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Reflex sympathetic dystrophy, or as it is now known, complex regional pain syndrome, Type 1, is an unusual complication of a variety of injuries whose development should be suspected in the presence of disproportionate pain coupled with autonomic disturbance. Early recognition and treatment with multimodality therapy offer a high probability of recovery.

Results of safety investigations conducted as an integral part of the development of a multichannel electrotactile speech processor (Tickle Talker) are reported. Electrical parameters of the stimulus waveform, design of the electrode handset and cabling, and the electrical circuitry of the speech processor/stimulator and programming interface have been analyzed for potential risks. Constant current biphasic square pulses delivered to electrodes positioned on the skin surface over the digital nerve bundles were chosen to optimize the safety, comfort, and function of the electrotactile stimulus. The device was battery-powered, and the user circuit was isolated from earth-referenced sources. Each electrode was isolated by capacitive coupling, preventing DC leakage of current to the user circuit. Studies of finger temperature showed slight cooling of the skin on the fingers of both stimulated and unstimulated hands for individual subjects following electrotactile stimulation through the Tickle Talker. Subsequent analysis of finger and hand vascular circulation in five subjects showed slight reductions in hand blood flow in some individuals. The results did not demonstrate a significant mean decrease in hand or finger blood flow following electrotactile stimulation. No evidence of sympathetic involvement was found, nor were any changes in vascular structure of the hand such as those associated with Raynaud's disease found. Evidence suggests that the decrease in temperature found in the initial study may be due to a change in the ratio of blood flow between arteriovenous anastomoses and nutritive capillary beds. Studies of: 1) changes in mean threshold and comfortable pulse widths over time; and, 2) changes in tactual sensitivity as measured by hot/cold, sharp/dull, and two-point difference limen discrimination, did not detect any systematic change in peripheral nervous system function following electrotactile stimulation. Analysis of electroencephalogram (EEG) recordings taken during electrotactile stimulation, and after relatively long periods of experience with the device did not show any pathological changes which might be associated with epileptic foci. In summary, no contraindications to long-term use of the Tickle Talker were detected in the studies performed.

Much has been published on the surgical treatment of leg ischaemia but relatively little is known about the incidence of claudication and the fate of the majority of patients presenting with chronic leg ischaemia who never come to surgery. A review of the available literature suggests the following conclusions: (1) about 1.5% of men under 49 and 5% of men over 50 will develop symptoms of intermittent claudication. The incidence of asymptomatic arterial disease is much higher; (2) the incidence of claudication in women is only slightly less, but the local disease follows a more benign course; (3) compared to the general population of comparable age the mortality of men presenting with chronic leg ischaemia is two to three times higher after 5 years; (4) about 50% of deaths will be due to myocardial ischaemia, 15% to stroke and 10% to vascular disease in the abdomen. In only 25% will the principal cause of death be unconnected with the circulation; (5) there is virtually no reliable information available at the moment on the incidence of non-fatal myocardial infarction or stroke in these patients.

Coronary artery disease (CAD) is a major cause of morbidity and mortality after elective surgical repair of abdominal aortic aneurysm (AAA). The aim of this study was to determine the relationship between the extent of CAD observed in coronary angiograms (more than 50% stenosis) and the frequency of postoperative myocardial ischemic complications in a consecutive series of 84 patients who underwent elective AAA repair. Ninety-four percent of the patients with clinical evidence of CAD had significant disease as observed in coronary angiograms and eight patients had left main CAD. Seventy-two patients underwent AAA repair with a mortality rate of 1.4%; five patients had preliminary myocardial revascularization, and AAA surgery was not recommended for four patients because of severe cardiac disease. Postoperative myocardial ischemic complications occurred in 13.4% of the patients who had undergone surgery--almost exclusively in patients with clinical evidence of CAD. Both myocardial ischemia and preoperative intervention were more frequent in patients with double- or triple-vessel disease than in patients with less extensive disease. Patients with symptoms and with double- or triple-vessel CAD have a high risk of developing myocardial ischemia after AAA surgery. Preliminary myocardial revascularization may be beneficial in this group of patients.

Conscious rabbits with previously implanted perivascular balloons for altering blood pressure were studied before and 6 days after: (i) sham-operation (n = 6); (ii) section of carotid sinus nerves alone (n = 7); (iii) section of aortic nerves alone (n = 5); and (iv) combined sino-aortic denervation (n = 5). Sigmoid mean arterial pressure (MAP)-heart period (HP) baroreflex curves were derived and were characterized by: (i) the HP range (HPR) between upper and lower plateau levels; (ii) the median blood pressure (BP50); and (iii) the average gain (G). Resting MAP and HP and the 3 baroreflex parameters were not altered significantly 6 days after sham-operation. After section of the carotid sinus nerves alone resting MAP and BP50 rose by 18 +/- 2.6 mm Hg, resting HP fell by 31 +/- 4.2 msec, whilst HPR and G fell to about 45% and 20 % respectively of initial preoperative control. After cutting the aortic nerves alone there was a similar fall in resting HP as after carotid denervation. However, the rises in resting MAP and BP50 were only about half of those observed after carotid denervation (P < 0.05) and the changes in HPR and G to 65% and 58% of control respectively were also less marked (P ¿ 0.01). The aortic baroreceptor zone also exerted smaller effects on the sympathetic efferent component of the baroreflex HP response. Despite the different effects exerted by each zone on the reflex parameters there was little difference in threshold pressure for producing cardiac slowing. After combined sino-aortic denervation there was a similar rise in resting MAP (19 mm Hg) as after carotid sinus denervation alone, but there was more marked tachycardia, with a fall in resting HP of 82 msec (P < 0.001) and both resting and baroreflex-mediated vagal tones were completely abolished. The small residual pressure-determined HP changes of about 8 msec were entirely sympathetic and probably mediated through cardiopulmonary baroreceptors.

The circulatory effects of Valsalva-like manoeuvers were studied before and during i.v. infusions of either ketamine, Althesin and thiopentone given in doses that produced similar levels of light anesthesia. The Valsalva-like manoeuvers were of 30 s duration and consisted of applying Valsalva pressures (VP) from 2.5 to 20 mm Hg to the animal's respiratory valve and to a cuff placed around its thorax and abdomen. In the conscious rabbit the major reflex responses to the Valsalva-like manoeuver were VP-related rises in total peripheral resistance (TPR) and in heart rate which were mainly mediated through intrathoracic baroreceptors and were completely abolished by sino-aortic denervation. Ketamine depressed the Valsalva-TPR response by about 30-40% but Althesin and thiopentone were without effect. Ketamine and thiopentone produced marked depression of the Valsalva-heart rate reflex, but Althesin had relatively little effect. We concluded that ketamine produces greater impairment of blood pressure homeostasis mediated through constrictor and heart rate reflexes evoked through arterial and cardiopulmonary baroreceptors than the other two anesthetics.

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.

Graded 30 s manoeuvers were used to elicit cardiovascular responses in conscious instrumented rabbits by applying pressures from 2.5 to 20 mm Hg (Valsalva Pressure, VP) to the animal's respiratory valve and to a sphygmomanometer cuff wrapped around its thorax and abdomen. In normal rabbits the Valsalva-like manoeuvers elicited VP-related rises in total peripheral resistance (TPR), heart rate and in right atrial pressure (RAP), VP-related fall in cardiac output (CO) and no change in mean arterial pressure (MAP). The rises in TPR and heart rate and the maintenance of MAP were reflexly mediated, whilst the CO and RAP changes were largely a mechanical consequence of the manoeuver as assessed from the responses after autonomic effector blockade. In rabbits with selective section of the carotid sinus nerves the reflex responses were little altered from normal, but after selective section of the aortic nerves there was significant attenuation of the TPR response, indicating that the input from the aortic baroreceptors was more important for this response than that from the carotid receptors. After combined denervation of the aortic and carotid baroreceptor zones (but with the vagi intact) the reflex TPR and heart rate changes were completely abolished, with the responses the same as after autonomic effector block. The results indicate that the arterial baroreceptor zones make a major contribution to the reflex cardiovascular responses to the Valsalva manoeuver in the rabbit and that any reflex effects of cardiopulmonary baroreceptor stimulation are only expressed in the presence of an intact arterial baroreceptor input.

Eleven normal volunteers were given an acute and two chronic doses of desipramine (DMI). The plasma norepinephrine (NE), 3-methoxy-4-hydroxyphenylglycol (MHPG), and dihydroxyphenylglycol (DHPG) concentrations were measured before and during drug administration. DMI reduced plasma concentrations of MHPG by 13% and DHPG by 17%. After two weeks of drug administration, the MHPG/NE ratio was reduced, and there was a significant negative correlation with the concurrent drug concentration. These results suggest that DMI: (1) reduces the turnover of NE; and (2) diminishes the oxidative deamination of NE. In addition, the drug concentration response relationship indicates that the effects of uptake inhibition may not be maximal until concentrations in the apparent therapeutic range are achieved.

Plasma noradrenaline measurements are a fallible guide to sympathetic nervous tone, being dependent on noradrenaline plasma clearance. We have developed radiotracer techniques, based on measurement of the rate of spillover of noradrenaline to plasma, to simultaneously estimate total, and organ-specific, sympathetic nervous activity in humans. In 27 unmedicated subjects without renal or liver disease, or cardiac failure, regional noradrenaline spillover rates were as follows: lungs 138 +/- 36 ng/min (mean +/- SE) (33% of total noradrenaline spillover), kidneys 77 +/- 10 ng/min (22% of total), skeletal muscle 64 +/- 11 ng/min (20%), hepatomesenteric 29 +/- 9 ng/min (9%), skin 18 +/- 4 ng/min (5%), and heart 11 +/- 4 ng/min (3%). Organ-specific noradrenaline spillover measurements are well suited to the elucidation of sympathetic nervous system pathophysiology in human diseases. Since the sympathetic nervous system outflow to individual organs is not activated or suppressed uniformly in different disease states, biochemical measures of "overall sympathetic nervous activity" are insufficiently specific for this purpose.