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Biomedical subjects

F Bonde-Petersen

Publications and source records attributed to F Bonde-Petersen.

At least 37 records · Page 2Linked to original sources
PubMed1987

Plasma arginine vasopressin during neck suction in upright sitting man.

In order to examine the influence of carotid baroreceptor stimulation on arginine vasopressin secretion, 8 normal healthy males were subjected to static neck suction of -3.3 kPa for 20 min in the upright sitting position after overnight food and fluid restriction. The plasma concentration of arginine vasopressin did not change significantly during neck suction. However, in 3 subjects the termination of neck suction induced large increases in plasma arginine vasopressin from 1.8 to 63.7 ng/l, from 0.7 to 34.3 ng/l and from 2.1 to 19.0 ng/l, respectively. Two subjects experienced symptoms such as nausea and paleness during neck suction. Systolic arterial pressure increased slightly but significantly during neck suction from 15.3 +/- 0.3 to 15.7 +/- 0.4 kPa (N = 7, P less than 0.05), whereas mean arterial pressure, diastolic arterial pressure, central venous pressure, heart rate, plasma osmolality, plasma sodium and potassium were unchanged. Haemoglobin concentration in blood and haematocrit increased significantly during and after neck suction, whereas plasma volume decreased. We conclude that neck suction with a negative pressure of 3.3 kPa in upright sitting man does not significantly affect plasma arginine vasopressin. However, termination of the stimulation induces large increases in some subjects. This may be explained by a direct effect on the vagus nerve or by a selective deloading of carotid baroreceptors.

Adult↗
PubMed1987

Cardiovascular reflexes during isometric exercise--role of muscle mass and gravitational stress.

Six healthy males performed sustained static contractions of five arm- and leg muscle groups for 2 min at 40% maximum voluntary contraction (MVC) sitting and supine. Delta heart rate, blood pressure, forearm vascular resistance, and cardiac output increased during contraction incrementing increasingly in the following order: dorsi flexion of ankle, plantar flexion, third finger flexion, handgrip, and knee extension. Muscle ischemia during recovery did not change this order. The cardiovascular responses to static contraction did not relate to muscle mass involved in a simple rectilinear manner. The increments in cardiovascular responses were not reduced in the supine position, although the values were at a lower level, probably due to the combination of a decreased sympathetic nervous activity in the supine position and an increased aortic baroreceptor stimulation induced by the increased stroke volume.

Adult↗
PubMed1986

Central transmural venous pressure and plasma arginine vasopressin during negative pressure breathing in man.

After overnight food and fluid restriction, 8 normal healthy males were examined in the upright sitting position before (prestudy), during and after (recovery) negative pressure breathing (NPB) with a pressure (P = difference between airway pressure and barometric pressure) of -9.6 +/- 0.5 to -10.4 +/- 0.4 mm Hg for 30 min. Plasma arginine vasopressin (pAVP) did not change significantly comparing prestudy with 10 and 30 min of NPB or comparing recovery with NPB at 10, 20 or 30 min. However, at 20 min of NBP, pAVP was slightly lower than at prestudy (p less than 0.05). Central venous pressure (CVP) decreased significantly during NPB, and central transmural venous pressure (CVP-P) increased significantly from -0.9 +/- 0.8 mm Hg to 3.8 +/- 0.7, 4.3 +/- 0.7 and 4.5 +/- 0.6 mm Hg (p less than 0.001) after 10, 20 and 30 min, respectively. Systolic, diastolic and mean arterial pressure and heart rate did not change significantly during NPB. Diuresis, natriuresis, kaliuresis, osmotic excretion and clearance were slightly increased during the recovery hour after NPB compared to prestudy, while urine osmolality decreased during NPB (n = 6). However, none of these changes were significant. There was no significant correlation between CVP-P and pAVP. In conclusion, -10 mm Hg NPB for 30 min in upright sitting subjects did not change pAVP consistently, while CVP-P was significantly increased and HR and arterial pressures were unchanged. This lends support to the concept that arterial baroreceptors and not cardiopulmonary mechanoreceptors are of importance in regulating AVP secretion in man.

Adult↗
PubMed1986

Central venous pressure and plasma arginine vasopressin in man during water immersion combined with changes in blood volume.

To investigate the influence of central venous pressure (CVP) changes on plasma arginine vasopressin (pAVP), 8 normal male subjects were studied twice before, during and after immersion to the neck in water at 35.1 degrees +/- 0.1 degrees C (mean +/- SE) for 6 h. After 2 h of immersion, blood volume was either expanded (WIEXP) by intravenous infusion of 2.0 1 of isotonic saline during 2 h or reduced by loss of 0.5 1 of blood during 30 min (WIHEM). The two studies were randomised between subjects. WIEXP increased CVP, systolic arterial pressure (SAP), diuresis, natriuresis, kaliuresis and osmolar clearance compared to WIHEM while haematocrit, haemoglobin concentration and urine osmolality decreased. Heart rate, mean arterial (MAP) and diastolic arterial pressure, plasma osmolality, plasma sodium, plasma potassium and free water clearance did not differ significantly in the two studies. pAVP was significantly higher after 6 h in WIHEM than after 6 h in WIEXP (2.0 +/- 0.2 vs. 1.6 +/- 0.2 pg X ml-1, mean +/- SE; P less than 0.05). pAVP values were corrected for changes in plasma volume due to infusion in order properly to reflect AVP secretion. In conclusion, there was a weak, but significant, negative correlation between CVP and pAVP during the two studies, while during recovery from WIHEM and WIEXP decrements in SAP and MAP correlated significantly and strongly with increases in pAVP. It is therefore concluded that it is the arterial baroreceptors rather than the cardiopulmonary mechanoreceptors which are of importance in AVP regulation in man.

Adult↗
PubMed1986

Arginine vasopressin, circulation, and kidney during graded water immersion in humans.

Ten normal males rested sitting upright at an air temperature of 28 degrees C for 5.5 h (control, C) and underwent 4 h of graded water immersion (WI) to the umbilicus (UI), to the chest (CI), and to the neck (NI), respectively (water temperature = 34.5 degrees C), on different experimental days. Plasma arginine vasopressin (PAVP) was suppressed during WI compared with C and maximally so during NI. However, there was no change in PAVP comparing CI with UI even though central venous pressure (CVP) increased. CVP increased during CI and NI compared with C but was unchanged during UI, whereas cardiac output (rebreathing method), stroke volume, and plasma volume increased to approximately the same level during all three steps of WI compared with C. Heart rate and total peripheral vascular resistance decreased during UI, CI, and NI. Systolic arterial pressure (SAP) and pulse pressure (PP) were increased gradually from prestudy related to the degree of WI. Also diuresis, natriuresis, kaliuresis, osmotic excretion, and clearance were increased gradually compared with C, whereas free water clearance (CH2O) gradually decreased. There were weak negative but statistically significant correlations between PAVP and CVP and between changes in PAVP from prestudy and corresponding changes in SAP and PP. Furthermore, a statistically significant and negative correlation between CH2O and natriuresis could be established. We conclude that graded immersion gradually increases central blood volume and decreases PAVP. However, not only cardiopulmonary mechanoreceptors but also arterial baroreceptors may play a role in AVP suppression during WI in humans. In hydropenic subjects the suppression of PAVP during WI is apparently not effective in counteracting the decrease in CH2O induced by increased solute excretion.

Adult↗
PubMed1986

Influence of central venous pressure change on plasma vasopressin in humans.

After overnight food and fluid restriction, nine healthy males were examined before, during, and after lower body positive pressure (LBPP) of 11 +/- 1 mmHg (mean +/- SE) for 30 min and before, during, and after graded lower body negative pressure (LBNP) of -10 +/- 1, -20 +/- 2, and -30 +/- 2 mmHg for 20 min each. LBPP and LBNP were performed with the subject in the supine position in a plastic box encasing the subject from the xiphoid process and down, thus including the splanchnic area. Central venous pressure (CVP) during supine rest was 7.5 +/- 0.5 mmHg, increasing to 13.4 +/- 0.8 mmHg (P less than 0.001) during LBPP and decreasing significantly at each step of LBNP to 2.0 +/- 0.5 mmHg (P less than 0.001) at 15 min of -30 +/- 2 mmHg LBNP. Plasma arginine vasopressin (AVP) did not change significantly in face of this large variation in CVP of 11.4 mmHg. Mean arterial pressure increased significantly during LBPP from 100 +/- 2 to 117 +/- 3 Torr (P less than 0.001) and only at one point during LBNP of -30 +/- 2 mmHg from 102 +/- 1 to 115 +/- 5 mmHg (P less than 0.05). Heart rate did not change during LBPP but increased slightly from 51 +/- 3 to 55 +/- 3 beats/min (P less than 0.05) only at 7 min of LBNP of -30 +/- 2 mmHg. Plasma osmolality, sodium, and potassium did not change during the experiment. Hemoglobin concentration increased during LBPP and LBNP, whereas hematocrit only increased during LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Haemodynamic and humoral effects of lower body negative pressure in normal, sodium-replete man during angiotensin-converting enzyme inhibition with captopril.

The significance of the renin-angiotensin system (RAS) for circulatory homeostasis during gravitational stress (10 min of lower body negative pressure, LBNP, at -40 mmHg) was investigated in eight men on liberal sodium intake. The function of RAS was inhibited by a single oral dose of 100 mg captopril, an angiotensin-converting enzyme inhibitor. Plasma concentrations of renin and angiotensin I were normal before and increased after captopril and during LBNP. Plasma concentration of angiotensin II was normal before captopril, increased during LBNP, and fell to low values after captopril. Systolic blood pressure decreased more during LBNP after captopril than in the control situation. In three cases, the LBNP experiment after captopril had to be interrupted due to marked hypotension. Heart rate and plasma concentration of adrenaline increased above pre-captopril levels. In six subjects, plasma concentration of noradrenaline increased more during LBNP after captopril, less in two subjects, whereas the arginine vasopressin concentration increased more after captopril in all five subjects where measurements were available. The results demonstrate that RAS participates in blood pressure homeostasis also in sodium-replete, normal man. The enhanced increases in heart rate and plasma catecholamines after captopril do not suggest that sympathetic reflex activity during gravitational stress is blunted after captopril, in contrast to the evidence from animal experiments.

Adult↗
PubMed1986

The influence of the renin-angiotensin system on adrenergic vasoconstrictor responses in the forearm and splanchnic region in sodium deplete man.

In sodium deplete subjects forearm (FBF) and splanchnic (SBF) blood flows were measured at rest and during lower body negative pressure (LBNP) before and during angiotensin II (ANG II) blockade. Both FBF and SBF were reduced by LBNP. Forearm blood flow and forearm vascular resistance were unaffected by ANG II blockade (intra-arterial saralasin, n = 6; i.v. enalapril, n = 9) both at rest and during LBNP. In contrast, resting SBF increased and splanchnic vascular resistance decreased after i.v. enalapril (n = 10). The low resistance was completely unchanged during the following LBNP. It is concluded that acute ANG II blockade has no influence on the vascular resistance in the human forearm, but increases basal SBF in sodium depleted subjects and 'paralyses' the vasoconstrictor response to LBNP.

Angiotensin II↗
PubMed1985

Central venous pressure and plasma arginine vasopressin during water immersion in man.

The influence of increased central venous pressure (CVP) on the plasma concentration of arginine vasopressin (pAVP) was examined in 7 healthy males subjected to water immersion (WI) up to the neck following overnight food- and fluid restriction. During WI the subject sat upright in a pool (water temperature = 35.0 degrees C) for 6 h. In control experiments the subject assumed the same position outside the pool wearing a water perfused garment (water temperature = 34.6 degrees C). CVP increased markedly during WI and after 20 min of immersion it attained a level which was significantly higher than the control value (10.9 +/- 1.5 (mean +/- SE) vs. 2.2 +/- 1.3 mm Hg, p less than 0.01). This increase was sustained throughout the 6 h WI period. Simultaneously, after 20 min pAVP during WI was significantly lower than control values (1.8 +/- 0.3 vs. 2.2 +/- 0.3 pg X ml-1, p less than 0.05) and sustained throughout WI. Systolic arterial pressure increased significantly by 7-10 mm Hg (p less than 0.05) after 2 h of WI, while diastolic arterial pressure was unchanged. Heart rate was decreased by 10 bpm throughout immersion. There was no change in plasma osmolality when comparing control with immersion. A pronounced osmotic diuresis, natriuresis and kaliuresis occurred during WI, counteracting an acute significant increase in plasma volume of 6.5 +/- 1.9% (P less than 0.01 within 20 min of immersion). We conclude that an increase in CVP due to WI is accompanied by suppressed pAVP.

Adult↗
PubMed1985

Changes in plasma volume, in transcapillary escape rate of albumin and in subcutaneous blood flow during hypoglycaemia in man.

Hypoglycaemia was induced by insulin injected intravenously (0.15 i.u./kg body weight) in seven healthy young males. Plasma volume was measured before and during hypoglycaemia by intravenous injection of 125I before hypoglycaemia and of 131I during hypoglycaemia. Plasma volume decreased and transcapillary escape rate increased significantly during hypoglycaemia. Skin temperature and local subcutaneous adipose tissue blood flow were measured in four different regions. Both tended to decrease during hypoglycaemia and decreased significantly 2 h after hypoglycaemia. There was no correlation between changes in the two measurements, suggesting that there is no simple relationship between subcutaneous blood flow and skin temperature during hypoglycaemia.

Adult↗
PubMed1985

Evidence that the arterial baroreceptors influence muscle blood flow and not subcutaneous flow in man.

Studies in man indicate that skeletal muscle blood flow is modulated via high pressure baroreceptors located in the carotid body. However, whether subcutaneous blood flow is influenced in this way remains controversial. Therefore, the aim of the present study was to determine whether subcutaneous as well as skeletal muscle blood flow was influenced by direct carotid body stimulation; this was done by means of neck suction. Six young healthy males were investigated. Subcutaneous and skeletal muscle blood flow in the forearm was measured by the local 133Xe washout technique. Neck suction of -20 mmHg was applied through a tight helmet covering the head and neck. In the supine position heart rate increased about 10%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged, but skeletal muscle blood flow increased about 70%. Measurements were repeated during neck suction, -20 mmHg, and 45 degrees head-up tilt (which is known to decrease subcutaneous blood flow and skeletal muscle blood flow by increasing sympathetic vasoconstrictor activity). Heart rate increased by about 20%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged and skeletal muscle blood flow increased about 100%. These results indicate that skeletal muscle blood flow is modulated through carotid baroreceptors. Subcutaneous blood flow seems not to be influenced by high pressure baroreceptor modulation, although a vasoconstrictor response to head-up tilt was demonstrated in this as well as other recent studies.

Adult↗
PubMed1985

The effect of metabolic control on hemodynamics in short-term insulin-dependent diabetic patients.

Hemodynamics variables (heart rate, arterial blood pressure, cardiac output, hepato-splanchnic blood flow, forearm blood flow, and plasma catecholamines) were measured during good (median blood glucose 4.7 mmol/L) and poor (median blood glucose 16.3 mmol/L) metabolic control in eight young, short-term, insulin-dependent diabetic patients. The measurements were performed twice within 2 wk, in random order. Continuous subcutaneous insulin infusion (CSII) was applied for 1 wk in order to obtain good control. All eight patients had elevated cardiac output (median 9%) and forearm blood flow (median 34%) during poor compared with good metabolic control, P less than 0.01. In contrast, hepato-splanchnic blood flow was lower (median 12%) during poor compared with good metabolic control, P less than 0.05. Heart rate remained unchanged, while mean arterial blood pressure was slightly higher during poor control, P less than 0.05. Five of six patients had elevated plasma noradrenaline concentration during poor metabolic control. Due to the small number of patients investigated, no valid conclusion regarding the activity of the sympathoadrenal system can be drawn. Our study suggests that both increased cardiac output and reduced hepato-splanchnic blood flow (redistribution) contribute to the elevated blood flow previously demonstrated in various other organs and tissues in diabetic patients during poor metabolic control.

Adult↗
PubMed1984

Haemodynamic changes in insulin-induced hypoglycaemia in normal man.

Haemodynamic variables (plasma volume, heart rate, blood pressure, cardiac output, stroke volume, pulmonary tissue volume, total peripheral vascular resistance, hepato-splanchnic vascular resistance, lower extremity vascular resistance and plasma catecholamines) were measured before and after insulin-induced hypoglycaemia in seven healthy men. Plasma volume decreased significantly at the nadir of glucose (mean decrease 222 +/- 41 ml) and subsequently increased to pre-hypoglycaemic values within 30 min. Cardiac output increased in response to hypoglycaemia (mean increase 2.8 +/- 0.61/min). The early rise in cardiac output was primarily due to an increase in heart rate, but later mainly due to increased stroke volume. Since pulmonary tissue volume was constant, the observed changes in cardiac output are unlikely to be due to a Frank-Starling mechanism but rather to increased sympatho-adrenal activity. Total peripheral vascular resistance as well as lower extremity vascular resistance decreased, whereas hepato-splanchnic vascular resistance was unaffected. Thus insulin-induced hypoglycaemia has marked transient effects on the circulation.

Adult↗
PubMed1984

Cardiovascular responses to heat stress and blood volume displacements during exercise in man.

Subjects exercised in the upright position at approximately 50% of maximal oxygen consumption in four situations: in 25 degrees C air, in 45 degrees C air [mean skin temperature (Tsk) 35 degrees C], in 35 degrees C water immersed to the level of the xiphoid process, and finally wearing a suit perfused with 35 degrees C water. The water immersion prevented gravitational shifts of blood volume to the legs. In this situation the forearm blood flow (FBF) rose continually with increasing core temperature (Tes) in contrast to the attenuation in rise above 38 degrees C Tes in 45 degrees C air. The differences were significant above 38.6 degrees C Tes in experiments in eight subjects. The effects of immersion on cardiac output (CO), stroke volume (SV), and heart rate (HR) were studied in five of the subjects in relation to Tes, since the rate of rise of Tes was different in the four situations. CO and SV tended to be higher during both rest and exercise in the water than in the other three conditions, while HR rose in the same manner with increasing core temperature, except that it was lower in 25 degrees C air, where Tsk was lower. Thus, the prevention of hydrostatic shifts of peripheral venous volume permitted the maintenance of a higher SV and peripheral blood flow, and enhanced the ability of the circulation to deal with the combined exercise and heat stress.

Adolescent↗
PubMed1984

Cardiovascular, hormonal and body fluid changes during prolonged exercise.

During prolonged heavy exercise a gradual upward drift in heart rate (HR) is seen after the first 100 min of exercise. This "secondary rise" might be caused by a reduction in stroke volume due to reduced filling of the heart, which is dependent upon both hemodynamic pressure and blood volume. Swimming and bicycling differ with respect to hydrostatic pressure and to water loss, due to sweating. Five subjects were studied during 90 min of bicycle exercise, and swimming the leg kick of free style. The horizontal position during swimming resulted in a larger cardiac output and stroke volume. After the initial rise in heart rate the "secondary rise" followed parallel courses in the two situations. The rises were positively related to the measured increments in plasma catecholamine concentrations, which continued to increase as exercise progressed. The secondary rise in HR could not be explained by changes in plasma volume or in water balance, nor by changes in plasma [K]. The plasma volume decreased 5-6% (225-250 ml) within the first 5 to 10 min of exercise both in bicycling and swimming, but thereafter remained virtually unchanged. The sweat loss during bicycling was four times greater than during swimming; but during swimming the hydrostatic conditions induced a diuresis, so that the total water loss was only 25% less than during bicycling.

Adult↗
PubMed1984

Cardiovascular and hormonal responses to bicycle exercise during lower body negative pressure.

UNLABELLED: The purpose was to combine bicycle exercise and LBNP as a model to investigate the mechanisms regulating circulation during gravitational stresses. METHODS: Cardiac Output (CO) by acetylene-, argon-, oxygen rebreathing; Heart Rate (HR) from ECG; Mean Arterial Pressure (MAP) by arm cuff; Plasma Nor-Epinephrine (NE), Epinephrine (E), and Lactate (HLa) by isotope and enzymatic techniques respectively. Total Peripheral Resistance (TPR) = MAP/CO and stroke volume (SV) = CO/HR. Six subjects exercised at 180-200 Watts in the upright position on a mechanically braked computer controlled small bicycle ergometer placed in a LBNP box. The above parameters were measured at rest and at 5 and 9 min of exercise without and with LBNP at -30 or -40 mmHg (depending on LBNP tolerance). RESULTS AND CONCLUSIONS: In the face of an increased sympathetic nervous activity (NE+E,TPR, and HR increased) during exercise in LBNP, there was a decrease in CO and SV indicating that the venous return was insufficient. However, HLa was unchanged demonstrating that the blood flow to the working muscles did not suffer.

Adult↗
PubMed1984

Cardiac output determined by the CO2 rebreathing method with correlation of lung-bag volume shrinkage.

The purpose of this study was to elucidate the effect of lung-bag volume shrinkage on P'VCO2 estimated by the CO2 rebreathing method and to correct its effect in calculation of cardiac output. The P'VCO2 was extrapolated with the linear relationship between dPACO2/dt and PACO2 during rebreathing. The P'VCO2 was higher than real mixed PCO2 by 0.82 mmHg at rest, by 1.35 mmHg at 50W, 1.57 mmHg at 100W, and 3.06 mmHg at 150W considering the effect of lung-bag volume shrinkage detected by argon concentration. The cardiac output obtained by the CO2 rebreathing method with correction of above differences was in good agreement with that determined by the acetylene method (r = 0.930, p less than 0.001). When the cardiac output was plotted against O2 uptake, our results and the regression line were fairly close to the reported regression lines.

Carbon Dioxide↗