Autonomic nervous function at rest in aerobically trained and untrained oldermen

Therelationship between aerobictraining, vagal influence on the heart and ageing was examined by assessing aerobic fitness andresting heart rate variability in trained and untrained older men. Subjects were 11 trained cyclistsand runners (mean age=6±61·6 years) and 11 untrained, age-matchedmen (mean age=66±1·2 years). Heart rate variability testing involvedsubjects lying supine for 25 min during which subjects’ breathing was paced andmonitored (7·5 breaths min^?1). Heart rate variability was assessedthrough time series analysis (HRV_ts) of the interbeat interval. Results indicated thattrained older men (3·55±0·21 l min^?1) hadsignificantly (P<0·05) greater VO _2maxthan that of control subjects (2·35±0·15 l min^?1).Also, trained older men (52±1·8 beats min^?1) hadsignificantly (P<0·05) lower supine resting heart rate than that of controlsubjects (65±4·2 beats min^?1). HRV_ts at highfrequencies was greater for trained men (5·98±0·22) than for untrainedmen (5·23±0·32). These data suggest that regular aerobic exercise inolder men is associated with greater levels of HRV_ts at rest.     

Reduced cardiac sympathetic autonomic tone after long-term nasal continuous positive airway pressure in obstructive sleep apnoea syndrome

The increased sympathetic activation that occurs in obstructive sleep apnoea (OSA) may play an important role in associated morbidity. We investigated the effect of long-term (3 month) nasal continuous positive airway pressure (CPAP) on the autonomic nervous system assessed by heart rate variability (HRV). Fourteen patients (12 men), mean age 61·4 ± 8·1 years, with OSA underwent continuous synchronized electrocardiographic and polysomnographic monitoring. The apnoea/hypopnoea index (AHI) decreased from 50·6 ± 13·7 to 2·2 ± 2·5 events h^?1 after CPAP. HRV analysis showed significant decreases in low frequency (LF; from 7·12 ± 1·06 to 6·22 ± 1·18 ln ms² Hz^?1; P<0·001), high frequency (HF; from 5·91 ± 0·87 to 5·62 ± 0·92 ln ms² Hz^?1; P<0·05) and LF/HF (from 1·21 ± 0·12 to 1·11 ± 0·15 ln ms² Hz^?1; P<0·001) when the patients were asleep. The decrease in LF/HF was prolonged into the daytime (from 1·33 ± 0·22 to 1·24 ± 0·21 ln ms² Hz^?1; P<0·001). Treatment of OSA by CPAP significantly reduced the parameters of cardiac sympathetic tone, a favourable effect.     

High dose ascorbic acid does not reverse central sympathetic overactivity in chronic heart failure

What is known and Objective: The increased central sympathetic activity typically associated with chronic heart failure (CHF) is probably mediated by formation of reactive oxygen species (ROS) in the brain. Our objective was to undertake a trial to test our hypothesis that administration of the well‐known antioxidant and ROS scavenger ascorbic acid, would reverse or reduce the sympathetic overactivity in CHF patients. Methods: In a prospective, randomized, placebo‐controlled, double‐blind, cross‐over trial, 11 CHF patients were treated with ascorbic acid 2 g/day or placebo for 3 days. At the end of each treatment period, sympathetic nervous system activity was measured by microneurography for direct muscle sympathetic nerve activity (MSNA) recording, analysis of heart rate variability (HRV) and measurement of plasma norepinephrine concentrations. Results: During ascorbic acid administration, plasma vitamin C levels were higher than during placebo (74·9 ± 6·0 μmol/L vs. 54·8 ± 4·6 μmol/L, P = 0·03). Ascorbic acid had no effect on sympathetic activity: MSNA (ascorbic acid: 66·8 ± 3·3 vs. placebo 66·9 ± 3·2 bursts/100 beats, P = 0·98). In addition, HRV and plasma norepinephrine levels did not differ. What is new and Conclusion: Short‐term administration of the antioxidant ascorbic acid in CHF patients does not reverse the increased sympathetic activity as measured by microneurography, HRV and plasma norepinephrine levels. The use of higher oral dosages seems not feasible due to accompanying side effects.     

Determination of baroreflex gain using auto-regressive moving-average analysis during spontaneous breathing

The heart rate component of the arterial baroreflex gain (BRG) was determined with auto-regressive moving-average (ARMA) analysis during each of spontaneous (SB) and random breathing (RB) protocols. Ten healthy subjects completed each breathing pattern on two different days in each of two different body positions, supine (SUP) and head-up tilt (HUT). The R–R interval, systolic arterial pressure (SAP) and instantaneous lung volume were recorded continuously. BRG was estimated from the ARMA impulse response relationship of R–R interval to SAP and from the spontaneous sequence method. The results indicated that both the ARMA and spontaneous sequence methods were reproducible (r=0·76 and r=0·85, respectively). As expected, BRG was significantly less in the HUT compared to SUP position for both ARMA (mean ± SEM; 3·5 ± 0·3 versus 11·2 ± 1·4 ms mmHg^–1; P<0·01) and spontaneous sequence analysis (10·3 ± 0·8 versus 31·5 ± 2·3 ms mmHg^–1; P<0·001). However, no significant difference was found between BRG during RB and SB protocols for either ARMA (7·9 ± 1·4 versus 6·7 ± 0·8 ms mmHg^–1; P=0·27) or spontaneous sequence methods (21·8 ± 2·7 versus 20·0 ± 2·1 ms mmHg^–1; P=0·24). BRG was correlated during RB and SB protocols (r=0·80; P<0·0001). ARMA and spontaneous BRG estimates were correlated (r=0·79; P<0·0001), with spontaneous sequence values being consistently larger (P<0·0001). In conclusion, we have shown that ARMA-derived BRG values are reproducible and that they can be determined during SB conditions, making the ARMA method appropriate for use in a wider range of patients.     

The exercise heart rate profile in master athletes compared to healthy controls

Endurance exercise protects the heart via effects on autonomic control of heart rate (HR); however, its effects on HR indices in healthy middle‐aged men are unclear. This study compared HR profiles, including resting HR, increase in HR during exercise and HR recovery after exercise, in middle‐aged athletes and controls. Fifty endurance‐trained athletes and 50 controls (all male; mean age, 48·7 ± 5·8 years) performed an incremental symptom‐limited exercise treadmill test. The electrocardiographic findings and HR profiles were evaluated. Maximal O₂ uptake (52·6 ± 7·0 versus 34·8 ± 4·5 ml kg^?1 min^?1; P<0·001) and the metabolic equivalent of task (15·4 ± 1·6 versus 12·2 ± 1·5; P<0·001) were significantly higher in athletes than in controls. Resting HR was significantly lower in athletes than in controls (62·8 ± 6·7 versus 74·0 ± 10·4 beats per minute (bpm), respectively; P<0·001). Athletes showed a greater increase in HR during exercise than controls (110·1 ± 11·0 versus 88·1 ± 15·4 bpm; P<0·001); however, there was no significant between‐group difference in HR recovery at 1 min after cessation of exercise (22·9 ± 5·6 versus 21·3 ± 6·7 bpm; P = 0·20). Additionally, athletes showed a lower incidence of premature ventricular contractions (PVCs) during exercise (0·0% versus 24·0%; P<0·001). Healthy middle‐aged men participating in regular endurance exercise showed more favourable exercise HR profiles and a lower incidence of PVCs during exercise than sedentary men. These results reflect the beneficial effect of endurance training on autonomic control of the heart.     

Cholinergic blockade and the mesenteric artery response to head-up tilt-induced central hypovolaemia

The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head-up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.v. glycopyrron. During supine rest, cholinergic blockade increased heart rate from 58 ± 3 to 106 ± 6 beats min^?1 (mean ± SE) and mean arterial pressure from 81 ± 3 to 97 ± 4 mmHg (P<0·01) and it reduced the cardiac stroke volume from 89 ± 6 to 59 ± 7 ml (P<0·01) with no significant effect on the SMA diameter and blood flow velocities. HUT provoked a further increase in heart rate to 134 ± 5 beats min^?1(P<0·01) and a reduction in stroke volume to 45 ± 4 ml (P<0·01). The early diastolic velocity increased from ?51 ± 4 to 6 ± 8 cm s^?1 during the normotensive stage of HUT and further to 21 ± 9 cm s^?1 during the hypotensive stage with a reduction in mean arterial pressure from 97 ± 4 to 73 ± 7 mmHg (P<0·01) but, in contrast to control HUT (without cholinergic blockade), the end-diastolic velocity did not change significantly. Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance. Likewise, during hypovolaemia, a glycopyrron-induced inhibition in diastolic velocity supports an increase in SMA impedance. The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.     

Effects of physical exercise on insulin absorption in insulin-dependent diabetics. A comparison between human and porcine insulin

Summary. Nine insulin-dependent diabetics with undetectable plasma C-peptide (<0·05 nmol 1^-1) and without insulin antibodies (insulin binding to IgG<0·05 Ul^-1) received subcutaneous injections of 10 U ¹²⁵I-labelled soluble human or porcine insulin in the thigh on 2 consecutive days. Disappearance rates of ¹²⁵I were monitored continuously by external counting and plasma insulin levels were determined during rest for 30 min, bicycle exercise of moderate intensity for 40 min, and 60 min recovery. Subcutaneous blood flow was measured concomitantly in the contralateral thigh by the ¹³³Xenon clearance technique. During the initial period of rest human insulin was absorbed approximately 40% faster than its porcine analogue (first order rate constants 0·37±0·06 vs 0·27±0·06% min^-1, P<0·05) and the increment of the area under the plasma insulin curve was greater after hum-ii than after porcine insulin (184±46 vs 112±42 mUl^-1 min, P<0·05). Exercise enhanced the absorption rates for both ¹²⁵I-insulins to 0·50±0·06 and 0·48±0·10% min^-1 for human and porcine insulin, respectively (P<0·05). This increase was less pronounced for human compared to porcine insulin (49±19 vs 105±40%, P=0·06). During exercise plasma insulin rose to 37±5 mUl^-1 after human and 30±5 mUl^-1 after porcine insulin and the areas under the plasma insulin curves were similar. During the recovery phase the absorption rates decreased slightly compared to the exercise value for both insulins. The blood glucose lowering effect was similar for the two insulins. Subcutaneous blood flow was not significantly altered by exercise in either group. It is concluded that during rest human soluble insulin is more rapidly absorbed than porcine insulin. Physical exercise tends to increase porcine insulin absorption more and eliminates the basal difference in the absorption kinetics between human and porcine insulin. The increased insulin absorption during exercise is not coupled to corresponding changes in the subcutaneous blood flow.     

Leg uptake of calcitonin gene‐related peptide during exercise in spinal cord injured humans

Exercise‐induced increases in cardiac output (CO) and oxygen uptake (VO₂) are tightly coupled, as also in absence of central motor activity and neural feedback from skeletal muscle. Neuromodulators of vascular tone and cardiac function – such as calcitonin gene related peptide (CGRP) – may be of importance. Spinal cord injured individuals (six tetraplegic and four paraplegic) performed electrically induced cycling (FES) with their paralyzed lower limbs for 29 ± 2 min to fatigue. Voluntary cycling performed both at VO₂ similar to FES and at maximal exercise in six healthy subjects served as control. In healthy subjects, CGRP in plasma increased only during maximal exercise (33·8 ± 3·1 pmol l^?1 (rest) to 39·5 ± 4·3 (14%, P<0·05)) with a mean extraction over the working leg of 10% (P<0·05). Spinal cord injured individuals had more pronounced increase in plasma CGRP (33·2 ± 3·8 to 46·9 ± 3·6 pmol l^?1, P<0·05), and paraplegic and tetraplegic individuals increased in average by 23% and 52%, respectively, with a 10% leg extraction in both groups (P<0·05). The exercise induced increase in leg blood flow was 10–12 fold in both spinal cord injured and controls at similar VO₂ (P<0·05), whereas CO increased more in the controls than in spinal man. Heart rate (HR) increased more in paraplegic subjects (67 ± 7 to 132 ± 15 bpm) compared with controls and tetraplegics (P<0·05). Mean arterial pressure (MAP) was unchanged during submaximal exercise and increased during maximal exercise in healthy subjects, but decreased during the last 15 min of exercise in the tetraplegics. It is concluded that plasma CGRP increases during exercise, and that it is taken up by contracting skeletal muscle. The study did not allow for a demonstration of the origin of the CGRP, but its release does not require activation of motor centres. Finally, the more marked increase in plasma CGRP and the decrease in blood pressure during exercise in tetraplegic humans may indicate a role of CGRP in regulation of vascular tone during exercise.     

Effect of bicycle exercise on insulin absorption and subcutaneous blood flow in the normal subject

Summary. Elimination of 8 units ¹²⁵I-insulin and ^99mTc-pertechnetate from a subcutaneous depot on the thigh or the abdomen was studied at rest and during intense bicycle exercise in healthy postabsorptive volunteers. Disappearance rates of the tracers as well as plasma insulin and glucose concentrations were determined before, during and after the 20 min exercise period, and compared to corresponding values obtained during a non-exercise, control study on another day. Leg exercise caused a two-fold increase in the rate of ¹²⁵I-insulin disappearance from a leg depot (first-order rate constants rose from 0·68 ± 0·15 to 1·12 ± 0·12%·min^-1, P <0·05), but had no significant effect on the rate of disappearance from an abdominal depot (rate constants were 0·75 ±0·17 and 0·87±0·18%·min^-1 at rest and during exercise, respectively). ^99mTc-pertechnetate clearance from leg or abdomen showed no significant change during exercise, indicating that subcutaneous blood flow was unaltered. Leg, but not abdominal, injection of insulin was associated with a greater rise in plasma insulin during exercise than at rest. The average difference between exercise and control insulin area-under-curve in the leg group (1426 ± 594%·min) was significantly greater (P <0·05) than that from the abdominal group (298 ±251%· min). When the data from the two study groups were pooled, a direct relationship was found to exist between the change in ¹²⁵I-insulin disappearance rate and the change in plasma insulin concentration (r=0·61, P <0·02). Plasma glucose levels fell throughout the observation period both during the exercise and the control study, following leg as well as abdominal injection. The glucose decremental area was greater during exercise than at rest both following leg (P <0·05) and abdominal injection (P <0·01). The exercise-induced mean reduction in plasma glucose was 60% lower following abdominal injection, but this difference was not significant.     

Systemic interleukin-1 α and interleukin-2 secretion in response to acute stress and to corticotropin-releasing hormone in humans*

Abstract Acute stress results in activation of the hypothalamic-pituitary-adrenal (HPA) axis. ACTH and cortisol secretion is stimulated by corticotropin-releasing hormone (CRH). It has also been shown that activation of the HPA axis during stress is accompanied by changes in the immune response. However, little is known about the influence of acute stress on the release of cytokines such as inteleukin-1 (IL-1) or interleukin-2 (IL-2). In this study, we determined serum IL-1 α and IL-2 levels in 19 patients undergoing the acute stress of angioplasty for coronary artery disease. A second protocol was devised to determine serum IL-1 α and IL-2 concentrations as well as lymphocyte subpopulations in 10 normal volunteers receiving 1 μ kg^-1 human CRH intravenously. Finally, IL-1 α concentrations were measured in CRH-incubated mononuclear cell (MNC) and monocyte cultures. In response to the stress of angioplasty, ACTH and cortisol as well as IL-1 α and IL-2 concentrations were clearly above baseline levels (IL-1 α, mean ± SEM, baseline: 1·39 ± 0·34 ng ml^-1, after angioplasty: 2·64 ± 0·73 ng ml^-1, P < 0·05; IL-2, baseline: 1·2 ± 0·13 ng ml^-1, after angioplasty: 2·8 ± 1·14 ng ml, P < 0·05). A similar pattern was obtained in normal subjects in response to CRH (IL-1 α, baseline: 0·8 ± 0·2 ng ml^-1, after angioplasty: 3·7 ± 1·4 ng ml^-1, P < 0·05; IL-2, baseline: 1·9 ± 0·4 ng ml^-1, after angioplasty: 5·4 ± 2·2 ng ml^-1, P < 0·02). The percentage of IL-2 receptor-positive lymphocytes rose from 3·9 ± 1·2% to 6·2 ± 1·6% (P < 0·05), the relative number of CD-3 lymphocytes rose from 74·5 ± 1·6% to 78·3 ± 2·0% (P < 0·05). No significant changes were observed in the number of CD-4, CD-8, natural killer and B cells. In vitro, IL-1 α concentrations in cultures containing CRH were not significantly different from control cultures. Our data demonstrate significant activation of the HPA axis and secretion of IL-1 α and IL-2 in response to both angioplasty and CRH. Furthermore, CRH administration resulted in activation of the cellular immune system (indicated by an increase in IL-2 receptor positive lymphocytes). Our in vitro data suggest that CRH may not directly act on blood mononuclear cells to induce IL-1 α release or, alternatively, sources other than blood mononuclear cells may account for the elevated IL-1 α levels observed in vivo. We conclude that CRH may play a major role in neuroendocrine-immune interactions during acute stress.     

Endothelin‐1: increased plasma clearance,pulmonary affinity and renal vasoconstriction in young smokers

Pulmonary and renal haemodynamics and elimination of endothelin‐1 (ET‐1) were studied in six young smokers in response to 20 min intravenous infusion of ET‐1 (4 pmol kg^–1 min^–1) after smoking. At 20 min of ET‐1 infusion fractional ET‐1 extractions in the lungs and kidneys were 60 ± 2 and 60 ± 7%, respectively. Cardiac output and renal blood flow (RBF) fell by 18 ± 4% (P<0·05) and 34 ± 5% (P<0·01). Mean systemic arterial pressure increased (P<0·05) whereas pulmonary pressures were unchanged. Compared with previously published data in non‐smokers ( 38 , 39 ) basal arterial ET‐1 and ET‐1‐values during ET‐1 infusion were lower with a more rapid return to basal value. Smokers had higher pulmonary extraction of ET‐1 at the same pulmonary arterial concentration (P<0·05). RBF reduction was more pronounced (P<0·05). Systemic vascular resistance increased while pulmonary vascular resistance did not increase as in non‐smokers. Increased plasma clearance and more efficient pulmonary elimination of ET‐1 lowers the arterial level in young smokers. In addition ET‐1 evokes more pronounced renal vasoconstriction in these individuals.     

Impact of functional training on cardiac autonomic modulation,cardiopulmonary parameters and quality of life in healthy women

Functional training (FT) promotes benefits in various physical abilities; however, its effect on autonomic modulation, cardiorespiratory parameters and quality of life in the healthy adult population is unknown, and thus, the aim of this study was to evaluate the influence of FT on these variables in healthy young women. The study consisted of 29 women, distributed into two groups: the FT Group (FTG; n = 13; 23 ± 2·51 years; 21·90 ± 2·82 kg m^?²) and the Control Group (CG; n = 16; 20·56 ± 1·03 years; 22·12 ± 3·86 kg m^?²). The FTG performed periodized FT for 12 weeks, three times a week. The following were evaluated: autonomic modulation (heart rate variability), cardiorespiratory parameters and quality of life (SF‐36 Questionnaire). The Student's t‐test for unpaired data or the Mann–Whitney test was used to compare the differences obtained between the final moment and the initial moment of the studied groups (P<0·05). The FTG demonstrated significant improvements in quality of life and autonomic modulation (P<0·05), but not in the cardiorespiratory parameters. Functional training was able to produce improvements in autonomic modulation and quality of life.     

Release of atrial natriuretic peptide during pulmonary arteryclamping in man

The vasodilating hormone atrial natriuretic peptide (ANP) issecreted from the heart in response to atrial wall stretch, but knowledge of the time course ofANP secretion after acute releasing stimuli is limited. The time from stimulus to release ofimmunoreactive atrial natriuretic peptide (irANP) was investigated by unilaterally clamping thepulmonary artery in 12 patients undergoing pulmonary surgery. The second messenger toANP-induced vascular relaxation, plasma cyclic guanosine mono-phosphate (p-cGMP), wasmeasured as an indirect marker of the vascular effects of ANP. Immediately after appliedclamping, p-irANP (baseline level 15·4±2·9 pmol l^?1) started to increase, reaching a significant, although moderate, increase(11±4%, P<0·05) after 2 min. This elevation of p-irANPremained during the entire clamping period (+13±6%, P<0·05 vs. baseline). Within 1 min of declamping, p-irANP returned to the baselinelevel. No conclusive alterations in p-cGMP were observed. The prompt ANP response to theapplied stimulus, and the return to baseline after declamping, may indicate the presence of ashort time-acting releasing mechanism of ANP.     

Haemodynamic response to exercise in patients with alcoholic liver cirrhosis

Summary. Physical work capacity was evaluated by a multistage bicycle exercise test in 29 patients, 22 men and seven women aged 35–61 years (mean 49) with alcoholic liver cirrhosis and in a sex- and age-matched control group. The maximal work load was reduced in the patient group, mean 122 vs. 186 watts in men (P < 0·001), and 60 vs. 119 watts in women (P < 0·005). Resting heart rate was higher in patients (91 vs. 78 beats × min¹, (P < 0·005), and the maximal heart rate was lower (159 vs. 170 beats × min^-1, (P < 0·001) compared with controls. Thirteen of 29 (45%) patients compared with 5 of 29 (17%) control subjects had an increase in left ventricular ejection fraction of ≤5% during exercise (P < 0·05). The present results suggest that an impaired capacity of the cardiac function to respond adequately to physical stress may at times contribute to the reduced physical work capacity seen in patients with alcoholic liver cirrhosis.     

Effects of intense exercise training on endothelium-dependent exercise-induced vasodilatation

To determine whether intense exercise training affects exercise-induced vasodilatation, six subjects underwent 4 weeks of handgrip training at 70% of maximal voluntary contraction. Exercise forearm vascular conductance (FVC) responses to an endothelium-dependent vasodilator (acetylcholine, ACH; 15, 30, 60 μg min^?1) and an endothelium-independent vasodilator (sodium nitroprusside, SNP; 1·6, 3·2, 6·4 μg min^?1) and FVC after 10 min of forearm ischaemia were determined before and after training. Training elicited significant (P<0·001) increases in grip strength (43·4 ± 2·3 vs. 64·1 ± 3·5 kg, before vs. after, mean ± SEM), forearm circumference (26·7 ± 0·4 vs. 27·9 ± 0·4 cm) and maximal FVC (0·4630 ± 0·0387 vs. 0.6258 ± 0·0389 units, P<0·05). Resting FVC did not change significantly with training (0·0723 ± 0·0162 vs. 0.0985 ± 0·0171 units, P>0·4), but exercise FVC increased (0·1330 ± 0·0190 vs. 0.2534 ± 0·0387 units, P<0·05). Before and after the training, ACH increased exercise FVC above the control (no drug) exercise FVC, whereas SNP did not. Training increased (P<0·05) the exercise FVC responses to ACH (0·3344 ± 0·1208 vs. 0.4303 ± 0·0858 units, before vs. after training, 60 μg min^?1) and SNP (0·2066 ± 0·0849 vs. 0.3172 ± 0·0628 units, 6·4 μg min^?1). However, these increases were due to the increase in control (no drug) exercise FVC, as the drug-associated increase in exercise FVC above control did not differ between trials (P>0·6). These results suggest that exercise FVC is increased by both exercise training and stimulating the release of endothelium-dependent vasodilators. However, training does not affect the vascular response to these vasodilators.     

Mixed venous blood temperature response to exercise in heart failure patients treated with short-term vasodilators

Summary. Deep-body or core temperature decreases during exercise in patients with heart failure, primarily due to the circulatory inadequacies associated with the pathophysiology of this condition. Vasodilators are commonly used to treat patients suffering from heart failure because these drugs improve total cardiac output and blood-flow to the regional circulations. In heart failure patients, the core temperature response to exercise should also be affected if the circulation is improved by vasodilators. Patients with severe heart failure were studied at rest and during upright bicycle exercise before, and after, short-term treatment with vasodilators (2-minoxidil, 3-hydralazine, 5-captopril). Their heart rate increased significantly (P<005) from rest to exercise before (87±15–109±14 beats/min), and after 89±13–112±15 beats/min) vasodilators, but there was no drug-related affect on these changes. Mean arterial and pulmonary capillary wedge pressures were significantly (P<0–05) decreased at rest and after the administration of vasodilators (mean arterial pressure 88±7 mmHg before; 77±8 mmHg after; pulmonary capillary wedge pressure 25±8 mmHg before, 19±9 mmHg after). During exercise, the increases in mean arterial and pulmonary capillary wedge pressures were not significantly different from the before vasodilator values (mean arterial pressure 92±14 mmHg before, 87±14 mmHg after; pulmonary capillary wedge pressure 31±11 mmHg before, 29± 11 mmHg after). Vasodilators increased cardiac output significantly (P<0–05) at rest (3-1 ±0–6 litre/min to 4-1 ± 1 1 litre/m) and during exercise (4–8±-2 litre/min-5–6±l-7 litre/min). The core temperature (mixed venous blood temperature) decreased significantly (P<0–05) during exercise from 37-04±0–62^oC to 36–65±0–65^oC, before treatment with vasodilators. After administration of vasodilators, resting core temperature was not significantly different (36–95±0–54^oC) and still decreased significantly (P<0–05) during exercise to 36–73±0–53^oC. This decrease was significantly (P<0–05) different from the core temperature response before the administration of vasodilators. We conclude that heart failure patients, treated with short-term vasodilators, have an     

Pulmonary vasodilatation and augmentation of right ventricular function following terbutaline infusion in severe chronic pulmonary disease

Summary. Twenty patients with a median age of 61 years and a median forced expired volume in 1 s (FEV₁) after bronchodilatating therapy of 0·55 1 were studied in order to measure the effect of intravenous terbutaline on bronchial tone, cardiac function, pulmonary haemodynamics, gas exchange, and oxygen transport capacity during rest and in 10 patients during exercise. Terbutaline infusion during rest resulted in an increase in heart rate from 84 to 103 beats min^-1 (P < 0·01), a decrease in mean systemic arterial pressure from 95 to 80 mmHg (P < 0·02), an unchanged mean pulmonary arterial pressure (18 mmHg), an increase in cardiac index from 2·89 to 3·86 1 min^-1 m^-2 (P < 0·01), an increase in right ventricular ejection fraction from 45 to 53% (P < 0·01), an increase in left ventricular ejection fraction from 63 to 67% (NS), an unchanged arterial oxygen tension, and an increase in calculated oxygen delivery from 533 to 638 ml O₂ min^-1 m^-2 (P < 0·01). During exercise terbutaline infusion resulted in an increase in heart rate from 108 to 120 beats min^-1 (P < 0·05), a decrease in mean systemic arterial pressure from 117 to 106 mmHg (P < 0·01), a decrease in mean pulmonary arterial pressure from 29 to 22 mmHg (P < 0·01), an increase in cardiac index from 4·53 to 4·64 min^-1 m^-2 (NS), an unchanged arterial oxygen tension, and an increase in the calculated oxygen delivery from 834 to 856 ml O₂ min^-1 m^-2 (NS). It was concluded that terbutaline augments right ventricular function: increases right ventricular ejection fraction and decreases right ventricular end-diastolic volume, and further decreases pulmonary vascular resistance without decreasing arterial oxygen tension, and increases oxygen delivery in patients with chronic pulmonary disease during rest and exercise.     

Electrocardiographic and vectorcardiographic findings in asymptomatic young men with primary T-wave abberations in the electrocardiogram. Relationship to sympatho-adrenal activity at rest and during different stress tests

Summary. Twelve asymptomatic men aged 18–19 years with flat, notched or inverted precordial T waves without concomitant ST depression (group T) were compared to thirteen age-matched controls with normal electrocardiograms (group C). Orthogonal leads, spatial vectorcardiography and sympatho-adrenal activity, as reflected by plasma catecholamines, were studied at rest and during mental stress (Stroop's colour word conflict test), isometric exercise (hand grip) and a cold pressor test. The groups had similar heart volumes and physical work capacity. Group T showed higher resting supine systolic blood pressure (140±15 mmHg vs. 121±8 mmHg, P<0·001) and plasma noradrenaline (1·82±0·79 nmol 1^-1vs. 1·25±0·49 nmol 1<sp>^-1, P<0·05) whereas heart rate, diastolic blood pressure and plasma adrenaline were similar in the two groups at rest. Increases in diastolic blood pressure and plasma adrenaline were larger in group T in connection with each of the stressful provocations. The magnitude of the T-wave aberrations in the electrocardiogram and the orthogonal leads in the vectorcardiogram as well as the spatial QRS-T angle were positively correlated to the plasma noradrenaline levels at rest. Changes of the T-wave aberrations in connection with stress were variable. The changes were positively correlated to heart rate and adrenaline during mental stress, to adrenaline during isometric exercise and to heart rate and noradrenaline during cold provocation. The present study demonstrates increased sympathetic tone at rest and increased reactivity in connection with stress in otherwise healthy young subjects selected on the basis of T-wave aberrations often considered as indicative of organic heart disease. The findings suggest that the T-wave aberrations were caused by increased sympathetic discharge.     

Haematocrit,plasma volume and noradrenaline in humans during simulated weightlessness for 42 days

Previous results from our laboratory demonstrate that changes in haematocrit (Hct) and haemoglobin concentration (Hb) underestimate the relative (%) change in plasma volume (PV) in seated subjects during simulation of weightlessness by water immersion. Therefore, we examined whether changes in Hct and Hb would accurately reflect the changes in PV in seven subjects during simulation of weightlessness by another model, 6° head-down tilted bed rest (HDBR), for 42 days. Since we have previously observed unexpectedly high plasma levels of noradrenaline (NA) in astronauts during space flight, we also took the opportunity to measure this variable. The measurements were compared with those of the supine horizontal position before and after HDBR. During HDBR, PV measured by the Evans blue dye dilution technique decreased by 6·1±2·8% (P<0·05) on day 2 and 9·6±2·2% (P<0·05) on the 42nd day compared with that of the supine, horizontal position. Based on changes in Hct and Hb, PV decreased similarly by 8·3±2·8 and 10·2±3·2% (P<0·05) respectively. There were no differences comparing the results of the two methods (P>0·05). Forearm venous plasma NA was unchanged during the whole course of HDBR compared with that of the pre-HDBR supine position. It is concluded that changes in Hct and Hb reliably reflect the changes in PV comparing prolonged HDBR with the pre- and post-HDBR horizontal, supine position. Thus, changes in Hct and Hb might accurately reflect the change in PV during weightlessness in humans provided that the horizontal supine position is used as the ground-based reference. Furthermore, the results of this study, as well as of previous studies from space, confirm that NA release is unchanged or even increased during weightlessness.     

Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans

The purpose of this investigation was to test the hypothesis that peripheral vasoconstriction and orthostatic tolerance are associated with increased circulating plasma concentrations of noradrenaline, vasopressin and renin–angiotensin. Sixteen men were categorized as having high (HT, n=9) or low (LT, n=7) tolerance to lower body negative pressure (LBNP) based on whether the endpoint of their pre‐syncopal‐limited LBNP (peak LBNP) exposure exceeded ?60 mmHg. The two groups were matched for age, height, weight, leg volume, blood volume and maximal oxygen uptake, as well as baseline blood volume and plasma concentrations of vasoactive hormones. Peak LBNP induced similar reductions in mean arterial pressure in both groups. The reduction in legarterial pulse volume (measured by impedance rheography), an index of peripheral vascular constriction, from baseline to peak LBNP was greater (P<0·05) in the HT group (?0·041 ± 0·005 ml 100 ml^?1) compared to the reduction in the LT group (?0·025 ± 0·003 ml 100 ml^?1). Greater peak LBNP in the HT group was associated with higher (P<0·05) average elevations in plasma concentrations of vasopressin (pVP, Δ=+7·2 ± 2·0 pg ml^?1) and plasma renin–angiotensin (PRA, Δ=+2·9 ± 1·3 ng Ang II ml^?1 h^?1) compared to average elevations of pVP (+2·2 ± 1·0 pg ml^?1) and PRA (+0·1 ± 0·1 ng Ang II ml^?1 h^?1) in the LT group. Plasma noradrenaline concentrations were increased (P<0·05) from baseline to peak LBNP in both HT and LT groups, with no statistically distinguishable difference between groups. These data suggest that the renin–angiotensin and vasopressin systems may contribute to sustaining arterial pressure and orthostatic tolerance by their vasoconstrictive actions.