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Biomedical subjects

P Sleight

Publications and source records attributed to P Sleight.

At least 253 records · Page 14Linked to original sources
PubMed1975

The action of clonidine on the baroreflex control of heart rate in conscious animals and man, and on single aortic baroreceptor discharge in the rabbit.

Changes in mean arterial pressure (M.A.P.) have been produced in conscious rabbits by inflation of balloon cuffs previously implanted round the inferior vena cave and aorta; Sigmoid stimulus/response curves (M.A.P./Heart Period, H.P.) were constructed. Clonidine caused a striking dose dependent increase in gain of the reflex arc in both normal rabbits and rabbits with renal hypertension. The largest effect was upon vagal motorneurones but a similar but smaller effect was present in vagotomised animals. Similar changes in the baro-reflex arc were produced by injection of very much smaller doses of clonidine into the lateral cerebral ventricle. Recordings made from single aortic baroreceptor fibres in anaesthetised rabbits showed again a dose dependeent sensitisation. These results suggest that the bradycardia caused by clonidine is largely mediated via an action in the brain on the baroreflex arc, with an additional action on the baroreceptors themselves. Preliminary results in normal man show a similar increase in the gain of this reflex after intravenous clonidine (150 mug).

Animals↗
PubMed1974

The effects of raising alveolar PCO2 and ventilation separately and together on the sensitivity and setting of the baroreceptor cardiodepressor reflex in man.

1. The effects of changes in ventilation and/or alveolar P(CO2) on the baroreflex control of heart rate have been studied in seven experiments on six young men and women who had been trained to control tidal volume and respiratory frequency at various levels independent of alveolar P(CO2), during hyperoxia.2. Intravenous phenylephrine provoked transient rises of directly measured arterial pressure during which individual systolic pressures (P) were linearly related to the following pulse interval (I). Baroreflex sensitivity was expressed as the slope of the regression of I on P, and reflex setting (I(ref)) as I at a single reference arterial pressure (= mean P for the experiment).3. Voluntary control of breathing had little effect on heart rate and arterial pressure (baroreflex setting), but diminished reflex sensitivity.4. Hypercapnia regularly caused tachycardia at the reference pressure (i.e. baroreflex setting lowered). The response was completely or partly reproduced by change of P(A, CO2) at constant ventilation in four subjects but not in two others; in them change of ventilation at constant P(A, CO2) completely mimicked the effect of free-breathing hypercapnia.5. Values of baroreflex sensitivity were relatively scattered. Hypercapnia caused a fall in baroreflex sensitivity in three subjects whether ventilation was fixed or free to rise. After separating the effect of voluntarily controlling ventilation, ventilation per se was without effect on reflex sensitivity.6. It is concluded that hypercapnia and hyperpnoea have separate effects on the baroreflex, the relative magnitudes of which differ from one subject to another. Baroreflex setting and sensitivity vary independently in response to change of ventilation and of P(A, CO2).

Blood Pressure↗
PubMed1973

Direct arterial pressure and electrocardiogram during motor car driving.

Direct arterial pressure and electrocardiogram have been measured continuously over a period of 24 hours in 15 patients. Observations have been made on the behaviour of these variables during 30 separate episodes of motor car driving. The patients were divided into three groups: (1) five normotensive subjects, (2) five patients with essential hypertension who were not receiving therapy, and (3) five patients with angina pectoris who were either normotensive or hypertensive.In all but one subject, apart from variable changes in heart rate, no significant arrhythmias or S-T segment changes were observed in the electrocardiogram. The arterial pressure remained remarkably stable throughout the driving period in all three groups and there was no significant difference between the levels of blood pressure at the beginning and end of a journey. There were short periods of raised arterial pressure during driving related to such episodes as overtaking, but these quickly returned to baseline levels. Two patients experienced anginal pain during driving.It is concluded that motor car driving does not have such a pronounced effect on the blood pressure as might have been thought.

Adult↗
PubMed1972

Continuous recording of direct arterial pressure and electrocardiogram in unrestricted man.

A system has been devised which records direct arterial pressure, electrocardiogram, and other variables in man with no restriction of activity. The advantage of this system is that the record is on magnetic tape, and it is possible to replay the records at various speeds to analyse each beat or to produce an entire 24-hour record on a few feet of paper. A marker allows the timing of relevant events. Initial experience with this procedure indicates that is is safe and reliable.

Adult↗
PubMed1972

Nocturnal angina.

Explore the source record for details and available documents.

Angina Pectoris↗
PubMed1972

The reflex cardiovascular depression caused by occlusion of the coronary sinus in the dog.

1. Brief occlusions of the outflow from the cannulated coronary sinus in the open chest anaesthetized dog caused a rise in coronary venous pressure, bradycardia, and systemic hypotension.2. The bradycardia and hypotension were directly proportional to the peak systolic coronary venous pressures above a threshold value of about 50 mm Hg.3. The bradycardia, but not the systemic hypotension, was abolished by intravenous atropine. Both responses were abolished by cutting the cervical vagi, and reversibly abolished by cooling them to less than 7 degrees C.4. During occlusions, there was inhibition of activity in single and small multi-fibre preparations of sympathetic efferent nerves in the ansae subclaviae and the cervical sympathetic.5. On the right side, nearly all afferent fibres ran in the recurrent cardiac nerve. There was no concentration of afferents in one cardiac nerve on the left side.6. It was concluded that the cardiovascular depression was reflex, and was caused by the stimulation of nerves or nerve endings in the ventricles of the heart.

Action Potentials↗