Biomedical subjects

Roger Hainsworth

Publications and source records attributed to Roger Hainsworth.

At least 19 recordsLinked to original sources

PubMed2006

Autonomic regulation during orthostatic stress in highlanders: comparison with sea-level residents.

This report is a comparison of orthostatic tolerance and autonomic function in three groups of high-altitude dwellers: Andeans with and without chronic mountain sickness (CMS) and healthy Ethiopians. Results are compared with those from healthy sea-level residents. The aim was to determine whether different high-altitude populations adapted differently to the prevailing hypobaric hypoxia. Orthostatic tolerance was assessed using a test involving head-up tilt (HUT) and graded lower body suction. This was performed at the subjects' resident altitude. Blood pressure (Portapres) and R-R interval (ECG) were recorded during the test, and spectral and cross-spectral analyses of heart period and systolic blood pressure time series were performed using data obtained both while supine and during HUT. The transfer function gain in the low-frequency range (LF, approximately 0.1 Hz) at the point of maximal coherence was used as a measure of cardiac baroreflex sensitivity (BRS). As previously reported, Peruvians displayed an unusually good orthostatic tolerance, while Ethiopians showed an orthostatic tolerance comparable to that of healthy sea-level residents. There were no significant differences between groups in the supine values of the spectral analysis results. Head-up tilt induced the expected changes in Ethiopians (an increase in the LF components and a decrease in the respiratory components) but not in Andeans. Cross-spectral analysis showed abnormal results from all groups of high-altitude dwellers. These results indicate that Ethiopians, but not Peruvians, behave similarly to sea-level residents in terms of orthostatic tolerance and autonomic responses to orthostatic stress, as assessed from spectral analyses, and this indicates good adaptation to their environment. However, in all the high-altitude groups the results of cross-spectral analysis were atypical, suggesting some degree of impairment in baroreflex function.

Acclimatization↗

PubMed2006

Carotid baroreflex regulation of vascular resistance in high-altitude Andean natives with and without chronic mountain sickness.

We investigated carotid baroreflex control of vascular resistance in two groups of high-altitude natives: healthy subjects (HA) and a group with chronic mountain sickness (CMS), a maladaptation condition characterized by high haematocrit values and symptoms attributable to chronic hypoxia. Eleven HA controls and 11 CMS patients underwent baroreflex testing, using the neck collar method in which the pressure distending the carotid baroreceptors was changed by applying pressures of -40 to +60 mmHg to the chamber. Responses of forearm vascular resistance were assessed from changes in the quotient of blood pressure divided by brachial artery blood velocity. Stimulus-response curves were defined at high altitude (4338 m) and within 1 day of descent to sea level. We applied a sigmoid function or third-order polynomial to the curves and determined the maximal slope (equivalent to peak gain) and the corresponding carotid pressure (equivalent to 'set point'). The results showed that the peak gains of the reflex were similar in both groups and at both locations. The 'set point' of the reflex, however, was significantly higher in the CMS patients compared to HA controls, indicating that the reflex operates over higher pressures in the patients (94.4 +/- 3.0 versus 79.6 +/- 4.1 mmHg; P < 0.01). This, however, was seen only when subjects were studied at altitude; after descent to sea level the curve reset to a lower pressure with no significant difference between HA and CMS subjects. These results indicate that carotid baroreceptor control of vascular resistance may be abnormal in CMS patients but that descent to sea level rapidly normalizes it. We speculate that this may be explained by CMS patients having greater vasoconstrictor activity at altitude owing to greater hypoxic stimulation of chemoreceptors.

Adult↗

PubMed2006

Cerebral vasodilatation to exogenous NO is a measure of fitness for life at altitude.

BACKGROUND AND PURPOSE: Andean highlanders, unlike Ethiopians, develop chronic mountain sickness (CMS), a maladaptation to their native land. Ambient hypoxia induces NO-mediated vasodilatation. Fitness for life at altitude might be revealed by cerebrovascular responses to NO. METHODS: Nine altitude-native men were examined at 3622 and 794 m in Ethiopia and compared with 9 altitude-native Andean men tested at 4338 and 150 m in Peru. We assessed CMS scores, hematocrits, end-tidal pressure of carbon dioxide (P(ET)co2), oxygen saturations, and cerebral blood flow velocity (CBV). We evaluated fitness for life at altitude from the cerebrovascular response to an exogenous NO donor. RESULTS: At high altitude, CMS scores and hematocrits were higher in Andeans, and they had lower oxygen saturations. Ethiopians had higher P(ET)co2 at all study sites. At low altitude, saturations were similar in both groups. Responsiveness of the cerebral circulation to NO was minimal in Ethiopians at low altitude, whereas Andeans had a large response. In contrast, at high altitude, Ethiopians showed large responses, and Peruvians had minimal responses. CONCLUSIONS: By our measure, high altitude-native Peruvians were well-adapted lowlanders, whereas Ethiopian highlanders were well adapted to altitude life. Environmental pressures were sufficient for human adaptation to chronic hypoxia in Africa but not South America. The mechanisms underlying these differences are unknown, although studies of neurovascular diseases suggest that this may be related to a NO receptor polymorphism.

Acclimatization↗

PubMed2006

Phase of the menstrual cycle does not affect orthostatic tolerance in healthy women.

Women of child-bearing age have a lower orthostatic tolerance (OT) than older women or men, and women suffering from frequent syncopal episodes often comment that their symptoms occur at certain times of the menstrual cycle. However, it is not known whether, in asymptomatic women, OT varies at different phases of the menstrual cycle. We studied 8 healthy asymptomatic women aged 26.8 +/- 3.4 years. We determined OT using a test of combined head-up tilting and lower body suction. We continuously monitored beat-to-beat blood pressure (Finapres), heart rate (ECG), and cerebral and forearm blood flow velocities (Doppler ultrasound). On each test day we assessed carotid baroreceptor sensitivity from suction/pressure applied to a neck chamber. We also determined estradiol and progesterone levels from a venous blood sample. Tests were performed in early follicular and late luteal phases, and during ovulation. Serum concentrations of estradiol (pmol x l(-1)) and progesterone (nmol x l(-1)) were in follicular phase 464.1 +/- 63 and 6.3 +/- 2.8; ovulation 941.6 +/- 298 and 5.8 +/- 1.2; luteal phase 698 +/- 188 and 32.3 +/- 9.6. Progesterone levels were significantly higher in the luteal phase (p < 0.001). OT was not different on any test day: follicular 31.9 +/- 1.6 min, ovulation 31.3 +/- 0.7 min; luteal 31.1 +/- 2.2 min. Supine and tilted heart rates and blood pressures, the maximum heart rate, and the cerebral autoregulatory and forearm vascular resistance responses to the orthostatic stress were similar during all studies. Both cardiac and vascular resistance carotid baroreceptor sensitivities were also similar on all test days. These results suggest that there is no difference in either OT or cardiovascular control at the tested phases of the menstrual cycle in healthy women.

Adult↗

PubMed2006

Water drinking improves orthostatic tolerance in patients with posturally related syncope.

Water drinking improves OT (orthostatic tolerance) in healthy volunteers; however, responses to water in patients with PRS (posturally related syncope) are unknown. Therefore the aim of the present study was to examine whether water would improve OT in patients with PRS. In a randomized controlled cross-over fashion, nine patients with PRS ingested 500 ml and 50 ml (control) of water 15 min before tilting on two separate days. OT was determined using a combined test of head-up tilting and lower body suction and expressed as the time required to induce presyncope. We measured blood pressure and heart rate (using Portapres) and middle cerebral artery velocity (using transcranial Doppler). SV (stroke volume) and TPR (total peripheral resistance) were calculated using the Modelflow method. OT was significantly (P<0.02) greater after drinking 500 ml of water than after 50 ml (25.4+/-1.5 compared with 19.8+/-2.3 min respectively). After ingestion of 500 ml of water, blood pressure during tilting was higher, the tiltinduced reduction in SV was smaller and the increase in TPR was greater (all P<0.05). The correlation coefficient of the relationship between cerebral blood flow velocity and pressure was lower after 500 ml of water (0.43+/-0.1 compared with 0.73+/-0.1; P<0.05), indicating better autoregulation. In conclusion, drinking 500 ml of water increased OT and improved cardiovascular and cerebrovascular control during orthostasis. Patients with PRS should be encouraged to drink water before situations likely to precipitate a syncopal attack.

Adult↗

PubMed2005

Increased postural sway in control subjects with poor orthostatic tolerance.

OBJECTIVES: This study sought to evaluate postural sway in control subjects with good and poor orthostatic tolerance (OT). BACKGROUND: Some asymptomatic volunteers, when subjected to a progressive orthostatic stress test, show early presyncope. We hypothesized that normal subjects with poor OT do not usually faint because they adopt a strategy of increased lower limb movement, which helps maintain venous return. METHODS: In 12 asymptomatic subjects with good OT and 11 with poor OT, assessed by the combined orthostatic stress of head-up tilting and lower body suction, we determined postural sway using a force platform after 1, 5, and 10 min of motionless standing. RESULTS: The subjects with poor tolerance had greater distances and velocities of sway in the anteroposterior direction but not the mediolateral direction. There was a significant negative correlation between postural sway and orthostatic tolerance. CONCLUSIONS: We have shown that in normal subjects with poor OT during a passive orthostatic stress test, their leg movements tend to be greater when standing. These movements are likely to enhance venous return and may at least partly explain why, despite their poor test results, they do not normally faint.

Adult↗

PubMed2005

R-R interval-blood pressure interaction in subjects with different tolerances to orthostatic stress.

In addition to the gain, the time delay in the input-output response in a feedback system is crucial for the maintenance of its stability. Patients with posturally related (vasovagal) syncope have inadequate control of blood pressure and one possible explanation for this could be prolonged latency of the baroreflex. We studied 14 patients with histories of syncope and poor orthostatic tolerance (assessed by a progressive orthostatic stress test) and 16 healthy controls. We performed spontaneous sequence analysis of the fluctuations of R-R period (ECG) and systolic arterial pressure (SAP, Finapres) recorded during a 20 min supine period and during 20 min 60 deg head-up tilt (HUT). The baroreflex latency was determined by identifying the lag between the changes in SAP and in R-R interval from which the highest correlation coefficient was obtained. During the supine period, 74% of sequences in control subjects and 54% in patients occurred with zero beats of delay (i.e. R-R interval changed within the same R-R interval). The remaining sequences occurred with delays of up to four beats. HUT shifted the baroreflex delay to be approximately one heartbeat slower and again patients showed more sequences with prolonged response. The delay in heartbeats was transformed into delay in time. In control subjects, 75% of baroreflex responses occurred within 1 s. In patients, 75% of baroreflex responses took more than 2 s to occur. The results showed that syncopal patients with poor orthostatic tolerance have increased baroreflex latency. This may lead to instability and inadequate blood pressure control and may predispose to vasovagal syncope.

Adolescent↗

PubMed2005

Prolonged latency in the baroreflex mediated vascular resistance response in subjects with postural related syncope.

In addition to the gain, the delay of the baroreflex response plays an important role in the maintenance of cardiovascular system stability. Additionally when postural changes induce sudden drops in blood pressure, a delayed response may fail to maintain sufficient cerebral perfusion pressure. We tested the hypothesis that the delay of the carotid baroreceptor reflex is impaired in subjects with poor orthostatic tolerance. An orthostatic test with 60 degrees head-up tilt, and progressive lower-body negative pressure was performed on 27 patients with histories of unexplained syncope and 13 control subjects. The test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Twelve patients had normal tolerance and thirteen patients had low tolerance. We measured beat-to-beat blood pressure (Finapres) and brachial artery blood flow velocity (Doppler ultrasonography). Before the test, we determined the response of forearm vascular resistance (mean arterial pressure/mean brachial artery velocity) to loading/unloading of carotid baroreceptors by the application of neck suction/pressure (-/+30 mmHg) to a chamber fitted overlying the carotid sinus. We measured the gain in the response (maximum percentage change from baseline value in vascular resistance divided by the neck collar pressure) and the latency in the response (delay of the maximum change in vascular resistance after neck-collar stimulation). Results are reported as means +/- SEM. In the three groups, there were no differences in the sensitivity of the vascular resistance response after baroreceptor loading/unloading. Following baroreceptor unloading, the latency of the response was 14.0+/-1.3 seconds in early fainters, 9.3+/-0.7 seconds in normal patients and 10.1+/-1.2 seconds in controls. The latency in blood pressure rise was 11.1+/-1.3 seconds in early fainters, 7.9+/-0.9 seconds in normal patients and 7.2+/-1.0 seconds in controls. The results following baroreceptor loading were more scattered. The early fainters still had a tendency to show prolonged latency. These results suggest that the delay in the baroreflex response plays an important role in postural related syncope.

Adult↗

PubMed2005

Effects of dietary salt loading on the responses of isolated rat mesenteric arteries to leptin.

BACKGROUND: Leptin induces relaxation of vascular smooth muscle through an endothelium-dependent release of nitric oxide (EDNO) and administration of a high-salt diet reduces the relaxation of vessels to EDNO. We would, therefore, predict that salt loading would reduce the leptin-induced dilatation. However, in salt-loaded animals the relaxation to acetylcholine is maintained through an endothelial-dependent hypopolarizing factor instead of EDNO. These experiments were, therefore, designed to examine whether in salt-loaded animals the response to leptin would be reduced or whether, as for acetylcholine, an alternative mechanism would be substituted. METHODS: Weanling rats were given diets containing either 0.4% (n = 10) or 8% (n = 9) sodium chloride for 4 weeks. They were then killed and a length of second order mesenteric artery was mounted in a perfusion myograph with diameter changes measured using a microscope-video tracking system. The vessels were preconstricted with norepinephrine and then the effects of graded concentrations of leptin were determined. RESULTS: In vessels from the low salt animals leptin caused a dose-dependent dilatation (maximum change 31.4% +/- 5.8% of the initial norepinephrine-induced constriction) but in the high salt animals the change was only 3.4% +/- 1.1%. The nitric oxide synthase blocker Nomega-nitro-L-arginine methyl ester (L-NAME) abolished the responses, although responses could still be obtained in vessels from both groups to the NO donor, sodium nitroprusside. CONCLUSIONS: These results indicate that salt loading to rats almost completely abolishes the vasodilatation to leptin. This implies endothelial disruption and, unlike the response to acetylcholine, no other vasodilator mechanism is implicated. This could provide a link between high salt intake and hypertension because the known increase in sympathetic activity caused by leptin would not be countered by a direct vasorelaxation.

Acetylcholine↗

PubMed2004

Salt supplementation improves orthostatic cerebral and peripheral vascular control in patients with syncope.

Salt supplementation improves orthostatic tolerance in many patients with posturally related syncope (PRS). This study aimed to examine whether in those patients who responded to salt loading there was also evidence of improved cerebral autoregulation and more powerful peripheral vasoconstriction during orthostasis. Eleven PRS patients were studied before and after ingestion of 100 mmol/d slow sodium for 2 months. Subjects underwent an orthostatic stress test of combined head-up tilting and lower body suction. We continuously monitored heart rate (ECG), blood pressure (Finapres), forearm and cerebral blood flow velocities (Doppler ultrasound), and end-tidal carbon dioxide (CO2). Forearm vascular resistance was calculated from pressure divided by velocity. Cerebral autoregulation was assessed from the correlation coefficient of the relationship between cerebral blood pressure and velocity. Salt loading had no effect on resting heart rate or blood pressure. Symptoms and orthostatic tolerance significantly improved in 10 of the patients. This was associated with a significant increase in the maximal forearm vasoconstriction from 64.4%+/-13.7% (SEM) to 135.2%+/-23.9% (P<0.005). The relationship between cerebral velocity and pressure was less strong (before salt: r=0.74+/-0.8; after salt: r=0.41+/-0.1; P<0.02), indicating improved autoregulation. End-tidal CO2 levels were not different between the 2 tests. Salt loading in PRS patients increases orthostatic tolerance and improves cerebrovascular and peripheral vascular control without affecting blood pressures. These changes are likely to contribute to the beneficial effects of salt loading in these patients.

Adult↗

PubMed2004

Pulmonary arterial distension and vagal afferent nerve activity in anaesthetized dogs.

Distension of the main pulmonary artery and its bifurcation are known to result in a reflex vasoconstriction and increased respiratory drive; however, these responses are observed at abnormally high distending pressures. In this study we recorded afferent activity from pulmonary arterial baroreceptors to investigate their stimulus-response characteristics and to determine whether they are influenced by physiological changes in intrathoracic pressure. In chloralose-anaesthetized dogs, a cardiopulmonary bypass was established, the pulmonary trunk and its main branches were vascularly isolated and perfused with venous blood at pulsatile pressures designed to simulate the normal pulmonary arterial pressure waveform. Afferent slips of a cervical vagus were dissected and nerve fibres identified that displayed discharge patterns with characteristics expected from pulmonary arterial baroreceptors. Recordings were obtained with (a) chest open (b) chest closed and resealed, and (c) with phasic negative intrathoracic pressures in the resealed chest. Pressure-discharge characteristics obtained in the open-chest animals indicated that the threshold pulmonary pressure (corresponding to 5% of the overall response) was 17.1 +/- 2.9 and the inflexion point of the curve was 29.2 +/- 3.3 mmHg (mean +/-S.E.M). In closed-chest animals the threshold and inflexion pressures were reduced to 12.0 +/- 1.7 and 20.7 +/- 1.8 mmHg. Application of phasic negative intrathoracic pressures further reduced the threshold and inflexion pressures to 9.5 +/- 1.2 mmHg (P < 0.05 vs. open) and 14.7 +/- 0.8 mmHg (P < 0.003 vs. open and P < 0.02 vs. atmospheric). These results indicate that under physiological conditions, with closed-chest and phasic negative intrathoracic pressure changes similar to those associated with normal breathing, activity from pulmonary baroreceptors is obtained at physiological pulmonary arterial pressures in intact animals.

Animals↗

PubMed2004

Phasic negative intrathoracic pressures enhance the vascular responses to stimulation of pulmonary arterial baroreceptors in closed-chest anaesthetized dogs.

We investigated whether the reflex responses to stimulation of pulmonary arterial baroreceptors were altered by intrathoracic pressure changes similar to those encountered during normal breathing. Dogs were anaesthetized with alpha-chloralose, a cardiopulmonary bypass was established, and the pulmonary trunk and its main branches as far as the first lobar arteries were vascularly isolated and perfused with venous blood. The chest was closed following connection to the perfusion circuit and pressures distending the aortic arch, carotid sinus and coronary artery baroreceptors were controlled. Changes in the descending aortic (systemic) perfusion pressure (SPP; flow constant) were used to assess changes in systemic vascular resistance. Values of SPP were plotted against mean pulmonary arterial pressure (PAP) and sigmoid functions applied. From these curves we derived the threshold pressures (corresponding to 5% of the overall response of SPP), the maximum slopes (equivalent to peak gain) and the corresponding PAP (equivalent to 'set point'). Stimulus-response curves were compared between data obtained with intrathoracic pressure at atmospheric and with a phasic intrathoracic pressure ranging from atmospheric to around -10 mmHg (18 cycles min(-1)). Results were obtained from seven dogs and are given as means +/-S.E.M. Compared to the values obtained when intrathoracic pressure was at atmospheric, the phasic intrathoracic pressure decreased the pulmonary arterial threshold pressure in five dogs; average change from 28.4 +/- 5.9 to 19.3 +/- 5.9 mmHg (P > 0.05). The inflexion pressure was significantly reduced from 37.8 +/- 4.8 to 27.4 +/- 4.0 mmHg (P < 0.03), but the slopes of the curves were not consistently changed. These results have shown that a phasic intrathoracic pressure, which simulates respiratory oscillations, displaces the stimulus-response curve of the pulmonary arterial baroreceptors to lower pressures so that it lies within a physiological range of pressures.

Animals↗

PubMed2004

Contrasting effects of carbohydrate and water on blood pressure responses to postural maneuvers in patients with posturally related (vasovagal) syncope.

Crouching then standing induces large changes in arterial blood pressure. Ingestion of carbohydrate and water are known to have contrasting effects on cardiovascular control in patients with various forms of autonomic dysfunction. We tested the hypothesis that, in patients with attacks of posturally related (neurogenic or vasovagal) syncope, postural maneuvers would cause greater changes in blood pressure than in normal controls and that they would be affected differently by carbohydrate and water. We studied 7 patients with histories indicating posturally related syncope and who we had shown to have abnormal responses to an orthostatic stress test, and 7 healthy volunteers with normal orthostatic responses. Responses of blood pressure (Portapres finger photoplethysmography) were determined to crouching and subsequent standing, before and after ingestion of a high carbohydrate "meal" (2.5MJ) and (on a different day) water (500 ml). Before the "meal" or water there were no differences between groups in baseline blood pressures or in the responses to crouching and standing. In controls, neither carbohydrate nor water had any significant effect on baseline blood pressure or on the responses to the maneuvers. In the patients, the standing pressures were also unaffected by carbohydrate but they did increase after water. In the patients the increases in pressure during the crouch were larger after carbohydrate, but smaller after water. These results show that, in patients with posturally related syncope, unlike in control subjects, carbohydrate ingestion and water result in opposite effects on blood pressure during postural maneuvers. These results raise the possibility that these patients might have a mild form of autonomic dysfunction.

Adolescent↗

PubMed2004

Pathophysiology of syncope.

Syncope or near-syncope is a not uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value. It is not necessarily abnormal, and individuals who are usually asymptomatic show the same reaction if a stress is sufficiently great to result in hypotension. Blood pressure is regulated mainly by baroreceptor reflexes by their control of vascular resistance and heart rate. The ability to vasoconstrict powerfully is important in resisting syncope; heart rate responses are of much less physiological significance. The intriguing unanswered question is what suddenly changes vasoconstriction and tachycardia to vasodilatation and bradycardia. It is now known not to be due to stimulation of cardiac receptors and some cerebral signal is more probable. People are more likely to faint when upright, motionless, warm, following meals, dehydrated or emotionally stressed, and these factors may be involved in some reflex syncopes including micturition and defaecation syncopes. Plasma volume is of considerable importance and increasing this by interventions such as salt loading, exercise training, and even sleeping with the bed head raised can often be of clinical benefit.

Bradycardia↗

PubMed2004

Cardiac output by Portapres.

Portapres derives continuous estimates of cardiac output from the peripheral pulse and has the potential to be an extremely valuable physiological and clinical tool. We assessed Portapres estimates of cardiac output in healthy subjects at rest, during maximal treadmill exercise ( n = 8) and during decreases caused by orthostatic stress ( n = 8). Comparison with a rebreathing method indicated that Portapres tended to overestimate cardiac output. The random errors of the estimates (precision), expressed as +/- 2 S.D. of the differences between paired estimates during steady states, ranged between 1.2 and 2.6 litres/min. We conclude that these errors indicate that the method is probably only useful for assessing changes in individual subjects where large changes are anticipated, as during exercise. When smaller changes occur, as during orthostasis, the errors preclude the use of individual subject data and only permit group average data to be examined.

Adult↗

PubMed2003

Cerebral autoregulation during orthostatic stress in healthy controls and in patients with posturally related syncope.

Posturally related syncope (PRS) is a common and distressing problem, which frequently occurs in people with no apparent clinical disorder and is ultimately caused by a reduction in blood supply to the brain. The aim of this study was to compare cerebrovascular responses to orthostatic stress in otherwise healthy patients suffering from PRS, and who were shown to have a poor orthostatic tolerance (n=28), with those in healthy control subjects with good orthostatic tolerance (n=11). Responses of heart rate, arterial blood pressure, end tidal carbon dioxide and middle cerebral artery (MCA) blood flow velocity were determined during a progressive orthostatic stress test of combined head-up tilting and lower body suction, which was continued until presyncope. We assessed the efficiency of autoregulation of cerebral blood flow from the relationship between values of MCA velocity and pressure obtained over the expected range for autoregulation (> 55 mmHg). All patients with PRS had a significant correlation between MCA velocity and pressure, but this was seen in only two of the controls. Furthermore, the values of the correlation coefficients were significantly higher in patients than controls, (p<0.001). We interpret these data as indicating that autoregulation in patients with PRS is less effective than in controls and suggest that this provides evidence for a link between abnormalities of regulation of the cerebral circulation and predisposition to syncope.

Adult↗

PubMed2003

Influence of dietary salt intake on the response of isolated perfused mesenteric veins of the dog to vasoactive agents.

BACKGROUND: Previous work has established that a high dietary salt intake results in enhanced arterial vasoconstrictor responses to stimulation with agonists. This investigation was designed to investigate the effects of dietary salt on the responses of isolated capacitance vessels (third order mesenteric veins). METHODS: Dogs were fed diets containing low, intermediate, and high levels of dietary salt (0.4, 3.0, and 6.0 mmol kg/day). The animals were killed, and lengths of mesenteric vein were mounted in a perfusion myograph with changes in lumenal diameter measured using a video tracking device. Responses to cumulative doses of norepinephrine (NE) and acetylcholine (Ach) were then determined. RESULTS: The vasoconstrictor responses to NE were greater in the veins from dogs on a high salt diet. Acetylcholine also caused venoconstriction that also was greater in the high salt group of animals. Responses to Ach were unaffected by N(omega)-nitro-L-arginine methyl ester but were abolished by atropine. CONCLUSIONS: These results indicate that mesenteric veins from dogs fed a high salt diet constrict more powerfully in response to agonists, which could contribute to the hypertensive effects of high intakes of dietary salt.

Acetylcholine↗

PubMed2003

Cross-spectral analysis of cardiovascular parameters whilst supine may identify subjects with poor orthostatic tolerance.

An easy and low-cost method for identification of subjects prone to orthostatic vasovagal syncope would be of clinical benefit. An orthostatic test with 60 degrees head-up tilt and progressive lower-body negative pressure was performed on 79 patients with histories of unexplained syncope and 26 control subjects. The test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Spectral and cross-spectral analysis was performed on the supine time series of the R-R interval (ECG) and systolic pressure (Finapres) recorded before the beginning of the test. According to reference values, 38 patients and 11 controls were classified as having poor orthostatic tolerance (PPT and CPT respectively), whereas 41 patients and 15 controls displayed normal orthostatic tolerance (PNT and CNT respectively). The central frequency of the low-frequency (LF approximately equal to 0.1 Hz.) oscillations in PNT and CNT was significantly higher than that in PPT and CPT. In addition, it was significantly linearly correlated with the time of presyncope. Using our test of orthostatic tolerance as a comparison, the LF central frequency allows the classification of subjects with poor or normal tolerance with 80% sensitivity and 82% specificity. These results suggest that the LF central frequency in the supine position may provide a useful index in the diagnosis of orthostatic intolerance.

Adolescent↗