Human cerebral venous outflow pathway depends on posture and central venous pressure

Internal jugular veins are the major cerebral venous outflow pathway in supine humans. In upright humans the positioning of these veins above heart level causes them to collapse. An alternative cerebral outflow pathway is the vertebral venous plexus. We set out to determine the effect of posture and central venous pressure (CVP) on the distribution of cerebral outflow over the internal jugular veins and the vertebral plexus, using a mathematical model. Input to the model was a data set of beat-to-beat cerebral blood flow velocity and CVP measurements in 10 healthy subjects, during baseline rest and a Valsalva manoeuvre in the supine and standing position. The model, consisting of 2 jugular veins, each a chain of 10 units containing nonlinear resistances and capacitors, and a vertebral plexus containing a resistance, showed blood flow mainly through the internal jugular veins in the supine position, but mainly through the vertebral plexus in the upright position. A Valsalva manoeuvre while standing completely re-opened the jugular veins. Results of ultrasound imaging of the right internal jugular vein cross-sectional area at the level of the laryngeal prominence in six healthy subjects, before and during a Valsalva manoeuvre in both body positions, correlate highly with model simulation of the jugular cross-sectional area ( R ²= 0.97). The results suggest that the cerebral venous flow distribution depends on posture and CVP: in supine humans the internal jugular veins are the primary pathway. The internal jugular veins are collapsed in the standing position and blood is shunted to an alternative venous pathway, but a marked increase in CVP while standing completely re-opens the jugular veins.     

Systolic and diastolic changes in human coronary blood flow during Valsalva manoeuvre.

Valsalva manoeuvre is reported to be sometimes successful for the relief of angina pectoris. The present study investigated how haemodynamic changes produced by Valsalva manoeuvre can interact to improve the relationship between cardiac work and coronary blood flow. Ten male subjects aged 53 +/- 12 years (SD) were considered. Blood velocity in the internal mammary artery, previously anastomosed to the left descending coronary artery, was studied with Doppler technique. The subjects performed Valsalva manoeuvres by expiring into a tube connected to a mercury manometer, to develop a pressure of 40 mmHg. The arterial blood pressure curve was continuously monitored with a Finapres device from a finger of the left hand. During expiratory effort, an increase in heart rate and a decrease in arterial pulse pressure were followed by a more delayed and progressive increase in mean and diastolic pressures. Systolic blood velocity markedly decreased along with the reduction in pulse pressure and increase in heart rate. By contrast, diastolic and mean coronary blood velocities did not show any significant change. Since it is known that the Valsalva manoeuvre strongly reduces stroke volume and cardiac output, it is likely that a reduction in cardiac work also takes place. Since in diastole, i.e. when the myocardial wall is better perfused, coronary blood velocity did not show any significant reduction, it is likely that unchanged perfusion in the presence of reduced cardiac work is responsible for the relief from angina sometimes observed during Valsalva manoeuvre. It is also likely that the increase in heart rate prevents the diastolic and mean blood coronary velocity from decreasing during the expiratory strain, when an increased sympathetic discharge could cause vasoconstriction through the stimulation of the coronary alpha-receptors.     

Cardiac responses to the Valsalva manoeuvre in different body positions

Summary A standardized Valsalva manoeuvre (VM) with a 15-s straining period was repeated in each of four postures by six male subjects. The postures were supine (SUP), sitting leaning back (LB), sitting leaning forward (LF) and standing (ST). During straining, the increase in heart rate (f _c) was different between LB and LF (+50% and +23%, respectively P<0.05). The decrease in stroke volume (SV), which was monitored by means of impedance cardiography, was different (63%, 68%, 39%, and 72%, P<0.001) as well as the decrease in cardiac output (CO) (55%, 53%, 26%, and 61%, P<0.001) in SUP, LB, LF, and ST, respectively. Accordingly, after pressure release the smallest changes of SV, f _c and CO were found in LF. In conclusion, cardiovascular stability during straining was increased during LF. Consequently, this posture would appear to be superior to other postures during unavoidable VM (weight lifting and defaecation). To perform tests on autonomic function LB would appear to be superior to the other postures because of the large autonomic responses, combined with minimum risk for the subject. The impedance method provided simple and reproducible determinations of SV changes during VM.     

Use of non-invasive finger blood pressure monitoring in the estimation of aortic pressure at rest and during the Mueller manoeuvre.

The aim of this investigation was to evaluate whether reliable estimates of aortic pressure can be derived using non-invasive finger blood pressure monitoring. Finger blood pressure (Ohmeda 2300 Finapres device; Finapres, Englewood, CO) was compared with simultaneous ascending aortic pressure measured with a catheter-transducer system both at rest and during acute negative intrathoracic pressure (the Mueller manoeuvre). Thirty-eight patients aged 17-73 years were studied. All were undergoing routine diagnostic or therapeutic cardiac catheterization. Beat-to-beat values of systolic, diastolic and mean non-invasive finger and invasive aortic blood pressure were measured at rest and factors which might have an influence on the difference between methods were examined. The mean finger-aortic difference was +5 +/- 14 mmHg for systolic, -2 +/- 7 mmHg for diastolic, -5 +/- 8 mmHg for mean and +6 +/- 13 mmHg for pulse pressure. In multivariate linear regression analysis, the difference in systolic pressure was related to aortic systolic pressure (standardized coefficient beta = -0.33, P = 0.01), heart rate (beta = 0.49, P < 0.000), age (beta = -0.29, P < 0.025) and height (beta = 0.40, P < 0.005). The linear regression equations to derive resting aortic pressures from the non-invasive finger pressure readings had correlation coefficients between 0.83 and 0.87 and standard errors of estimate between 6 and 14 mmHg. During the Mueller manoeuvre, Finapres reproduced average pressure changes reliably compared with intra-aortic pressure. Due to moderate inter-individual variation in the finger-aortic differences the correlation coefficients ranged from 0.83 to 0.93 and the standard errors of estimate from 3 to 6 mmHg. Non-invasive finger blood pressure monitoring could be used to estimate central aortic mean and diastolic blood pressure fairly reliably at rest, but with respect to systolic pressure the variance in finger-aortic difference was marked. The average intra-aortic pressure changes caused by the Mueller manoeuvre were reliably reproduced by the Finapres device.     

Forced expiratory flow-volume curves during the application of lower-body negative pressure

Ten normal subjects were studied during supine rest and quiet standing, and when exposed, supine, to lower-body negative pressure (LBNP) of 30, 40 and 50 mmHg, each for a period of 7 min, in random order. Their partial and complete flow-volume curves, heart rate and blood pressure were recorded during the last 3 min in each condition. The expected reflex cardiovascular responses to the decrease in central blood volume during standing and during LBNP were seen. The forced vital capacity was somewhat greater during standing and during LBNP than while supine. The airflow variables measured from the flow-volume curve-except MEF25% (partial)--were significantly increased during progressive LBNP but did not reach the raised values found when the posture changed from supine to standing. The observations suggest that besides the redistribution of the central blood volume to the periphery, other factors must contribute to the increase in airflows during standing.     

Venous pressure in the saphenous vein near the ankle during changes in posture and exercise at different ambient temperatures

Summary The venous pressure in the saphenous vein at the ankle was measured in ten healthy subjects (5 men, 5 women) aged 19–33 years during supine posture, orthostasis and cycle ergometer exercise (50 W, 50 rpm). Measurements were made at 20, 28 and 36°C at 50% relative humidity. A custom-built setup consisting of two pressure transducers and a differential amplifier was used to compensate for the hydrostatic effects, temperature influences and movement artefacts that disturbed the pressure measurements. Pressure was lowest in the supine position and varied only slightly with the ambient temperature. The mean pressures were 7 (SEM 1) mmHg [0.9 (SEM 0.13) kPa], 7 (SEM 1) mmHg [0.9 (SEM 0.13) kPa], 4 (SEM 1) mmHg [0.5 (SEM 0.13) kPa] at 20, 28 and 36° C. The venous pressure increased when the subjects were passively tilted from a supine to an upright posture. The rate of the increase was smaller at 20°C than at 28° and 36° C. The final level the pressure reached during motionless standing differed slightly. The mean pressures were 76 (SEM 2) mmHg [10.1 (SEM 0.27) kPa], 79 (SEM 7) mmHg [10.5 (SEM 0.93) kPa] and 75 (SEM 3) mmHg [10.0 (SEM 0.40)] at the three temperatures. When starting exercising, venous pressure decreased within the 1st min to a level which remained virtually constant until the end of exercise. However, this level was found to be temperature dependent. It was lowest at 20° C 26 (SEM 3) mmHg [3.5 (SEM 0.40) kPa] and increased with temperature. The mean values were 30 (SEM 3) mmHg [4.0 (SEM 0.40) kPal at 28° C and 35 (SEM 3) mmHg [4.7 (SEM 0.40) kPa] at 36° C. The difference between the venous pressures at 20° and 36° C was statistically significant. Overall, posture and exercise influenced the venous pressure at the ankle more intensely than did ambient temperature. Muscle exercise reduced the venous pressure considerably, even in the warm environment.     

Effects of adenosine on autonomic control of heart rate in man

Six healthy subjects (two female) aged 23-40 years participated in a double-blind randomized cross-over study to investigate autonomic mechanisms involved in the chronotropic effect of adenosine in conscious man. Adenosine was infused in increasing doses following saline, propranolol (0.2 mg kg-1 body weight) or propranolol (0.2 mg kg-1 plus atropine (0.04 mg kg-1). Heart rate and blood pressure were measured supine, on standing and during a Valsalva manoeuvre. Plasma catecholamines were measured in the supine and standing positions. Following saline, adenosine (up to 120 micrograms kg-1 min-1) caused a dose-related increase in heart rate (mean +/- SD maximum increase 18 +/- 8 bpm; P less than 0.01). The change in heart rate with adenosine after propranolol (12 +/- 9 bpm; P less than 0.05) did not differ significantly from the corresponding change following saline but was abolished by propranolol plus atropine, which, in turn, was associated with a mean maximum decrease in heart rate of 5 +/- 3 bpm (P less than 0.01). The increase in heart rate during the initial 30 s on standing was augmented with adenosine compared with saline (16 +/- 5 bpm; P less than 0.01). A significant increase in plasma noradrenaline on standing was also found with adenosine compared with saline (6.37 +/- 2.86 vs. 4.77 +/- 1.79 nmol 1(-1); P less than 0.05). The heart rate response to the Valsalva manoeuvre was not affected by adenosine. These results suggest that the positive chronotropic effect of infused adenosine in conscious man may in part be caused by an inhibition of cardiac vagal tone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of age on the immediate cardiovascular response to orthostatic manoeuvre

The dynamics of cardiovascular changes following standing up from the supine position were investigated in 41 healthy men aged 20–59 years, classified into three groups: (22–26 years, n = 14), (33–49 years, n = 13) and (51–59 years, n = 14). The protocols consisted of a sequence repeated twice lying down-standing up-lying down. The initial period supine was for 20 min and then the subjects remained in each position for 8 min. Stroke volume, cardiac output (CO), ejection time (ET), pre-ejection period and heart rate (HR) were continuously calculated using automated impedance cardiography and electrocardiography. Blood pressure was measured by the auscultation method. The patterns of HR and haemodynamic orthostatic response were shown to be highly reproducible. Most of the indices characterizing the amplitude and rate of cardiovascular changes following standing up showed a tendency towards attenuation with age. However, only the indices of HR, CO and ET responses correlated significantly with age. The strongest relationships with age were observed in the sudden increase in HR (n = – 0.61, P < 0.01), the transient increase in CO (r = – 0.45, P < 0.001), and the rapid decrease in ET (r = 0.42, P < 0.01) after standing up. A few indices of HR and haemodynamic response also showed weak correlations with the subjects' heights and body masses.     

Reproducibility of the heart rate response to low-strain Valsalva manoeuvre in healthy subjects

To elucidate whether the intrastrain cardio-acceleration and cardio-deceleration responses to low-strain Valsalva manoeuvre at expiratory pressures 10 and 20 mmHg (VM10,VM20) are reproducible, a beat-to-beat heart rate study was undertaken in 46 subjects (40 male undergraduates aged 19-25 years and six laboratory workers (four females and two males aged 28-55 years). The intensity of the heart rate response (HRR) was assessed by a ratio of the mean value of the pre-strain heart rate (Valsalva means' ratio VMR). In each subject the HRR to VM10 and VM20 was measured by repeating each manoeuvre three times. Reproducibility was evaluated on a short-term (1 h), medium-term (1 and 6 months), and long-term (6 and 11 years) basis. With the individual differences the initial short-term reproducibility study revealed either an cardio-acceleration or cardio-deceleration response to VM10 and VM20, which persisted well in the repeated tests. On the ground of this result three individual modes of HRRs to VM10 and VM20 were distinguished: (i) Mode A, a deceleration response appeared both to VM10 and VM20; (ii) Mode B, a deceleration response appeared to VM10 and an acceleration response to VM20; (iii) Mode C, an acceleration response appeared both to VM10 and VM 20. All of these modes, as well as the separate acceleration and deceleration responses, were well reproducible at any cited time points. We suggest that the individual modes of HRR are induced by different states of autonomic cardiovascular reactivity: Mode A probably expresses a parasympathotonic (vagotonic), Mode C--a sympathotonic, and Mode B--an intermediate autonomic state. Thus, the individual modes of HRR to VM10 and to VM20 could be used as a method of non-invasive determination of cardiovascular autonomic reactivity.     

Mapping the cardiogenic impedance signal on the thoracic surface

The cardiogenic impedance signal from band electrodes placed in the traditional position around the neck and lower thorax was studied by mapping the location of the signal on the sternum using 10 cm strip electrodes in eight male subjects. The band current electrodes on the neck and waist were replaced with 10cm strip electrodes on the forehead and 10 cm below the xiphisternal joint, respectively, with only small changes in the dZ/dt peak amplitude and Z_o. Similarly, using a strip voltage pickup electrode at the level of the xiphisternal joint resulted in very small changes in the waveform. The amplitude of dZ/dt measured between the xiphisternal joint and points along the sternum remains small until approximately 10cm below the suprasternal notch, after which it increased linearly to the top of the neck. An average of 17 per cent and 24 per cent of the dZ/dt signal and 24 per cent and 22 per cent of the Z_o signal for supine and standing, respectively, occurs above the suprasternal notch. Replacing the current electrodes with strip electrodes on the forehead and waist caused only small changes in the signal. The position of the neck strip electrode is more critical.     

Influence of microgravity on astronauts' sympathetic and vagal responses to Valsalva's manoeuvre

When astronauts return to Earth and stand, their heart rates may speed inordinately, their blood pressures may fall, and some may experience frank syncope. We studied brief autonomic and haemodynamic transients provoked by graded Valsalva manoeuvres in astronauts on Earth and in space, and tested the hypothesis that exposure to microgravity impairs sympathetic as well as vagal baroreflex responses. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, respiration and peroneal nerve muscle sympathetic activity in four healthy male astronauts (aged 38–44 years) before, during and after the 16 day Neurolab space shuttle mission. Astronauts performed two 15 s Valsalva manoeuvres at each pressure, 15 and 30 mmHg, in random order. Although no astronaut experienced presyncope after the mission, microgravity provoked major changes. For example, the average systolic pressure reduction during 30 mmHg straining was 27 mmHg pre-flight and 49 mmHg in flight. Increases in muscle sympathetic nerve activity during straining were also much greater in space than on Earth. For example, mean normalized sympathetic activity increased 445 % during 30 mmHg straining on earth and 792 % in space. However, sympathetic baroreflex gain, taken as the integrated sympathetic response divided by the maximum diastolic pressure reduction during straining, was the same in space and on Earth. In contrast, vagal baroreflex gain, particularly during arterial pressure reductions, was diminished in space. This and earlier research suggest that exposure of healthy humans to microgravity augments arterial pressure and sympathetic responses to Valsalva straining and differentially reduces vagal, but not sympathetic baroreflex gain.     

Initial cardiovascular response on change of posture from squatting to standing

Summary The immediate cardiovascular responses on active change from the squatting (control) to the standing position differ from those obtained in the lying-to-standing manoeuvre. Without exception, the first beat after changing from squatting to standing showed a decrease in systolic, diastolic and mean pressure by 2.0±1.1 kPa (14.6±8.3 mm Hg), 1.4±1.7 kPa (10.6±12.6 mm Hg) and 1.9±1.0 kPa (13.9±7.3 mm Hg), respectively. During the 4^th or 5^th pulse after standing the pulse pressure was significantly higher than when lying (P<0.01). Mean pressure reached a minimum of 7.7±1.9 kPa (57.8±14.4 mm Hg) after 7.1±1.1s. Thereafter the blood pressure increased to a new level within about 15 s. 11 of 16 subjects demonstrated a biphasic heart rate (HR) response. The maximum HR was reached after 11.0±2.4 s of standing. In all experiments, the peaks in HR were distinctly delayed after the blood pressure clips. We conclude that an arterial baroreflex could be implicated in the immediate HR increase after a squatting-tostanding manoeuvre. The subsequent time course of the initial HR response, however, might be induced by other mechanisms.     

Haemodynamic and baroreflex responses to whole-body tilting in exercising men before and after 6 weeks of bedrest

We sought to determine whether the cardiovascular deconditioning that occurs in exercising men after prolonged (42 days) bedrest in the head-down tilt (HDT) position is primarily related to mechanical changes in the heart or to an impaired arterial-cardiac-chronotropic baroreflex. Seven subjects were studied before (C, control) and repeatedly after HDT with rapid tilting between the upright and supine positions during steady-state 50-W dynamic leg exercise. Ventricular interdependence was assumed to be an index of cardiac size; it was assessed on the basis of the initial dip of arterial pulse pressure (PP) induced by a sudden tilt from the upright to the supine position (down-tilt). Arterial-cardiac-chronotropic baroreflex sensitivity (ABS) was assessed as the ratio between tilt-induced heart rate transients and the preceding (and reciprocal) transient in arterial pressure. On the first day of recovery, the initial PP dip was −4 (2) mmHg (where 1 mmHg is 0.13 kPa), less than half of the control value; on subsequent recovery days, the initial PP dip was not significantly different from the control value. When tilting from the upright to the supine position, mean ABS ranged from 1.02 to 1.06 bpm/mmHg during three separate control sessions. Tilts in the opposite direction gave lower ABS values because of the more sluggish HR response and ranged from 0.43 to 0.45 bpm/mmHg in the control situations. ABS did not change after HDT. Our results indicate that impairments of the cardiovascular system after long-term bedrest are of haemodynamic rather than baroreflex origin. Accepted: 8 March 2000     

Systemic hypoxia affects cardiac autonomic activity and vascular hemodynamic control modulated by physical stimulation

This study investigates how various hypoxic interventions affect cardiac autonomic activity and hemodynamic control during posture change and the Valsalva maneuver. Ten healthy sedentary men exposed to 12, 15 and 21% O₂ for 1 h in a normobaric hypoxia chamber in a random order. Before and after various O₂ concentrations were administered, subjects performed the sit-up test and Valsalva maneuver, respectively. An impedance plethysmography was utilized to measure blood pressure (BP) and vascular hemodynamics, whereas spectral analysis of heart rate variability (HRV) was performed to determine cardiac autonomic activity. Analytical results can be summarized as follows: while the patient rests in a supine position, exposure to 12% O₂ reduces the ratio of lower to upper extremity systolic BP, which is accompanied by (1) suppressed arterial reactive hyperemia and increased venous flow resistance, as well as (2) decreased total power and high frequency (HF) and increased low frequency (LF) and the ratio of LF to HF. Moreover, the hypoxia-induced changes of time and frequency domains in HRV at resting supine disappear following the sit-up test, whereas this hypoxic exposure attenuates the BP and heart rate responses to the Valsalva maneuver. Conversely, resting and physical stimuli-mediated HRV and vascular hemodynamic values are unaltered by both 15 and 21% O₂ exposures. We conclude that acute hypoxic exposure affects cardiovascular autonomic functions, with reactions determined by the intervening O₂ concentrations. Moreover, the BP and cardiac autonomic responses to 12% O₂, but not 15% O₂, exposure are depressed while performing posture change and the Valsalva maneuver.     

An analysis of the relationship between transthoracic impedance variations and thoracic diameter changes

The relationship between transthoracic impedance variations and thoracic diameter changes (distance changes between the impedance-measuring electrodes) associated with both respiration and circulation was studied in 15 anaesthetised dogs. Respiratory records obtained by both impedance and inductance methods during respiration were very similar. After replacing oxygen within the lung and trachea with physiological saline, an injection of saline into the airway produced a decrease of impedance and an increase of thoracic diameter. The withdrawal of saline produced directly opposite effects. When a highly conducting solution of saline was injected into the inferior vena cava, the thoracic diameter increased simultaneously with a decrease of the impedance. Even though the thoracic-diameter response was constant and simultaneous with injections into the inferior vena cava, the orifice of the right atrium or right ventricle, the decrease of the impedance lagged behind the diameter change as the injection site was shifted distally to the lung. The impedance increased with a decrease of the thoracic diameter following reduced venous return to the right ventricle by an occlusion of the inferior vena cava. This experimental evidence suggests that the variations of the impedance on the surface of the thorax originate from conductivity changes within the lung irrespective of airway and pulmonary vascular spaces, and not from distance changes between electrodes.     

Difference in human cardiovascular response between upright and supine recovery from upright cycle exercise

Cardiovascular responses were examined in seven healthy male subjects during 10 min of recovery in the upright or supine position following 5 min of upright cycle exercise at 80% peak oxygen uptake. An initial rapid decrease in heart rate (f _c) during the early phase of recovery followed by much slower decrease was observed for both the upright and supine positions. The average f _c at the 10th min of recovery was significantly lower (P < 0.05) in the supine position than in the upright position, while they were both significantly greater than the corresponding pre-exercise levels (each P < 0.05). Accordingly, the amplitude of the high frequency (HF) component of R-R interval variability (by spectrum analysis) in both positions was reduced with a decrease in mean R-R interval, the relationship being expressed by a regression line – mean R-R interval = 0.006 × HF amplitude + 0.570 (r = 0.905, n = 28, P < 0.001). These results would suggest that the slower reduction in f _c following the initial rapid reduction in both positions is partly attributable to a retardation in the restoration of the activity of the cardiac parasympathetic nervous system. Post-exercise upright stroke volume (SV, by impedance cardiography) decreased gradually to just below the pre-exercise level, whereas post-exercise supine SV increased markedly to a level similar to that at rest before exercise. The resultant cardiac output (Q˙ _c) and the total peripheral vascular resistance (TPR) in the upright and supine positions returned gradually to their respective pre-exercise levels in the corresponding positions. At the 10th min of recovery, both average SV and Q˙ _c were significantly greater (each P < 0.005) in the supine than in the upright position, while average TPR was significantly lower (P < 0.05) in the supine than in the upright position. In contrast, immediately after exercise, mean blood pressure dropped markedly in both the supine and upright positions, and their levels at the 10th min of recovery were similar. Therefore we concluded that arterial blood pressure is maintained relatively constant through various compensatory mechanisms associated with f _c, SV, Q˙ _c, and TPR during rest and recovery in different body positions. Accepted: 4 September 1999     

Effect of propranolol on the tone of collateral arteries in patients with occlusion of the superficial femoral artery

The effect of administration of 0.5 mg propranolol into the femoral artery in eight patients with lower limb ischaemia and superficial femoral artery occlusion on collateral arterial resistance was studied in supine and tilted head-up position. Mean blood pressures were recorded directly from the femoral and popliteal artery and femoral blood flow was measured by an indicator dilution technique. After beta-receptor blockade in the supine position the collateral arterial resistance increased by 7 +/- 2%, femoral blood flow decreased 10 +/- 4%, and popliteal artery pressure increased by 4 mmHg (8 +/- 3%). During head-up tilt there was no change in femoral blood flow and collateral arterial resistance after propranolol. The peripheral vasoconstrictor effect of propranolol, therefore, seems not to be harmful to patients with vascular disease.     

Short-term cardiovascular responses to rapid whole-body tilting during exercise

Our objective was to characterize the responses of heart rate (HR) and arterial blood pressure (BP) to changes in posture during concomitant dynamic leg exercise. Ten men performed dynamic leg exercise at 50, 100, and 150 W and were rapidly and repeatedly tilted between supine (0°) and upright (80°) positions at 2-min intervals. Continuous recordings of BP and HR were made, and changes in central blood volume were estimated from transthoracic impedance. Short-lasting increases in BP were observed immediately upon tilting from the upright to the supine position (down-tilt), averaging +18 mmHg (50 W) to +31 mmHg (150 W), and there were equally short-lasting decreases in BP, ranging from −26 to −38 mmHg upon tilting from supine to upright (up-tilt). These components occurred for all pressure parameters (systolic, mean, diastolic, and pulse pressures). We propose that these transients reflect mainly tilt-induced changes in total peripheral resistance resulting from decreases and increases of the efficiency of the venous muscle pump. After 3–4 s (down-tilt) and 7–11 s (up-tilt) there were large HR transients in a direction opposite to the pressure transients. These HR transients were larger during the down-tilt (−15 to −26 beats · min⁻¹) than during the up-tilt (+13 to +17 beats · min⁻¹), and increased in amplitude with work intensity during the down-tilt. The tilt-induced HR fluctuations could be modelled as a basically linear function of an arterial baroreflex input from a site half-way between the heart and the carotid sinus, and with varying contributions of fast vagal and slow sympathetic HR responses resulting in attenuated tachycardic responses to hypotensive stimuli during exercise. Accepted: 24 August 1999     

Mechanisms of hypotensive effects of a posture change from seated to supine in humans.

The hypothesis tested was that the hydrostatic stimulation of carotid baroreceptors is pivotal to decrease mean arterial pressure at heart level during a posture change from seated to supine. In eight males, the cardiovascular responses to a 15-min posture change from seated to supine were compared with those of water immersion to the xiphoid process and to the neck, respectively. Left atrial diameter and cardiac output (rebreathing) increased similarly during the posture change and water immersion to the xiphoid process and further so during neck immersion. Mean arterial pressure decreased by 12 +/- 2 mmHg during the posture change, by 5 +/- 1 mmHg during xiphoid immersion, and was unchanged during neck immersion. Arterial pulse pressure increased by 12 +/- 3 mmHg during the posture change (P < 0.05) and less during xiphoid and neck immersion by 7 +/- 3 mmHg (P < 0.05). Total peripheral vascular resistance decreased similarly during the posture change and neck immersion and slightly less during xiphoid immersion (P < 0.05). In conclusion, the hydrostatic stimulation of carotid baroreceptors combined with some additional increase in arterial pulse pressure, which also stimulates aortic baroreceptors, accounts for more than half of the hypotensive response at heart level to a posture change from seated to supine.     

Long-term effects of captopril and atenolol in essential hypertension

Fifty patients with mild or moderate essential hypertension were randomized (double-blindly) to treatment with either captopril (n = 26) or atenolol (n = 24). Their mean supine diastolic blood pressure after placebo was 100-125 mmHg. The study included an initial dose finding phase (12 weeks) during which the dosages of captopril and atenolol were increased stepwise every second week in order to obtain normotension (supine diastolic blood pressure less than 95 mmHg). Hydrochlorothiazide was added when necessary. During the second phase of the study the patients were followed on active treatment for 2 years. After the initial 12 weeks of active treatment, recumbent and standing blood pressures had fallen significantly both in the captopril group (by 31/20 and 33/19 mmHg, p less than 0.001) and in the atenolol group (by 24/18 and 30/20 mmHg, p less than 0.01 (systolic), p less than 0.001 (diastolic)). The antihypertensive effect was maintained in both groups during long-term treatment. The antihypertensive effect of both agents was potentiated to the same extent by addition of hydrochlorothiazide. Side-effects were few and mild. It can be concluded that both captopril and atenolol are safe and effective antihypertensive drugs.