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Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 127 records · Page 7Linked to original sources
PubMed1995

Effect of epidural anaesthesia on dorsal pedis arterial diameter and blood flow.

In nine subjects the influence of low (LE: blockade at or below the umbilicus; Th. 10) and high epidural anaesthesia (HE: block above the umbilicus) on vascular tone was evaluated by high frequency ultrasound (20 mHz) determined luminal diameter and a Doppler (8 mHz) assessment of mean blood flow velocity (Vmean) in the dorsalis pedis artery. The LE was induced by 0.5% bupivacain through a catheter at L3-L4, and HE was established by further infusion. Resting blood pressure and heart rate were not affected by LE or HE. One subject developed selective thoracic anaesthesia, and another was blocked on the contralateral side only. In the seven adequately blocked subjects, the luminal diameter of the dorsalis pedis artery increased from 1.70 (1.25-1.93) to 1.90 (1.75-2.23) mm during LE (+12%) and further to 2.08 (1.83-2.96) mm during HE (22%; P < 0.05). The Vmean was similar during control (7[4-26] cm s-1) and LE (12[4-55] cm s-1), but increased during HE to 35(12-78 cm s-1 (+500%; P < 0.05). Thus, arterial blood flow was higher during LE (21[7-98] ml min-1; +263%) and HE (94[21-177] ml min-1; +1175%) than at rest (8[7-36] ml min-1; P < 0.05). This study quantified the importance of sympathetic nerve activity for vascular tone and in turn blood flow in an artery of a resting human limb, as the diameter and Vmean increased with progressive epidural anaesthesia.

Adult↗
PubMed1995

Brain and muscle oxygen saturation during head-up-tilt-induced central hypovolaemia in humans.

Near-infrared spectrophotometry-determined cerebral (ScO2) and muscle oxygen saturations (SmO2) were followed in 15 volunteers during passive 50 degrees head-up-tilt-induced central hypovolaemia, and in nine volunteers during ventilatory manoeuvres affecting arterial carbon dioxide tension. During head-up tilt, mean arterial pressure [MAP, 88 (77-118) to 97 (80-136) mmHg, median and range] and heart rate [HR; 66 (49-77) to 87 (42-132) beats min-1 P < 0.01] increased, but after 22 (1-45) min they declined [to 61 (40-91) mmHg and 69 (38-109) beats min-1, respectively, P = 0.001] and pre-syncopal symptoms developed. Central hypovolaemia was indicated by an increased thoracic electrical impedance, and a decreased cardiac output and central venous oxygen saturation. The arterial oxygen saturation, pulmonal oxygen uptake and skin temperatures remained constant. The ScO2 remained stable at 72 (62-77)% until the pre-syncopal incidence, when it decreased to 62 (31-73)% (P = 0.001), and tilt down made it increase to 75 (36-87)% (P < 0.05) before the recovery value was established. In contrast, SmO2 decreased during tilting [75(70-87) to 65 (53-70)%], and recovered to 70 (53-83)%, P < 0.01) during the hypotensive episode. The end-tidal CO2 tension decreased only during tilt-up. The ScO2 decreased, and SmO2 increased during hyperventilation, and ScO2 increased during breathing of 5% carbon dioxide. Rebreathing from a bag made SmO2 decrease and resulted in a biphasic ScO2 response: it first increased and subsequently decreased. Cardiovascular changes during tilt were not reflected in skin temperature. The ScO2 reflected the maintained autoregulation of cerebral blood flow until the perfusion pressure decreased markedly. In contrast, SmO2 mirrored muscle vasoconstriction early during tilt, and vasodilatation when pre-syncopal symptoms appeared.

Adult↗
PubMed1995

Reduced arterial diameter during static exercise in humans.

In eight subjects luminal diameter of the resting limb radial and dorsalis pedis arteries was determined by high-resolution ultrasound (20 MHz). This measurement was followed during rest and during 2 min of static handgrip or of one-leg knee extension at 30% of maximal voluntary contraction of another limb. Static exercise increased heart rate and mean arterial pressure, which were largest during one-leg knee extension. After exercise heart rate and mean arterial pressure returned to the resting level. No changes were recorded in arterial carbon dioxide tension, and the rate of perceived exertion was approximately 15 units after both types of exercise. The dorsalis pedis arterial diameter was 1.50 +/- 0.20 mm (mean and SE) and the radial AD 2.45 +/- 0.12 mm. During both types of contractions the luminal diameters decreased approximately 3.5% within the first 30 s (P < 0.05), and during one-leg knee extension they continued to decrease to a final exercise value 7.6 +/- 1.1% lower than at rest (P < 0.05). Thus, they became smaller than during the handgrip. After exercise resting values were reestablished. When the arterial diameter was expressed in relation to mean arterial pressure for the radial and dorsalis pedis artery was 22 +/- 3 and 28 +/- 3% lower during handgrip than the relation during rest, respectively. After one-leg knee extension both arteries reached 30 +/- 4% lower values. This study demonstrated arterial constriction in the resting limbs within the first 30 s of static exercise, and continued constriction during one-leg knee extension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Sympathetic influence on cardiovascular responses to sustained head-up tilt in humans.

Sympathetic beta-adrenergic influences on cardiovascular responses to 50 degrees head-up tilt were evaluated with metoprolol (beta 1-blockade; 0.29 mg kg-1) and propranolol (beta 1 and beta 2-blockade; 0.28 mg kg-1) in eight males. A normotensive-tachycardic phase was followed by a hypotensive-bradycardic episode associated with presyncopal symptoms after 23 +/- 3 min (control, mean +/- SE). Head-up tilt made thoracic electrical impedance (3.0 +/- 1.0 omega), mean arterial pressure (MAP, 86 +/- 4-93 +/- 4 mmHg), heart rate (HR, 63 +/- 3-99 +/- 10 beats min-1) and total peripheral resistance (TPR, 15 +/- 1-28 +/- 4 mmHg min L-1) increase, while central venous oxygen saturation (74 +/- 2-58 +/- 4%), cardiac output (5.7 +/- 0.1-3.1 +/- 0.3 L min-1), stroke volume (95 +/- 6-41 +/- 5 mL) and pulse pressure (55 +/- 4-49 +/- 4 mmHg) decreased (P < 0.05). Central venous pressure decreased during head-up tilt (7 +/- 2-0 +/- 1 mmHg), but it remained stable during the sustained tilt. At the appearance of presyncopal symptoms MAP (49 +/- 3 mmHg), HR (66 +/- 4 beats min-1) and TPR (15 +/- 3 mmHg min L-1) decreased (P < 0.05). Neither metoprolol or propranolol changed tilt tolerance or cardiovascular variables, except for HR that remained at 57 +/- 2 (metoprolol) and 55 +/- 3 beats min-1 (propranolol), and MAP that remained at 87 +/- 5 mmHg during the first phase with metoprolol. In conclusion, sympathetic activation was crucial for the heart rate elevation during normotensive head-up tilt, but not for tilt tolerance or for the associated hypotension and bradycardia.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1995

Dynamic exercise enhances regional cerebral artery mean flow velocity.

Dynamic exercise enhances regional cerebral artery mean flow velocity. J. Appl. Physiol. 78(1): 12-16, 1995.--Anterior (ACA) and middle (MCA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes were determined using transcranial Doppler in 14 subjects during dynamic exercise after assessment of the carbon dioxide reactivity for both arteries. Right hand contractions provoked an elevation in left MCA Vmean [19% (12-28); P < 0.01], whereas the pulsatility decreased in all four arteries (P < 0.05). During right foot movement, left ACA Vmean increased by 23% (11-37; P < 0.01) with lesser (approximately 10%; P < 0.05) increases in the other arteries, and pulsatility index decreased (P < 0.05). During cycling, ACA and MCA Vmean increased bilaterally by 23% (10-49) and 18% (5-32), respectively (P < 0.01), and the pulsatility was also elevated (P < 0.05). Cerebral artery pulsatility did not demonstrate a focal response but depended did not demonstrate a focal response but depended on the muscle mass involved during exercise. The data demonstrate a significant increase in Vmean for the artery supplying the cortical projection of the exercising limb. Insignificant and marginally significant increases in Vmean may be related to sympathetically mediated vasoconstriction and/or coactivation of untargeted muscle groups.

Adult↗
PubMed1995

Natural killer cell response to exercise in humans: effect of hypoxia and epidural anesthesia.

For the response of immunologically competent blood cells to exercise, the importance of afferent nerve impulses was evaluated. On separate days, seven males cycled in a recumbent position approximately 60% of maximal O2 uptake with and without sensory nerve blockade by lumbar epidural anesthesia. Blood samples were collected after 60 min of rest, 20 min of exercise, and 120 min postexercise. Subsequently, on each day, the subjects were exposed to 11.5% O2-88.5% N2 for 10 min. This was followed by 20 min of hypoxic exercise at the same work rate, and a final blood sample was obtained. The concentrations of lymphocytes expressing the cluster designation (CD) cell-surface antigens CD3, CD4, CD8, and CD14 became elevated during exercise, and these responses were enhanced by hypoxia (P < or = 0.01). The most pronounced changes were within the concentrations of CD16+ and CD56+ natural killer cells, which increased twofold during normoxic and fivefold during hypoxic exercise (P < or = 0.01). Sensory nerve blockade decreased the number of CD3+ and CD4+ cells and increased the percentage of CD16+ cells, independent of exercise and hypoxia (P < or = 0.05). Sensory nerve blockade caused minor enhancement in the increase of unstimulated natural killer cell activity during exercise (P = 0.07) and enhanced the interferon-alpha-stimulated activity at normoxia (P < or = 0.05), whereas no effect was detected at hypoxia. The results demonstrate that the responses of immunological competent cells to normoxic and hypoxic exercise are not abolished by blockade of nerve impulses from active muscle.

Adult↗
PubMed1995

Central command increases muscle sympathetic nerve activity during intense intermittent isometric exercise in humans.

During sustained isometric exercise, central command has very little effect on muscle sympathetic nerve activity (MSNA). To determine if central command has a greater effect on MSNA during intermittent than during sustained contractions, MSNA was recorded with microelectrodes (peroneal nerve) during intermittent isometric handgrip at 25%, 50%, and 75% maximum voluntary contraction (MVC) in 9 human subjects with paced breathing. Similar experiments were performed in 11 additional subjects before and after partial neuromuscular blockade (intravenous curare) to isolate the influence of central command while minimizing force output and thus muscle afferent feedback. Before curare, handgrip at 25% and 50% MVC had no effect on MSNA, whereas handgrip at 75% MVC synchronized the MSNA to the handgrip such that MSNA was 5.7 +/- 1.3 times higher (mean +/- SEM, P < .001) during the contraction periods than during the relaxation periods. After curare, this synchronization of MSNA persisted without attenuation, even though force output fell to < 25% of the initial MVC. From these observations, we conclude that central command causes synchronization of motor activity and muscle sympathetic activity during intense intermittent isometric exercise.

Adult↗
PubMed1995

Exercise-induced gastric mucosal acidosis.

Gastric acidosis as assessed by tonometry was applied to evaluate changes in splanchnic blood flow during exercise. In six healthy male oarsmen, we determined gastric acidosis in response to 30 min of maximal ergometer rowing. The gastric mucosa carbon dioxide tension was determined by equilibration of isotonic saline to the tonometer. Arterial bicarbonate (HCO3-), pH, arterial oxygen tension (PaO2), and saturation (SaO2) were obtained simultaneously, while pH (pHi) of the gastric mucosa was calculated using the Henderson-Hasselbach equation. During rowing PaO2 and SaO2 decreased to values of 73.7 mm Hg and 95.5%, respectively (P < 0.05). However, during the last minute of rowing the values were normalized with a hyperventilation reducing PaCO2 to 27.1 mm Hg (P < 0.05). Rowing decreased HCO3- from 25.8 (21.4-28.5) to 14.1 (11.6-17.4) mmol l-1, while the gastric carbon dioxide tension increased from 36.8 (24.1-63.9) to 61.7 (48.9-82.0) mm Hg (P < 0.05). Accordingly, pHi decreased from 7.25 (7.04-7.48) to 6.79 (6.67-6.85) (P < 0.05). Arterial pH also decreased (from 7.42 (7.41-7.44) to 7.29 (7.26-7.33) (P < 0.05)), with the enlarged difference between pH and pHi suggesting marked splanchnic hypoperfusion during rowing.

Acidosis↗
PubMed1995

Digoxin affects potassium homeostasis during exercise in patients with heart failure.

OBJECTIVE: The aim was to evaluate whether digitalisation of heart failure patients affects extrarenal potassium handling during and following exercise, and to assess digoxin receptor occupancy in human skeletal muscle in vivo. METHODS: In a paired study of before versus after digitalisation, 10 patients with congestive heart failure underwent identical exercise sessions consisting of three bouts of increasing work rates, 41-93 W, on a cycle ergometer. The final bouts were followed by exercise to exhaustion. The femoral vessels and brachial artery were catheterised. Arterial blood pressure, heart rate, leg blood flow, cardiac output, plasma potassium, haemoglobin, pH, and skeletal muscle receptor occupancy with digoxin in biopsies were determined. RESULTS: Occupancy of skeletal muscle Na/K-ATPase with digoxin was 9% (P < 0.05). Following digitalisation femoral venous plasma potassium increased by 0.2-0.3 mmol.litre-1 (P < 0.05) at work rates of 69 W, 93 W, and at exhaustion, as well as during the first 3 min of recovery. Following digitalisation the femoral venoarterial difference in plasma potassium increased by 50-100% (P < 0.05) during exercise, and decreased by 66-75% (P < 0.05) during early recovery. Total loss of potassium from the leg increased by 138%. The effects of digitalisation on plasma potassium were not the outcome of changes in haemodynamics, because cardiac output and leg blood flow increased by up to 13% and 19% (P < 0.05), nor was it the outcome of changes in haemoconcentration or pH. CONCLUSIONS: Extrarenal potassium handling is altered as a result of digoxin treatment. This is likely to reflect a reduced capacity of skeletal muscle Na/K-ATPase for active potassium uptake because of inhibition by digoxin, adding to the reduction of skeletal muscle Na/K-ATPase concentration induced by heart failure per se. In heart failure patients, improved haemodynamics induced by digoxin may, however, increase the capacity for physical conditioning. Thus the impairment of extrarenal potassium homeostasis by heart failure and digoxin treatment may be counterbalanced by training.

Cardiac Output↗
PubMed1995

Systemic vascular resistance during high-volume plasmapheresis in patients with fulminant hepatic failure: relationship with oxygen consumption.

BACKGROUND: In patients with fulminant hepatic failure, systemic vascular resistance and blood pressure are often reduced. OBJECTIVE: To determine whether systemic vascular resistance increases during high-volume plasmapheresis, which is assumed to eliminate endogenous vasodilatory substances from the bloodstream. DESIGN: A prospective study. PATIENTS AND METHODS: Ten patients [median age 48 (range 21-53) years] were admitted for liver transplantation. Systemic haemodynamic variables were determined using a catheter in a radial artery and a thermodilution catheter placed in a pulmonary artery. Ten (range 8-15) litres of fresh frozen plasma were exchanged, while body temperature [37.6 (range 36.6-38.4) degrees C], blood partial pressure of carbon dioxide [3.75 (range 3.30-4.50) kPa] and peak inspiratory ventilatory pressure [24 (range 20-26) mmHg] were kept constant. RESULTS: Mean arterial pressure increased from 74 (range 61-110) to 96 (range 68-103) mmHg and cardiac index decreased from 5.2 (range 3.6-7.5) to 4.2 (range 3.4-6.6) l/min/m2. The systemic vascular resistance index increased from 662 (range 430-1270) to 1060 (range 621-1520) dyn s/cm5/m2. In contrast, the pulmonary vascular resistance index [42 (range 20-110) dyn s/cm5/m2) remained constant. As cardiac index decreased, oxygen delivery decreased from 939 (range 680-1496) to 745 (range 601-1189) ml/min/m2 with no effect on oxygen consumption [171 (87-231) ml/min/m2], as the arteriovenous oxygen extraction ratio increased from 17 (range 9-22) to 25 (range 8-31)% (P < 0.02). CONCLUSION: In patients with fulminant hepatic failure, cardiac output, systemic vascular resistance and arterial blood pressure improved during high-volume plasmapheresis.

Acute Disease↗
PubMed1994

Reflex increase in blood pressure induced by leg compression in man.

1. We tested the hypotheses that the increase in mean arterial pressure with the application of external leg compression in man is (i) blocked with epidural anaesthesia, and (ii) dependent upon the level of external pressure applied, the quantity of leg muscle mass compressed and the vascular volume of the leg. Fourteen healthy subjects were fitted with an anti-shock trouser garment to provide three levels (30, 60 and 90 mmHg) of leg compression, while cephalad translocation of fluid was prevented by upper-thigh cuffs inflated to a supra-systolic pressure. Cardiovascular responses were recorded during leg compression before and after the administration of epidural anaesthesia in eight subjects, while blood pressure responses from six subjects were compared with their single leg pressor response. 2. Both mean arterial and diastolic pressures were elevated with increasing leg compression, with no changes in heart rate, cardiac output, thoracic impedance, and central venous pressure. The leg compression-induced blood pressure increases were abolished by epidural anaesthesia. Furthermore, when only one leg was compressed at 90 mmHg, the pressor response was less than that elicited from compression of both legs at the same external pressure. Changes in vascular volume of the leg did not influence the pressor response to leg compression. 3. The results indicate that the mean arterial pressure increases in response to external compression of the legs and that a reflex mechanism, mediated by muscle afferent nerves, is involved. The response is dependent upon both the changes in intramuscular pressure and the quantity of muscle mass compressed.

Adult↗
PubMed1994

Hypoxia and training-induced adaptation of hormonal responses to exercise in humans.

To establish whether or not hypoxia influences the training-induced adaptation of hormonal responses to exercise, 21 healthy, untrained subjects (2) years, mean (SE)] were studied in three groups before and after 5 weeks' training (cycle ergometer, 45 min.day-1, 5 days.week-1). Group 1 trained at sea level at 70% maximal oxygen uptake (VO2max), group 2 in a hypobaric chamber at a simulated altitude of 2500 m at 70% of altitude VO2max, and group 3 at a simulated altitude of 2500 m at the same absolute work rate as group 1. Arterial blood was sampled before, during and at the end of exhaustive cycling at sea level (85% of pretraining VO2max). VO2max increased by 12 (2)% with no significant difference between groups, whereas endurance improved most in group 1 (P < 0.05). Training-induced changes in response to exercise of noradrenaline, adrenaline, growth hormone, beta-endorphin, glucagon, and insulin were similar in the three groups. Concentrations of erythropoietin and 2,3-diphosphoglycerate at rest did not change over the training period. In conclusion, within 5 weeks of training, no further adaptation of hormonal exercise responses takes place if intensity is increased above 70% VO2max. Furthermore, hypoxia per se does not add to the training-induced hormonal responses to exercise.

Adaptation, Physiological↗
PubMed1994

Maximal oxygen deficit of sprint and middle distance runners.

Anaerobic energy capacity was evaluated by maximal oxygen deficit (MOD) as well as by blood gas and muscle biopsy variables during short exhausting running in six recreational (RR) and eight competitive sprint and middle distance runners (SMDR). On 3 days runs to exhaustion were executed. Two runs were performed at a treadmill gradient of 15% at speeds which resulted in exhaustion after approximately 1 (R15%,1 min) and 2-3 min (R15%,2-3 min), respectively. On the 3rd day, the subjects ran with the treadmill at a gradient of 1% at a speed which caused exhaustion after 2-3 min (R1%,2-3 min). The runner performance was assessed from 400 m [RR, median 64.8 (range 62.2-69.6) s; SMDR, median 49.4 (range 48.5-52.0) s] and 800 m [RR, median 158.8 (range 153.3-170.2) s; SMDR, median 115.2 (range 113.3-123.3) s] track times. Muscle biopsies from gastrocnemius muscle were obtained before and immediately after R15%,2-3 min, from which muscle lactate and creatine phosphate (CP) concentrations, fibre type distribution, capillaries per fibre, total lactate dehydrogenase (LDH) activity and the LDH isoenzyme pattern were determined. The MOD increased with the treadmill gradient and duration. During both treadmill and track runs, SMDR performance was superior to that of RR, but no significant differences were observed with respect to MOD, muscle fibre type distribution, total LDH activity, its iso-enzyme pattern, changes in muscle lactate or CP concentrations. However, after treadmill runs, peak venous lactate concentration and partial pressures of carbon dioxide were higher, and pH lower in SMDR. Also the number of capillaries per muscle fibre and the maximal oxygen uptake were larger in SMDR. These findings would suggest that the superior performance of SMDR depended more on their aerobic than on their anaerobic capacity.

Adult↗
PubMed1994

The immune system during exposure to extreme physiologic conditions.

It is not clear how the immune system is modulated in response to physical stress (e.g. trauma, surgery, burn and sepsis). In order to better understand the stress-induced immune changes, effects of isolated stressors are evaluated. Human experiments include hypoxia, head-up tilt, hyperthermina and exercise, which influence all lymphocyte subtypes and especially so the natural killer (NK) cells. In essence, the immune response is enhanced even by light physical stress, but suppressed after prolonged, intense stress.

Exercise↗
PubMed1994

Maximal inspiratory pressure following endurance training at altitude.

Effects of endurance training on maximal inspiratory pressure and fatigue were evaluated after 5 weeks. Twelve male and 9 female untrained subjects were matched in the three groups for sex and maximal oxygen uptake (VO2 max). Training was performed at 70% VO2max; 45 min day-1; 5 days week-1 (n = 7); and at the same relative (n = 7) and absolute (n = 7) work loads in a pressure chamber corresponding to 2500 m (560 mmHg). Work load was increased every week to maintain the training heart rate. Maximal respiratory pressure was measured at the mouth before and 30, 60 and 120 s after maximal exercise. With no significant difference between the three groups of subjects, VO2max increased from 2.96 (1.98-4.47) (median and range for 21 subjects) to 3.33 (2.50-4.72) 1 min-1 (p < 0.001) and ventilation (VE max) from 109 (57-147) to 123 (73-148) 1 min-1 (p < 0.001), while maximal heart rate decreased from 193 (180-211) to 192 (169-207) beats min-1 (p < 0.01). Maximal inspiratory pressure (87 (56-115) mmHg), inspiratory muscle fatigue (18 (-2-43)%, p < 0.001), and arterial oxygen tension during exercise (12.4 (9.9-15.6)kPa) were similar before and after training. The results demonstrate that training at simulated altitude at 2500 m does not increase VE max or VO2 max above the increases obtained from training at sea level. Furthermore, VEmax and VO2 max increased approximately 13% despite unchanged maximal inspiratory pressure and inspiratory muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Thoracic impedance and pulmonary atrial natriuretic peptide during head-up tilt induced hypovolaemic shock in humans.

Head up and down tilts were used for manipulating the central blood volume in eight volunteers. During head-up tilt thoracic electrical impedance (TI) increased from 36.7 (33.9-52.1) ohm (mean and range) to 41.9 (36.9-59.2) ohm, heart rate from 60 (49-72) to 80 (65-90) beats min-1 (P < 0.05) and decreased again to 57 (48-67) beats min-1 accompanying a fall in mean arterial pressure from 86 (76-97) to 54 (41-79) mmHg and in cardiac output from 9.2 (5.9-12.1) to 6.9 (3.4-8.8) 1 min-1 (n = 7, P < 0.07). Central venous pressure did not change significantly. Pulmonary arterial mean, 6 (3-12) mmHg, and wedge pressures, 4 (1-9) mmHg, decreased to 4 (1-11) and 1 (0-7) mmHg, respectively, and mixed, 78 (77-79%), and central venous oxygen saturations, 72 (71-73)%, fell to 62 (46-75) and 54 (44-58)%, respectively (P < 0.05). Atrial natriuretic peptide (ANP) was determined from blood of the superior vena cava and pulmonary and brachial arteries. Pulmonary artery ANP, 18.4 (7.5-30.7) pmol l-1, was higher than in vena cava, 13.3 (5.2-20.9) pmol l-1 (P < 0.05). At the time of presyncope, pulmonary artery ANP decreased from 20.8 (37.4-10.1) to 13.7 (19.7-5.7) pmol l-1, in vena cava from 13.8 (23.1-7.1) to 10.2 (17.9-6.7) pmol l-1 and in the brachial artery from 16.9 (34.1-5.2) to 11.3 (18.5-5.1) pmol l-1 (P < 0.05). Head-down tilt did not affect the recorded variables significantly. Thoracic electrical impedance, pulmonary artery pressure and venous oxygen saturations were sensitive indices of the central blood volume as reflected in the release of atrial natriuretic peptide from the right side of the heart.

Adult↗
PubMed1994

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans.

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 +/- 2.7 min (mean, SE) (fatigue) and oxygen uptake (VO2) increased to 1.90 +/- 0.13 1 min-1. Compared with voluntary exercise at the same VO2, increases in heart rate (HR) (135 +/- 7 vs. 130 +/- 9 beats min-1) and cardiac output (16.9 +/- 1.1 vs. 17.3 +/- 0.91 min-1) were similar, and ventilation (54 +/- 5 vs. 45 +/- 41 min-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 +/- 4 (rest) to 119 +/- 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 +/- 3 (rest) to 95 +/- 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.

Adult↗