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Background-Orthostatic symptoms and syncope are common, even in apparently healthy subjects. In patients with severe autonomic dysfunction, water drinking elicits an acute pressor response and improves orthostatic hypotension. We tested the hypothesis that water drinking also improves orthostatic tolerance in healthy subjects. Methods and Results-In a randomized, controlled, crossover fashion, 13 healthy subjects (9 men, 4 women, 31Ϯ2 years) ingested 500 mL and 50 mL of mineral water 15 minutes before head-up tilt on two separate days. Finger blood pressure, brachial blood pressure, heart rate, thoracic impedance, and blood flow velocity in the brachial artery and the middle cerebral artery were measured. Orthostatic tolerance was determined as the time to presyncope during a combined protocol of 20 minutes of 60°head-up tilt alone, followed by additional increasing steps of lower body negative pressure (Ϫ20, Ϫ40, and Ϫ60 mm Hg for 10 minutes each or until presyncope). Drinking 500 mL of water improved orthostatic tolerance by 5Ϯ1 minute (range, Ϫ1 to ϩ11 minutes, PϽ0.001). After drinking 500 mL of water, supine mean blood pressure increased slightly (PϽ0.01) as the result of increased peripheral resistance (PϽ0.01). It also blunted both the increase in heart rate and the decrease in stroke volume with head-up tilt. Cerebral blood flow regulation improved after water drinking. Conclusions-Water drinking elicits an acute hemodynamic response and changes in cerebrovascular regulation in healthy subjects. These effects are associated with a marked improvement in orthostatic tolerance.

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Objective-To determine whether in patients presenting with posturally related syncope administration of salt increases plasma volume and improves orthostatic tolerance. Patients with poor tolerance of orthostatic stress tend to have lower than average plasma and blood volumes. Design-A double blind placebo controlled study in 20 patients and an open study in 11 of the effects of giving 120 mmoUday of sodium chloride. Patients-31 patients presenting with episodes of syncope who had no apparent cardiac or neurological disease. Plasma volume was determined by Evans blue dye dilution, orthostatic tolerance by time to presyncope in a test of combined headup tilt and lower body suction, and baroreceptor sensitivity by the effect of neck-suction on pulse interval. Results-8 weeks after treatment, 15 (70%) of the 21 patients given salt and three (30%) of the placebo group showed increases in plasma and blood volumes and in orthostatic tolerance, and decreases in baroreceptor sensitivity. Improvement was related to initial salt excretion in that patients who responded to salt had a daily excretion below 170 mmol. The patients in the placebo group who improved also showed increases in salt excretion. Conclusions-In patients with unexplained syncope who had a relatively low salt intake administration of salt increased plasma volume and orthostatic tolerance, and in the absence of contraindications, salt is suggested as a first line of treatment.

A combined tilt-table and lower body suction chamber to provide a progressive test of orthostatic tolerance which avoided the use of drugs and had a defined end point even in most asymptomatic subjects has been constructed and evaluated. An air-tight cover, sealed to a tilt-table and to the subject at the level of the iliac crest, was used to study the responses to: head-up tilting for 20 min, then tilting plus lower body suction at -20 and -40 mmHg for 10 min at each. Blood pressure, heart rate and cardiac output were measured noninvasively and orthostatic tolerance was assessed as the time to imminent onset of syncope. All subjects tolerated tilt alone but 84% developed signs and symptoms of presyncope during the suction. Younger women had a lower orthostatic tolerance than other groups. Values of the variables measured during tilting alone did not correlate with the measured orthostatic tolerance, but during the suction subjects who developed early syncope showed larger decreases in cardiac output and smaller maximal heart rates than the more resistant subjects. The test is repeatable and is likely to be of value in the assessment of orthostatic tolerance in patients and for evaluating the effects of various interventions.

IntroductionHigh altitude places are amongst the most inhospitable on earth. According to WHO [70] in 1966 there were approximately 140 million people living at altitudes over 2,500 m and there are several areas of permanent habitation at over 4,000 m. These are in three main regions of the world: the Andes of South America, the highlands of Eastern Africa, and the Himalayas of South-Central Asia. This review is concerned with the effects of the altitude on visitors and the ways by which the permanent high altitude dwellers have adapted to their environment.The two main challenges to life at high altitude come from hypobaric hypoxia and the low ambient temperatures. Temperature decreases about 1°C for each 150 m elevation, so that at 4,500 m temperature is roughly 30°C lower than at sea level. Barometric pressure falls progressively with increasing altitude. Up to about 2,500 m there are few if any effects of hypoxia. Above 3,000 m some effects of hypoxia are likely to be experienced and above 4,000 m adverse effects would be experienced by most unacclimatized visitors. However, many people live and work at altitude with no apparent adverse effects. One such example is Cerro de Pasco a busy mining town of Roger Hainsworth Mark J. Drinkhill Maria Rivera-ChiraThe autonomic nervous system at high altitude j Abstract The effects of hypobaric hypoxia in visitors depend not only on the actual elevation but also on the rate of ascent. Sympathetic activity increases and there are increases in blood pressure and heart rate. Pulmonary vasoconstriction leads to pulmonary hypertension, particularly during exercise. The sympathetic excitation results from hypoxia, partly through chemoreceptor reflexes and partly through altered baroreceptor function. High pulmonary arterial pressures may also cause reflex systemic vasoconstriction. Most permanent high altitude dwellers show excellent adaptation although there are differences between populations in the extent of the ventilatory drive and the erythropoiesis. Some altitude dwellers, particularly Andeans, may develop chronic mountain sickness, the most prominent characteristic of which being excessive polycythaemia. Excessive hypoxia due to peripheral chemoreceptor dysfunction has been suggested as a cause. The hyperviscous blood leads to pulmonary hypertension, symptoms of cerebral hypoperfusion, and eventually right heart failure and death. j

Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor-vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied 11 healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of −40 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus-response curves were defined during (i) air breathing, (ii) hypoxia (12% O 2 in N 2 ), and (iii) hypercapnia (5% CO 2 in 95% O 2 ). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to 'set point'). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post-stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or 'set point' for the control of RR interval, heart rate or mean arterial pressure. Peak sensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from −2.5 ± 0.4 units to −1.4 ± 0.1 units (P < 0.05) and this was restored in the post-stimulus period to −2.6 ± 0.5 units. There was no effect on 'set point'. Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post-stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post-control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, 'set point' was significantly increased from 74.7 ± 4 to 87.0 ± 2 mmHg (P < 0.02). This was not completely restored to pre-stimulus control levels in the post-stimulus control period (82.2 ± 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex 'set point'. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemorecepto...