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R F Rea

Publications and source records attributed to R F Rea.

43 records · Page 3Linked to original sources
PubMed1989

Enhancement of sympathetic nerve activity by single premature ventricular beats in humans.

This is the first systematic study of the effects of ventricular premature beats on sympathetic nerve activity in humans. Microneurographic techniques were used to record efferent sympathetic activity from the peroneal nerve, and an intracardiac electrode catheter was used to introduce ventricular premature beats after every 6 to 10 sinus heartbeats. Studies were performed in eight patients, aged 22 to 74 years (mean 57), undergoing cardiac electrophysiologic studies. Three patients did not have apparent heart disease and five had coronary artery disease. During sinus rhythm, 19 to 93% (mean 42%) of heartbeats were followed by a pulse-synchronous burst of sympathetic activity. Provoked ventricular premature beats had obvious effects on this activity. Premature beats with coupling intervals less than 80% of sinus cycle length were consistently followed by a burst of sympathetic activity, and this activity was greater in amplitude, duration and area (all p less than 0.05) than were burst of such activity during sinus rhythm. The magnitude of this burst of activity increased as the coupling interval of the ventricular premature beat decreased (p less than 0.0001). In contrast, postextrasystolic beats were followed by nearly complete neural silence. These effects were seen in all patients regardless of baseline burst incidence and the presence or absence of heart disease. Total nerve activity per 10 heartbeats was 6,520 +/- 770 U during ventricular extrastimulation and 5,720 +/- 440 U during normal sinus rhythm (difference not significant). It is concluded that single ventricular premature beats provoke fluxes of muscle sympathetic nerve activity in humans, comprising surges of sympathetic activity larger than those occurring during sinus rhythm, followed by neural silence.

Adult↗
PubMed1989

Carotid baroreflex resetting during drug-induced arterial pressure changes in humans.

We studied human baroreflex resetting during 25 min of drug-induced arterial pressure changes in 10 healthy volunteers. Average (+/- SE) base-line systolic pressure of 113 +/- 4 fell to 102 +/- 3 during nitroprusside infusions and rose to 135 +/- 6 mmHg during phenylephrine infusions. Average base-line R-R intervals of 932 +/- 37 shortened to 820 +/- 39 during nitroprusside infusions and lengthened to 1,251 +/- 61 ms during phenylephrine infusions. Carotid baroreceptor-cardiac reflex responses were evaluated with a complex series of neck chamber pressure changes, and R-R intervals were plotted as functions of carotid distending pressure. Baroreceptor-cardiac reflex relations shifted on both R-R interval and arterial pressure axes during drug infusions, but there was no significant change of the maximum slope or range of R-R interval responses. The position of baseline R-R intervals on the reflex relation (operational point) changed significantly. Resting R-R intervals were closer to threshold during pressure reductions and closer to saturation for baroreceptor-cardiac responses during pressure elevations. These results document short-term partial resetting of human baroreceptor-cardiac reflex responses as early as 25 min after the onset of arterial pressure changes.

Adult↗
PubMed1989

Sympathetic nerve activity in arm and leg muscles during lower body negative pressure in humans.

Nonhypotensive lower body negative pressure (LBNP) is reported to decrease forearm but not calf blood flow as measured by strain-gauge plethysmography. This suggests that unloading of cardiopulmonary receptors increases sympathetic outflow to arm but not to leg. To test this hypothesis we measured muscle sympathetic nerve activity (MSA) in the arm (radial nerve) and leg (peroneal nerve) simultaneously during LBNP. In eight healthy subjects, we measured heart rate, blood pressure, and radial and peroneal MSA during LBNP at 10 and 20 mmHg. There was no difference between radial and peroneal MSA at rest, and there were successive parallel increases of MSA in both nerves during LBNP at 10 and 20 mmHg. These data indicate that there are nearly identical increases of sympathetic outflow to the arm and leg during mild to moderate degrees of orthostatic stress.

Adult↗
PubMed1988

Baroreflex modulation of sympathetic activity and sympathetic neurotransmitters in humans.

We raised and lowered arterial pressures with stepwise intravenous infusions of phenylephrine and nitroprusside in ten healthy young men and measured changes of R-R intervals, post-ganglionic peroneal nerve muscle sympathetic activity, and antecubital vein plasma noradrenaline and neuropeptide Y concentrations. Respiratory peak-valley R-R interval changes declined with arterial pressure reductions, but did not rise with pressure elevations. Sympathetic activity was modulated by respiration over the entire range of pressures and, at each pressure, was more prominent in expiration than inspiration. Levels of muscle sympathetic nerve activity were low during supine rest, were suppressed almost completely during small increases of pressure, and were increased proportionally during pressure reductions. Over a range of average diastolic pressures from 69 to 89 mmHg, antecubital vein plasma noradrenaline levels were related linearly (r = 0.86, P = 0.0001) to muscle sympathetic nerve activity. Neuropeptide Y levels increased proportionally with muscle sympathetic nerve activity during pressure reductions, but did not decline during pressure elevations. Our results suggest that in man, muscle sympathetic outflow is modulated finely by small changes of baroreceptor input, and that during pharmacologically induced changes of arterial pressure, changes of antecubital vein plasma noradrenaline concentrations provide excellent estimates of changes of sympathetic nerve traffic to skeletal muscle.

Adult↗
PubMed1987

Carotid baroreceptor-muscle sympathetic relation in humans.

The purpose of this study was to define the relation between carotid distending pressure and muscle sympathetic activity in humans. Carotid baroreceptors of nine healthy subjects were compressed or stretched for 5 s with graded neck pressure or suction (+40 to -65 mmHg), and muscle sympathetic nerve activity was recorded. The results delineate several features of human baroreflex function. First, the carotid-muscle sympathetic relation is well described by an inverse sigmoid function. Second, a linear relation exists between carotid distending pressure and sympathetic outflow over a range of approximately 25 mmHg. Third, sympathetic responses to changes of carotid pressures are asymmetric; increases of sympathetic activity during carotid compression are much greater than reductions of sympathetic activity during carotid stretch. Fourth, at rest, normal subjects operate near the threshold level for sympathetic excitation. Thus the carotid-muscle sympathetic baroreflex is poised to oppose reductions more effectively than elevations of arterial pressure, and the range of pressures over which the reflex is active is wider than thought hitherto.

Adult↗