. which started in less than 20 s; this occurred with either spontaneous or controlled ventilation, and whether or not there was also a rise in arterial blood pressure; the time course was similar to that of the arterial chemoreceptor reflex responses of ventilation and blood pressure. Division bilaterally of the sinus and vagus nerves in six cats showed that the intracranial pressure response was not dependent on these chemoreceptor afferent pathways. The results suggest a rapid vasodilatation starting at a time when cerebral arterial oxygen tension is unlikely to be below 7 kPa (50 mmHg). The mechanism remains unexplained.

Anesthesia↗

The human ventilatory response to stimulation by transient hypoxia.

1. The detailed pattern of transient changes in breathing pattern has been studied following a brief hypoxic stimulus (three breaths of nitrogen) in nine healthy subjects. All showed an increase in ventilation of which the magnitude and relative contributions of volume and frequency varied between subjects. 2. Ventilation, tidal volume, inspiratory, expiratory and total breath time were recorded or derived breath-by-breath; for each of these variables, several test sequences were time-averaged at half-second intervals for each individual; similarly, time-averages were obtained for percentage changes from base line over all nine subjects. 3. There ws an increase in inspiratory time accompanying the increasing tidal volume, in all but two subjects. This was statistically significant over all subjects, and in five individuals. Frequency changes were the resultant of alterations in the two phases; when total breath duration decreased it was always linked to a decrease in expiratory time. 4. Further analysis of the initial part of the response suggests that an increase of the duration of an inspiration may be the first change allowing an increase in tidal volume, before the 'drive' increases; this may be a dynamic feature of the control system whatever the nature and site of action of the stimulus.

Adolescent↗

Responses of systemic vascular smooth muscle to hypoxia.

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes. Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10(-6) noradrenaline (NA). Reduction of Po2 to less than 3KPa during NA constraction led to relaxation which was rapid and 90% complete in RPV, rapid and 60% in REA: the relaxation began when tissue Po2 was decreasing and was not lower than 5.5 K Pa. RCC responded slowly and only some strips relaxed. The rapidity and magnitude of relaxation for each type of vessel was comparable to that produced by removal of external calcium. Also for any one type of VSM the response to NA was abolished or diminished to a similar extent by preliminary exposure to hypoxia, or by preliminary removal of calcium. Preliminary hypoxia diminished 50 mmol.1(-1) K+ contractions as much as it diminished NA contractions. Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.

Animals↗

Brain death, apneic diffusion oxygenation, and organ transplantation.

This paper presents a simple method of maintaining good donor organ oxygenation during a prolonged test of apnea used to determine brain death prior to cadaver transplantation. Apneic diffusion oxygenation can maintain arterial pO2 above 200 torr for periods exceeding 15 minutes, thereby allowing a more definitive determination of brain death without concomitant tissue hypoxia and possible damage to donor organs.

Adult↗

Response of ventilation and of intracranial pressure during rebreathing of carbon dioxide in patients with acute brain damage.

A study of the ventilatory response to rising CO2 in 43 patients with acute brain damage, using a rebreathing method, has revealed several instances of abnormally low responsiveness. The increased responsiveness previously reported in chronic brain damage was not observed in these patients by this method. The incidence of a very low response to CO2 tended to be associated with hyperventilation and brain-stem damage, but the numbers were insufficient to define a statistical relationship. There was no association between responsiveness to CO2 and either bilateral forebrain damage or periodic breathing. Studies of changes in intracranial pressure with rising CO2 suggest that such a rebreathing test might provide a simple means of confirming the presence or absence of cerebrovascular response to changing CO2.

Brain Injuries↗