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Biomedical subjects

R Hainsworth

Publications and source records attributed to R Hainsworth.

At least 19 recordsLinked to original sources
PubMed2003

Cardiovascular regulation in the period preceding vasovagal syncope in conscious humans.

To study cardiovascular control in the period leading to vasovagal syncope we monitored beat-to-beat blood pressure, heart rate (HR) and forearm blood flow in 14 patients with posturally related syncope, from supine through to tilt-induced pre-syncope. Signals of arterial blood pressure (BP) from a Finapres photoplethysmograph and an electrocardiograph (ECG) were fed into a NeuroScope system for continuous analysis. Non-invasive indices of cardiac vagal tone (CVT) and cardiac sensitivity to baroreflex (CSB) were derived on a beat-to-beat basis from these data. Brachial vascular resistance (VR) was assessed intermittently from brachial blood flow velocity (Doppler ultrasound) divided by mean arterial pressure (MAP). Patients underwent a progressive orthostatic stress test, which continued to pre-syncope and consisted of 20 min head-up tilt (HUT) at 60 deg, 10 min combined HUT and lower body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg. Pre-syncope was defined as a fall in BP to below 80 mmHg systolic accompanied by symptoms. Baseline supine values were: MAP (means +/- S.E.M.) 84.9 +/- 3.2 mmHg; HR, 63.9 +/- 3.2 beats min-1; CVT, 10.8 +/- 2.6 (arbitrary units) and CSB, 8.2 +/- 1.6 ms mmHg-1. HUT alone provoked pre-syncope in 30 % of the patients whilst the remaining 70 % required LBNP. The cardiovascular responses leading to pre-syncope can be described in four phases. Phase 1, full compensation: where VR increased by 70.9 +/- 0.9 %, MAP was 89.2 +/- 3.8 mmHg and HR was 74.8 +/- 3.2 beats min-1 but CVT decreased to 3.5 +/- 0.5 units and CSB to 2.7 +/- 0.4 ms mmHg-1. Phase 2, tachycardia: a progressive increase in heart rate peaking at 104.2 +/- 5.1 beats min-1. Phase 3, instability: characterised by oscillations in BP and also often in HR; CVT and CSB also decreased to their lowest levels. Phase 4, pre-syncope: characterised by sudden decreases in arterial blood pressure and heart rate associated with intensification of the symptoms of pre-syncope. This study has given a clearer picture of the cardiovascular events leading up to pre-syncope. However, the mechanisms behind what causes a fully compensated system suddenly to become unstable remain unknown.

Adult↗
PubMed2003

Syncope: what is the trigger?

Although a syncopal attack is frequently preceded by prodromal symptoms, sometimes the onset can be so abrupt that there is no warning at all. The switch in autonomic responses responsible for such an attack is quite rapid and dramatic, but the trigger for this remains one of the unresolved mysteries in cardiovascular physiology.

Autonomic Nervous System↗
PubMed2002

Change in endothelial function in mesenteric arteries of Sprague-Dawley rats fed a high salt diet.

A high salt diet in some species results in elevated arterial blood pressure and alterations in vascular smooth muscle responses to agonists. Weanling male Sprague-Dawley rats were given either a high salt diet containing 8 % or a low salt diet of 0.4 % sodium chloride for a period of 4 weeks. At the end of the feeding period, tail systolic pressure was higher in the high salt than in low salt rats. The rats were then killed and the intestines removed. Vascular smooth muscle (VSM) responses were estimated from the changes in lumenal diameter of pressurised second order mesenteric resistance arteries. High salt diet resulted in enhanced VSM responses to noradrenaline. The vessels dilated in response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels from both high and low salt rats. However, vessels from high salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L-NAME and the responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin. These results show that in Sprague-Dawley rats, a high salt diet enhances the vasoconstriction in response to noradrenaline. The vasodilatory responses to acetylcholine were not significantly changed. However, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.

Acetylcholine↗
PubMed2002

Effects of head-up tilting on baroreceptor control in subjects with different tolerances to orthostatic stress.

During orthostatic stress, an increase in peripheral vascular resistance normally results in arterial blood pressure being well maintained, despite a decrease in cardiac output. The present study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was increased during orthostatic stress and whether failure to develop this increase was associated with poor orthostatic tolerance. Three groups of subjects were studied: asymptomatic controls; patients investigated for suspected posturally related syncope but who had normal responses to an orthostatic stress test (normal patients); and patients who were shown to have low orthostatic tolerance (early fainters). We determined responses of R-R interval and forearm vascular resistance (mean arterial pressure/brachial artery velocity by Doppler ultrasonography) to the loading and unloading of carotid baroreceptors by application of pressures of -30 and +30 mmHg to a chamber fitted over the neck. Responses were determined after 20 min of supine rest and after 10 min of head-up tilt at 60 degrees. Responses of cardiac interval were not significantly different between the three groups, and they were not altered by the postural change. Vascular responses also did not differ between the groups during supine rest. However, in healthy volunteers and in normal patients, responses to both neck suction and pressure were significantly enhanced during head-up tilt. In controls, responses to suction were increased by tilt from 0.04+/-0.1 to -1.01+/-0.2%.mmHg(-1) (means+/-S.E.M.; P<0.001) and those to neck pressure from -0.6+/-0.3 to -3.1+/-1.1%.mmHg(-1) (P<0.05). In the normal patients, the corresponding changes were: during suction, from -0.2+/-0.1 to -0.7+/-0.1%.mmHg(-1) (P<0.05); during pressure, from -0.7+/-0.1 to -1.5+/-0.3%.mmHg(-1) (P<0.05). In contrast, in patients with low orthostatic tolerance, posture had no effect on the reflex (neck suction, from -0.3+/-0.1 to -0.3+/-0.1%.mmHg(-1); neck pressure, from -1.0+/-0.3 to -0.9+/-0.2%.mmHg(-1)). We suggest that an increase in the sensitivity of the carotid baroreceptor/vascular resistance reflex may be important in the maintenance of blood pressure during orthostatic stress, and that failure of this to occur in patients with posturally related syncope may go some way towards explaining their poor orthostatic tolerance.

Adolescent↗
PubMed2001

Reflex vascular responses to independent changes in left ventricular end-diastolic and peak systolic pressures and inotropic state in anaesthetised dogs.

1. Ventricular mechanoreceptors are known to exist and can when stimulated induce reflex vasodilatation, but the nature of the effective stimuli and the physiological role of the reflex remain to be established. 2. Dogs were anaesthetised with chloralose and a cardiopulmonary bypass established. Ventricular pressures were separated from those in the aortic root and coronary arteries by a balloon inflated in the ventricular outflow tract. Ventricular filling was controlled by adjusting the rate of inflow of blood through an apical cannula and peak pressure by regulating the outflow pressure from the same cannula. Carotid and aortic pressures were also controlled and vascular resistance was assessed from changes in perfusion pressure (constant flow conditions) to the descending abdominal aorta. 3. Increased coronary or carotid sinus pressure induced a significant vasodilatation. Changes in ventricular peak systolic pressure, without associated changes in end-diastolic pressure, had no significant effect on vascular resistance. In contrast, changes in end-diastolic pressure did induce vasodilatation that, although small, was proportional to the magnitude of the end-diastolic pressure change. 4. Changes in ventricular inotropic state induced by dobutamine infusion or by stimulation of efferent cardiac sympathetic nerves did not induce significant responses. Furthermore, the combined effects of reduced ventricular filling and increased inotropic state were also ineffective in inducing responses. 5. We conclude that, to induce reflex responses, the only effective stimulus to ventricular mechanoreceptors was an increase in filling. Compared with other mechanoreflexes, however, responses to ventricular distension were small and seem unlikely to be of importance except perhaps during abnormal ventricular distension.

Animals↗
PubMed2001

Why do we faint?

Explore the source record for details and available documents.

Blood Pressure↗
PubMed2001

Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance.

The mechanisms leading to vasovagal syncope are still unclear. A simple discriminating test for the identification of syncope-prone subjects is not presently available. Fifty-two subjects had a stepwise orthostatic test with 60 degrees tilt and -20 and -40 mm Hg lower-body negative pressure before the appearance of impending syncope symptoms. Spectral and cross-spectral analyses of heart period and systolic pressure time series were performed to estimate the power of the high-frequency (approximately equals 0.25 Hz) and low-frequency (approximately equals 0.1 Hz) oscillations, the coherence between heart period and systolic pressure, and the mean low-frequency and high-frequency central frequency, phase shift, and transfer function at maximal coherence. According to time to presyncope, the 52 subjects were divided into two groups: 25 with normal orthostatic tolerance, and 27 with poor orthostatic tolerance. In the supine positions, the mean central low-frequency was significantly lower in poor-tolerance group than in normal-tolerance group, discriminating poor from normal orthostatic tolerance with 80% specificity and 83% sensitivity, and was significantly correlated to time to presyncope. In the 2 to 3 minutes preceding syncope, subjects with poor orthostatic tolerance had less tachycardia, lower low-frequency power of systolic pressure, higher respiratory frequency, and a less negative phase shift in high-frequency range. In presyncope, sympathetic activation is reduced in subjects with poor orthostatic tolerance. In addition, the higher breathing frequency and the smaller negativity of phase shift in high-frequency range, which may indicate an inadequate engagement of the baroreflex, suggest a causal role of respiration in the development of syncope. Supine central values of low frequency may be proposed as a valuable clinical index of orthostatic intolerance.

Adult↗
PubMed2001

Responses to stimulation of coronary and carotid baroreceptors and the coronary chemoreflex at different ventricular distending pressures in anaesthetised dogs.

Stimulation of left ventricular mechanoreceptors was believed not only to exert important effects on the circulation, but also to influence the responses to baroreceptor reflexes. However, most previous work is flawed due to inadequate localisation of stimuli to specific reflexogenic areas. In this study, we applied a discrete stimulus to left ventricular mechanoreceptors to examine other reflexes known to effect the circulation. Dogs were anaesthetised, artificially ventilated and a cardiopulmonary bypass established. The pressure distending the left ventricle was controlled through an apical cannula with the aortic valve obstructed by a balloon. Changes in ventricular systolic and end-diastolic pressure had only a small effect on vascular resistance, assessed as perfusion pressure in the systemic circulation (flow constant). Responses to changes in carotid or coronary pressure or to stimulation of chemosensitive afferents by injecting veratridine into the coronary circulation were always much larger. Responses to stimulation of these reflexes were little affected by the level of stimulus to the ventricular receptors. These experiments confirm that responses to stimulation of ventricular mechanoreceptors are very small and show that they remain small at different levels of input to other baroreceptive regions. There was no evidence of interaction between ventricular mechanoreceptor reflexes and carotid or coronary baroreceptors or ventricular chemosensitive reflexes.

Anesthesia↗
PubMed2001

Carotid baroreceptor reflexes in humans during orthostatic stress.

Orthostatic stress, including standing, head-up tilting and lower body suction, results in increases in peripheral vascular resistance but little or no change in mean arterial pressure. This study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was enhanced during conditions of decreased venous return. We studied eight healthy subjects and determined responses of pulse interval (ECG) and forearm vascular resistance (mean finger blood pressure divided by Doppler estimate of brachial artery blood velocity) to graded increases and decreases in carotid transmural pressure, effected by a neck suction/pressure device. Responses were determined with and without the application of lower body negative pressure (LBNP) at -40 mmHg. Stimulus-response curves were determined as the responses to graded neck pressure changes and the differential of this provided estimates of reflex sensitivity. Changes in carotid transmural pressure caused graded changes in R-R interval and vascular resistance. The cardiac responses were unaffected by LBNP. Vascular resistance responses, however, were significantly enhanced during LBNP and the peak gain of the reflex was increased from 1.2 +/- 0.3 (mean +/- S.E.M.) to 2.2 +/- 0.3 units (P < 0.05). The increased baroreflex gain may contribute to maintenance of blood pressure during orthostatic stress and limit the pressure decreases during prolonged periods of such stress.

Adult↗
PubMed2001

Randomized controlled trial of home-based exercise training to evaluate cardiac functional gains.

There is evidence that multiple benefits can be obtained through exercise training that leads to increases in peak oxygen consumption (V(O(2))). It is unclear whether significant improvements can also be achieved through unsupervised low-budget home-based training regimes, especially in terms of cardiac functional gains. A randomized cross-over trial was conducted to investigate the effects of a home-based unsupervised exercise training programme of moderate intensity on aerobic capacity, cardiac reserve and peak cardiac power output in healthy middle-aged volunteers. Nine subjects with no known cardiovascular diseases performed symptom-limited treadmill cardiopulmonary exercise tests after an 8-week period of exercise training, and results were compared with those obtained after a similar 'non-exercising' control period. Cardiac output was measured non-invasively during exercise tests using the CO(2)-rebreathing method. With exercise training, resting heart rate decreased significantly from 88.3+/-3.4 to 78.7+/-3.2 beats.min(-1) (P<0.05), heart rate at a submaximal workload (V(O(2))=1.5 litres.min(-1)) decreased from 125.5+/-2.4 to 115.5+/-1.6 beats.min(-1), and peak V(O(2)) increased by 9% from 2.62+/-0.19 to 2.85+/-0.18 litres.min(-1) (P<0.01). Baseline cardiac power output was 1.11+/-0.05 W, and this remained unchanged with training. Peak cardiac power output increased by 16% from 4.1+/-0.3 to 4.7+/-0.3 W (P<0.001), and cardiac reserve increased by 21% (P<0.01). A major contribution to these increases was from the 11% increase in stroke volume, from 100.1+/-5.3 to 111.2+/-6.2 ml (P<0.001). All subjects reported more positive perceptions of their health (P<0.05), fitness (P<0.01) and levels of activity (P<0.01) after the training period. These results show that motivated subjects undergoing low-budget unsupervised home-based exercise training of moderate intensity can derive benefit in terms of symptoms, aerobic capacity and cardiac functional reserve.

Analysis of Variance↗
PubMed2000

Reflex effects of independent stimulation of coronary and left ventricular mechanoreceptors in anaesthetised dogs.

Previous studies which have indicated that the stimulation of ventricular mechanoreceptors induces significant reflex responses can be criticised because of the likelihood of concomitant stimulation of coronary arterial baroreceptors. We therefore undertook this investigation to examine the coronary and ventricular mechanoreflexes in a preparation in which the pressure stimuli to each region were effectively separated. Dogs were anaesthetised, artificially ventilated and placed on cardiopulmonary bypass. A balloon at the ventricular outflow separated pressure in the left ventricle from that perfusing the coronary arteries. Ventricular pressures were changed by varying inflow and outflow of blood entering and leaving the ventricle through an apical cannula, and coronary pressure by changing pressure in a reservoir connected to a cannula tied in the aortic root. Pressures distending carotid and aortic baroreceptors were controlled. Changes in descending aortic perfusion pressure (flow constant) were used to assess systemic vascular responses. Large changes in carotid sinus and coronary pressures decreased vascular resistance by 35+/-1.9 and 40+/-2.5%, respectively. Intracoronary injections of veratridine (30-60 microg) decreased vascular resistance by 31+/-2.5%. However, large increases in ventricular pressure decreased resistance by only 9+/-2.2%. Significant changes in vascular resistance were obtained with increases in coronary arterial pressure from 60 to 90 mmHg. However, ventricular pressures had to increase to 152/18 mmHg (systolic/end-diastolic) before there was a significant response. These results show that coronary mechanoreceptors are likely to play an important role in cardiovascular control. If ventricular receptors have any function at all, it is as a protective mechanism during gross distension, possibly associated with myocardial ischaemia.

Anesthesia↗
PubMed2000

Forearm vascular responses during orthostatic stress in control subjects and patients with posturally related syncope.

The aim of this study was to compare the changes in forearm vascular resistance that occurred during orthostatic stress in asymptomatic volunteer subjects with those in patients with posturally related syncope. The authors hoped firstly that it would indicate the importance of vasoconstriction in the maintenance of blood pressure, and secondly that it might have diagnostic value if there were differences between symptomatic patients and asymptomatic volunteers. Twelve volunteers and 67 patients with unexplained syncope were classified as early or late fainters, based on their endurance of a test of combined head-up tilting and lower-body suction. Responses of vascular resistance were assessed from the ratio of arterial blood pressure (Finapres) to brachial artery blood velocity (Doppler). Changes in vascular resistance were greater in volunteers at all stages of the procedure than in patients. There was, however, no significant difference between the responses of early and late-fainting volunteers. These results demonstrate the importance of vasoconstriction in the resistance to posturally related syncope, and they indicate that assessments of responses of vascular resistance may improve the accuracy of the diagnosis.

Adult↗
PubMed2000

Vascular responses to orthostatic stress in patients with postural tachycardia syndrome (POTS), in patients with low orthostatic tolerance, and in asymptomatic controls.

Patients with postural tachycardia syndrome (POTS) are characterized by development of symptoms of orthostatic intolerance during standing that are not because of hypotension but are associated with tachycardia. The goal of this study was to compare the cardiac and vascular responses to orthostatic stress for patients with POTS (n = 8) with those for patients with low orthostatic tolerance (n = 29) and for healthy control subjects (n = 12). Responses of heart rate (ECG), arterial blood pressure, and brachial artery blood velocity (Doppler) were determined during a progressive orthostatic stress test of head-up tilt and lower body suction. Changes in forearm vascular resistance (mean arterial pressure/brachial velocity) were less for patients with POTS than for healthy persons, and also less than for most of the patients with low orthostatic tolerance. However, patients with POTS did not have a low tolerance to orthostatic stress (measured as time to discontinuation of the test). For the patients with POTS, the test was discontinued often because of symptoms associated with tachycardia but not hypotension, whereas for the other two groups, the test was discontinued because of hypotension. This study shows that for patients with POTS, abnormal sympathetic responses exist, with an increased sympathetic drive to the heart but deficient peripheral vascular responses, as measured in the forearm. This supports the hypothesis that patients with POTS may have a selective peripheral neuropathy, with small responses in some regions being compensated by overactivity in other regions.

Adolescent↗
PubMed2000

Reflex responses from the main pulmonary artery and bifurcation in anaesthetised dogs.

This study was undertaken to determine the reflex cardiovascular and respiratory responses to discrete stimulation of pulmonary arterial baroreceptors using a preparation in which secondary modulation of responses from other reflexes was prevented. Dogs were anaesthetised with -chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The main pulmonary arterial trunk, bifurcation and extrapulmonary arteries as far as the first lobar arteries on each side were vascularly isolated and perfused through the left pulmonary artery and drained via the right artery through a Starling resistance which controlled pulmonary arterial pressure. Pressures distending systemic baroreceptors and reflexogenic regions in the heart were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic systemic circulation, both of which were perfused at constant flows. Respiratory responses were assessed from recordings of efferent phrenic nerve activity. Increases in pulmonary arterial pressure consistently evoked increases in both perfusion pressures and in phrenic nerve activity. Both vascular and respiratory responses were obtained when pulmonary arterial pressure was increased to above about 30 mmHg. Responses increased at higher levels of pulmonary arterial pressures. In 13 dogs increases in pulmonary arterial pressure to 45 mmHg increased systemic perfusion pressure by 24 +/- 7 mmHg (mean +/- S.E.M.) from 162 +/- 11 mmHg. Setting carotid sinus pressure at different levels did not influence the vascular response to changes in pulmonary arterial pressure. The presence of a negative intrathoracic pressure of -20 mmHg resulted in larger vascular responses being obtained at lower levels of pulmonary arterial pressure. This indicates that the reflex may be more effective in the intact closed-chest animal. These results demonstrate that stimulation of pulmonary arterial baroreceptors evokes a pressor reflex and augments respiratory drive. This reflex is likely to be elicited in circumstances where pulmonary arterial pressure increases and the negative excursions of intrathoracic pressure become greater. They are likely, therefore, to be involved in the cardio-respiratory response to exercise as well as in pathological states such as pulmonary hypertension or restrictive or obstructive lung disease.

Animals↗
PubMed2000

Absence of reflex vascular responses from the intrapulmonary circulation in anaesthetised dogs.

The aim of this investigation was to determine whether reflex cardiovascular responses were obtained to localised distension of the intrapulmonary arterial and venous circulations in a preparation in which the stimuli to other major reflexogenic areas were controlled and the lung was shown to possess reflex activity. Dogs were anaesthetised with -chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The intrapulmonary region of the left lung was isolated and perfused through the left pulmonary artery and drained through cannulae in the left pulmonary veins via a Starling resistance. Intrapulmonary arterial and venous pressures were controlled by the rate of inflow of blood and the pressure applied to the Starling resistance. Pressures to the carotid, aortic and coronary baroreceptors and heart chambers were controlled. Responses of vascular resistance were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic circulation (flows constant). The reactivity of the preparation was demonstrated by observing decreases in vascular resistance to large step changes in carotid sinus pressure (systemic vascular resistance decreased by -40 +/- 5%), chemical stimulation of lung receptors by injection into the pulmonary circulation of veratridine or capsaicin (resistance decreased by -32 +/- 4%) and, in the four dogs tested, increasing pulmonary stroke volume to 450 ml (resistance decreased by -24 +/- 6%). However, despite this evidence that the lung was innervated, increases in intrapulmonary arterial pressure from 14 +/- 1 to 43 +/- 3 mmHg or in intrapulmonary venous pressure from 5 +/- 2 to 34 +/- 2 mmHg or both did not result in any consistent changes in systemic or limb vascular resistances. In two animals tested, however, there were marked decreases in efferent phrenic nerve activity. These results indicate that increases in pressure confined to the intrapulmonary arterial and venous circulations do not cause consistent reflex vascular responses, even though the preparation was shown to be reflexly active and the lung was shown to be innervated.

Animals↗