The purpose of this study was to relate baroreflex sensitivity to age and arterial pressure in 61 male and 20 female untreated subjects, aged 19-66 years, whose mean arterial pressures ranged from 70 to 150 mm Hg. In this selected group of subjects there was no correlation between age and arterial pressure. The index of sensitivity used was the increase in pulse interval which occurs reflexly in response to a rise in systolic pressure induced by the intravenous injection of phenylephrine and is measured as the increase in pulse interval in milliseconds per mm Hg rise in systolic blood pressure. It ranged from 1.9 to 48.9 msec/mm Hg. Increasing age and arterial pressure act independently to reduce baroreflex sensitivity. Eight subjects who had normal blood pressure at the time of testing but whose pressure had been elevated in the past, had reflex sensitivities significantly less than expected in persons of the same age and mean arterial pressure. The heart rate in these subjects was not significantly different from that in the controls; the heart rate of the 12 hypertensive subjects aged under 40 years was significantly faster than that of age-matched normotensive subjects but not that of older hypertensive subjects.

The reflex bradycardia produced by a transient phenylephrine-induced rise of arterial pressure was investigated in man during rest and supine exercise, before and after autonomic blockade of the heart. Reflex bradycardia diminished proportionally to the tachycardia of exercise. Propranolol slowed the heart at rest and during exercise, but increased the reflex response only at rest, having no effect during exercise. Atropine, or atropine with propranolol, blocked the reflex during rest and exercise. The tachycardia following hypotension induced by amyl nitrite was similarly affected by the two drugs. Tachycardia induced by standing up and by isoprenaline also diminished the reflex bradycardia. It is concluded that reflex heart rate changes following sudden changes of arterial pressure are predominantly parasympathetic, and diminish during exercise in parallel with the decrease of parasympathetic tone. The reflex response is determined partly by the interaction of parasympathetic and sympathetic impulses at the sinoatrial node, shown by the effects of peripheral sympathetic stimulation and blockade at rest. During exercise central depression of the reflex may also occur. KEY WORDSphenylephrine atropine propranolol amyl nitrite posture parasympathetic nerves sympathetic nerves

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The use of arterial pulse wave velocity (PWV) as a continuous measure of blood pressure changes is outlined. Theoretical considerations indicate that changes in PWV reflect changes in blood pressure, and an experiment was carried out to assess this relationship. PWV along an arm artery was monitored in 26 subjects at a time when the arterial distending pressure of the limb was altered over a wide range by means of externally applied positive and negative pressures. The results show that changes in PWV reliably follow changes in blood pressure. This method can be considered suitable for studies requiring changes rather than absolute values of blood pressure.

An adaptation of the technique for measuring pulse wave velocity is described in which the interval between the R wave of the ECG and the radial pressure pulse is monitored. The resulting transit time (TT) is suitable for use as an indirect measure of blood pressure change. The reliability of the measure was assessed in 5 subjects who volunteered for arterial cannulation on 2 occasions. Simultaneous recordings of intra‐arterial pressure and TT were taken during a variety of maneouvres, including mental arithmetic, isometric exercise, and amyl nitrite inhalation. The dependence of changes in TT on arterial pressure was confirmed for all procedures except amyl nitrite inhalation. Linear correlations between TT and mean arterial pressure were high, varying between −.913 and −.98. The regression coefficients were reproducible and similar in all individuals. The reasons for the anomalous amyl nitrite response are discussed, together with the limits of application of the measure.

1. Serial studies of the baroreflex control of heart rate (baroreflex sensitivity) were made in thirty-two patients on long-term haemodialysis by relating the reflex slowing of the heart to the arterial pressure rise produced by repeated sudden injections of phenylephrine.2. Baroreflex sensitivity was less in the older patients and in those with higher pressures. The response was about 50% of that found previously for other subjects of comparable ages and arterial pressures without renal failure.3. Haemodialysis improved reflex sensitivity over the long term, but did not have any consistent immediate effect. 4. Patients who had malignant hypertension in the past had lower reflex sensitivities than others (with similar ages and pressures at the time of study) whose blood pressures had never been raised, but there were individual exceptions. 5. Reflex sensitivity changed very little with different blood pressures in any one subject.6. Three patients in whom hypertension was thought to have preceded renal failure had reflex sensitivities similar to eleven others in whom the hypertension was secondary to renal disease. 7. Reflex sensitivity was no different in three patients whose blood pressure could be controlled only by bilateral nephrectomy from that in others in whom the pressure could be controlled by salt restriction.8. Reflex sensitivity was slightly reduced in two patients studied in the diuretic phase of acute renal failure; it was markedly reduced in a third who was also pregnant.

Coagulase-negative staphylococci cause about 5% of native-valve endocarditis. Staphylococcus lugdunensis, a recently-described species of coagulase-negative staphylococci, has been reported to cause destructive native-valve endocarditis with a high mortality. We report four consecutive cases of definite Staphylococcus lugdunensis native-valve endocarditis by the Duke criteria over a 4-year period. All patients required urgent aortic valve replacement 1-5 days after admission, and recovered. An intriguing, aspect in the presentation of these patients was a history of vasectomy and inguinal skin breaks in the immediate period preceding the occurrence of endocarditis.

It is unclear whether the stiffened arterial tree in systolic hypertension is the cause or the effect of the disease. In this study, brachial and radial arterial pulses were sensed by external Pixie transducers and measurements of pulse wave velocity converted to volume distensibility using the Bramwell-Hill equation. Blood pressure was controlled as a variable by repeating the measurements at a variety of transmural arterial pressures. This was accomplished by encasing the forearm in a rigid plastic cylinder within which pressures were varied. Twenty-nine patients with systolic hypertension were compared with 22 age-matched control subjects. At ambient pressures the volume distensibility of patients was lower than that of control subjects (0.10 versus 0.18% delta volume/mm Hg, p less than 0.001) but there was no difference in volume distensibility between the two groups at any comparable transmural pressure. Nineteen patients were treated for 1 month with a thiazide diuretic agent and the studies were then repeated. Systolic and diastolic blood pressure decreased significantly and volume distensibility increased (0.10 to 0.15% delta volume/mm Hg, p less than 0.001) at ambient pressures. But at comparable transmural pressures, volume distensibility was unchanged. It is concluded that, in the forearm, increased arterial stiffness is the result and not the cause of systolic hypertension, but these data cannot exclude increased aortic stiffness as a significant factor. Thiazide diuretic drugs increase forearm arterial compliance by lowering blood pressure without a demonstrable drug effect on this arterial wall.