Search PubMed⌕ Search

Biomedical subjects

P Norsk

Publications and source records attributed to P Norsk.

At least 37 records · Page 2Linked to original sources
PubMed2000

Forearm vascular and neuroendocrine responses to graded water immersion in humans.

The hypothesis that graded expansion of central blood volume by water immersion to the xiphoid process and neck would elicit a graded decrease in forearm vascular resistance was tested. Central venous pressure increased (P < 0.05) by 4.2 +/- 0.4 mmHg (mean +/- SEM) during xiphoid immersion and by 10.4 +/- 0.5 mmHg during neck immersion. Plasma noradrenaline was gradually suppressed (P < 0.05) by 62 +/- 8 and 104 +/- 11 pg mL-1 during xiphoid and neck immersion, respectively, indicating a graded suppression of sympathetic nervous activity. Plasma concentrations of arginine vasopressin were suppressed by 1.5 +/- 0.5 pg mL-1 (P < 0.05) during xiphoid immersion and by 2.0 +/- 0.5 pg mL-1 during neck immersion (P < 0.05 vs. xiphoid immersion). Forearm subcutaneous vascular resistance decreased to the same extent by 26 +/- 9 and 28 +/- 4% (P < 0.05), respectively, during both immersion procedures, whereas forearm skeletal muscle vascular resistance declined only during neck immersion by 27 +/- 6% (P < 0.05). In conclusion, graded central blood volume expansion initiated a graded decrease in sympathetic nervous activity and AVP-release. Changes in forearm subcutaneous vascular resistance, however, were not related to the gradual withdrawal of the sympathetic and neuroendocrine vasoconstrictor activity. Forearm skeletal muscle vasodilatation exhibited a more graded response with a detectable decrease only during immersion to the neck. Therefore, the forearm subcutaneous vasodilator response reaches saturation at a lower degree of central volume expansion than that of forearm skeletal muscle.

Adult↗
PubMed2000

Water and sodium balances and their relation to body mass changes in microgravity.

BACKGROUND: Since the very beginning of space physiology research, the deficit in body mass that is often observed after landing has always been interpreted as an indication of the absolute fluid loss early during space missions. However, in contrast to central hypervolemic conditions on Earth, the acute shift of blood volume from the legs to the upper part of the body in astronauts entering microgravity (microG) has neither stimulated diuresis and natriuresis nor resulted in negative water-and sodium-balances. DESIGN: We therefore examined the kinetics of body mass changes in astronauts (n = 3) during their several weeks aboard the space station MIR. A continuous diet monitoring was performed during the first mission (EuroMIR94, 30 days). The second mission (MIR97, 19 days) comprised a 15-day metabolic ward period (including predefined constant energy and sodium intake). Water and sodium balances were calculated and the kinetic of changes in basal concentrations of fluid-balance-related hormones during flight were determined. CONCLUSION: The data suggest firstly that loss of body mass during space flight is rather a consequence of hypocaloric nutrition. Secondly, microG provokes a sodium retaining hormonal status and may lead to sodium storage without an accompanying fluid retention.

Astronauts↗
PubMed2000

Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure.

The hypothesis was tested that cardiovascular and neuroendocrine (norepinephrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York Heart Association class II-III, ejection fraction = 0.28 +/- 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 +/- 0.03) underwent 30 min of thermoneutral (34.7 +/- 0.02 degrees C) water immersion (WI) to the xiphoid process. WI increased (P < 0.05) central venous pressure by 3.7 +/- 0.6 and 3.2 +/- 0.4 mmHg and stroke volume index by 12.2 +/- 2.1 and 7.2 +/- 2.1 ml. beat(-1). m(-2) in controls and HF patients, respectively. During WI, systemic vascular resistance decreased (P < 0.05) similarly by 365 +/- 66 and 582 +/- 227 dyn. s. cm(-5) in controls and HF patients, respectively. Forearm subcutaneous vascular resistance decreased by 19 +/- 7% (P < 0.05) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vasopressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved.

Adaptation, Physiological↗
PubMed2000

Arterial pulse pressure and vasopressin release during graded water immersion in humans.

Previous results indicate that arterial pulse pressure modulates release of arginine vasopressin (AVP) in humans. The hypothesis was therefore tested that an increase in arterial pulse pressure is the stimulus for suppression of AVP release during central blood volume expansion by water immersion. A two-step immersion model (n = 8) to the xiphoid process and neck, respectively, was used to attain two different levels of augmented cardiac distension. Left atrial diameter (echocardiography) increased from 28 +/- 1 to 34 +/- 1 mm (P < 0.05) during immersion to the xiphoid process and more so (P < 0.05), to 36 +/- 1 mm, during immersion to the neck. During immersion to the xiphoid process, arterial pulse pressure (invasively measured in a brachial artery) increased (P < 0.05) from 44 +/- 1 to 51 +/- 2 mmHg and to the same extent from 42 +/- 1 to 52 +/- 2 mmHg during immersion to the neck. Mean arterial pressure was unchanged during immersion to the xiphoid process and increased during immersion to the neck by 7 +/- 1 mmHg (P < 0.05). Arterial plasma AVP decreased from 2.5 +/- 0.7 to 1.8 +/- 0.5 pg/ml (P < 0. 05) during immersion to the xiphoid process and significantly more so (P < 0.05), to 1.4 +/- 0.5 pg/ml, during immersion to the neck. In conclusion, other factors besides the increase in arterial pulse pressure must have participated in the graded suppression of AVP release, comparing immersion to the xiphoid process with immersion to the neck. We suggest that when arterial pulse pressure is increased, graded distension of cardiopulmonary receptors modulate AVP release.

Adult↗
PubMed2000

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system.

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.

Adaptation, Physiological↗
PubMed2000

Does gender influence human cardiovascular and renal responses to water immersion?

We hypothesized that women and men exhibit similar cardiovascular and renal responses to thermoneutral water immersion (WI) to the neck. Ten women and nine men underwent two sessions in random order: 1) seated nonimmersed for 5.5 h (control) and 2) WI for 3 h, with subjects seated nonimmersed for 1.5 h pre- and 1 h postimmersion. We measured left atrial diameter, heart rate, arterial pressure, urine volume and osmolality, and urinary endothelin, urodilatin, sodium, and potassium excretion. No significant difference existed between groups in cardiovascular responses. The groups also exhibited mostly similar renal responses to immersion after adjustment for body mass. However, female urodilatin excretion per kilogram during immersion was over twofold that of men, and the female kaliuretic response to immersion was delayed and less pronounced relative to that in men. Men may excrete more potassium than women during immersion because men possess greater lean body mass (potassium per kilogram). Results obtained in men during WI may be cautiously extrapolated to women, yet urodilatin and potassium responses exhibit gender differences.

Adult↗
PubMed1999

Contribution of the leg vasculature to hypotensive effects of an antiorthostatic posture change in humans.

1. Previous results from our laboratory have shown that vasodilatation in the legs prevents mean arterial pressure (MAP) from increasing during water immersion. Therefore, we tested the hypothesis that vasodilatation in the legs is necessary for the hypotensive effects to occur during a moderate antiorthostatic posture change. 2. Ten healthy males underwent a 5 min posture change from upright seated to horizontal supine (SUP) and back to seated again with (OCCL-SUP) and without simultaneous total arterial (154 +/- 1 mmHg) thigh occlusion, and a control seated period, also with and without arterial occlusion. Cardiac output (CO) was measured by a non-invasive foreign (N2O) gas rebreathing technique. 3. MAP (brachial auscultation) decreased during SUP from 94 +/- 3 to 84 +/- 2 mmHg (P < 0.0001) and total peripheral vascular resistance (TPR = MAP/CO, n = 8) decreased by 15 +/- 4 % (P < 0.001). During OCCL-SUP, MAP decreased from 98 +/- 2 to 90 +/- 2 mmHg (P < 0.005) and TPR decreased by 14 +/- 3 % (P < 0.01). 4. In conclusion, vasodilatation in the legs is not necessary for the decrease in MAP to occur during a moderate antiorthostatic manoeuvre. Therefore, vasodilatation in more central vascular beds (e.g. abdomen) can alone account for the hypotensive effects.

Adult↗
PubMed1999

[Space medicine].

Explore the source record for details and available documents.

Aerospace Medicine↗
PubMed1999

Mechanisms of inhibition of vasopressin release during moderate antiorthostatic posture change in humans.

The hypothesis was tested that the carotid baroreceptor stimulation caused by a posture change from upright seated with legs horizontal (Seat) to supine (Sup) participates in the suppression of arginine vasopressin (AVP) release. Ten healthy males underwent this posture change for 30 min without or with simultaneous application of lower body negative pressure (LBNP) adjusted to maintain left atrial diameter (LAD) at the Seat level. Throughout Sup, mean arterial pressure and heart rate decreased from 98 +/- 2 to 91 +/- 2 mmHg and from 63 +/- 2 to 55 +/- 2 beats/min (P < 0.05), respectively, whereas the corresponding decreases during Sup + LBNP were attenuated and of shorter duration (98 +/- 2 to 93 +/- 2 mmHg and 62 +/- 2 to 58 +/- 3 beats/min, P < 0.05). During Sup, LAD increased from 30 +/- 1 to 33 +/- 1 mm, and arterial pulse pressure (PP) increased from 40 +/- 2 to 47 +/- 2 mmHg, whereas plasma AVP decreased from 0.9 +/- 0.2 to 0.5 +/- 0.1 pg/ml (P < 0.05), and plasma norepinephrine (NE) decreased from 176 +/- 20 to 125 +/- 16 pg/ml (P < 0.05). During Sup + LBNP, there were no changes in LAD, PP, plasma AVP, or NE. In conclusion, vasopressin secretion is suppressed during an antiorthostatic posture change, which increases carotid sinus pressure, PP, and LAD. The suppression is absent when PP and LAD are prevented from increasing and is thus critically dependent on at least one of these stimuli.

Adult↗
PubMed1999

Arterial pressure in humans during weightlessness induced by parabolic flights.

Results from our laboratory have indicated that, compared with those of the 1-G supine (Sup) position, left atrial diameter (LAD) and transmural central venous pressure increase in humans during weightlessness (0 G) induced by parabolic flights (R. Videbaek and P. Norsk. J. Appl. Physiol. 83: 1862-1866, 1997). Therefore, because cardiopulmonary low-pressure receptors are stimulated during 0 G, the hypothesis was tested that mean arterial pressure (MAP) in humans decreases during 0 G to values below those of the 1-G Sup condition. When the subjects were Sup, 0 G induced a decrease in MAP from 93 +/- 4 to 88 +/- 4 mmHg (P < 0.001), and LAD increased from 30 +/- 1 to 33 +/- 1 mm (P < 0.001). In the seated position, MAP also decreased from 93 +/- 6 to 87 +/- 5 mmHg (P < 0.01) and LAD increased from 28 +/- 1 to 32 +/- 1 mm (P < 0.001). During 1-G conditions with subjects in the horizontal left lateral position, LAD increased compared with that of Sup (P < 0.001) with no further effects of 0 G. In conclusion, MAP decreases during short-term weightlessness to below that of 1-G Sup simultaneously with an increase in LAD. Therefore, distension of the heart and associated central vessels during 0 G might induce the hypotensive effects through peripheral vasodilatation. Furthermore, the left lateral position in humans could constitute a simulation model of weightlessness.

Adult↗
PubMed1999

Preservation of veno-arteriolar reflex in the skin following 20 days of head down bed rest in humans.

A decrease in orthostatic tolerance following exposure to microgravity or head down bed rest (HDBR) is frequently observed and is thought to be multifactorial in origin. Recently published observations by Buckey et al. indicate that the inability to regulate peripheral vascular resistance during an orthostatic stress after spaceflight could be another important mechanism for orthostatic intolerance. Previous investigations have revealed that a local veno-arteriolar reflex is present in cutaneous, subcutaneous and muscle tissue. The reflex response is elicited in response to an increase in transmural venular pressure of about 25 mmHg or more. The local veno-arteriolar reflex acts in concert with centrally elicited sympathetic activity to regulate vascular resistance. During standing, the local veno-arteriolar reflex participates as a mechanism to increase peripheral vascular resistance independently of sympathetically mediated vasoconstrictor responses. During HDBR the local veno-arteriolar reflex is inactive for a prolonged period of time. Therefore we hypothesized that the veno-arteriolar reflex in the skin is attenuated immediately after prolonged HDBR and that an attenuation of the response may contribute to post-HDBR orthostatic intolerance.

Bed Rest↗
PubMed1998

Vasopressin, angiotensin II and renal responses during water immersion in hydrated humans.

1. The hypothesis was tested that in hydrated humans the release of arginine vasopressin and angiotensin II is suppressed by water immersion (WI) and that this is a mechanism of the immersion-induced diuresis and natriuresis. Seven male subjects on controlled sodium (65-75 mmol per 24 h for 4 days) and water intake were studied. 2. Plasma vasopressin was promptly suppressed by WI, declining from 0. 76 +/- 0.13 to 0.23 +/- 0.08 pg ml-1 (P < 0.05), with a concomitant increase in renal water output (CH2O) from -0.4 +/- 0.2 to 4.4 +/- 0.7 ml min-1 (P < 0.05). Subsequently, CH2O returned to the level of control, whereas plasma vasopressin remained suppressed. Plasma osmolality gradually increased from 285 +/- 1 to 289 +/- 1 mosmol kg-1 (P < 0.05). WI caused a 9-fold increase in renal sodium excretion. Plasma angiotensin II decreased from 27.1 +/- 5.3 to 4.3 +/- 0.7 pg ml-1 (P < 0.05), and the intraindividual correlation coefficients between sodium excretion rates and angiotensin II concentrations varied between 0.73 and 0.96 (P < 0.002). 3. The data demonstrate that plasma vasopressin and angiotensin II concentrations decrease during WI in hydrated humans, concomitantly with initial increases in CH2O and sodium excretion. Therefore, vasopressin could constitute a mediator of CH2O and angiotensin II of the natriuresis of WI. The subsequent return of CH2O to the level of control is, however, also caused by other factors.

Adult↗
PubMed1998

Underestimation of plasma volume changes in humans by hematocrit/hemoglobin method.

During water immersion in humans, the use of changes in hematocrit (Hct) and hemoglobin concentration (Hb) underestimates the relative changes in plasma volume (PV) as measured directly with Evans blue (EB). It is not known whether the same is the case during posture changes. Therefore, changes in PV were determined with an EB dilution technique in 10 males before, during, and after an acute posture change from seated to 6 degrees head-down tilt (HDT). The EB method was improved to take into account changes in transcapillary escape rate of albumin-bound EB. Furthermore, blood was sampled from a central venous catheter. Hct and Hb were simultaneously measured. During HDT, PV determined with EB increased by 9.3 +/- 2.0% but increased only 4.5 +/- 0.9% when calculated with the Hct/Hb method (P < 0.05 vs. EB measurements). Thus use of the Hct/Hb method in humans leads to underestimation of the change in PV by as much as 50% during an acute change in posture. Therefore, a direct tracer-dilution method must be used for accurate estimations of changes in PV during changes in posture or other antiorthostatic maneuvers.

Adult↗
PubMed1998

Preventing hemodilution abolishes natriuresis of water immersion in humans.

The hypothesis was tested that hemodilution is one of the determinants of the water immersion (WI)-induced natriuresis. Eight males were subjected to 3 h of 1) WI to the midchest (Chest), 2) WI to the neck combined with thigh cuff-induced (80 mmHg) venous stasis (Neck + stasis), and 3) a seated time control (n = 6). Central venous pressure and left atrial diameter increased to the same extent during Chest and Neck + stasis (P < 0.05), whereas renal sodium excretion only increased during Chest from 77 +/- 7 to 225 +/- 13 micromol/min (P < 0.05). During Chest, plasma colloid osmotic pressure (COP) decreased from 27.7 +/- 0.7 to 25.1 +/- 0.7 mmHg (P < 0.05), and plasma volume (PV) increased from 3,263 +/- 129 to 3,581 +/- 159 ml (P < 0.05), whereas these variables remained unchanged during Neck + stasis. Plasma norepinephrine concentration decreased similarly during Chest and Neck + stasis by 45 +/- 7 and 34 +/- 4%, respectively (P < 0.05), whereas plasma renin activity decreased only during Chest (P < 0.05). In conclusion, during WI in humans 1) hemodilution (decrease in COP and increase in PV) is a pivotal stimulus for the natriuresis and 2) central blood volume expansion without hemodilution does not augment renal sodium output.

Adult↗
PubMed1998

Osmoregulatory control of renal sodium excretion after sodium loading in humans.

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by approximately 4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 +/- 8 vs. 110 +/- 17 micromol/min). However, after HiNa+ the corresponding natriureses were identical (135 +/- 33 vs. 139 +/- 39 micromol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23-52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

Adult↗
PubMed1998

Indirect evidence of CNS adrenergic pathways activation during spaceflight.

BACKGROUND: Microgravity causes cephalad fluid shift and compensatory mechanisms. Hormonal changes suggestive of peripheral sympathetic (catecholaminergic) nervous system activation have been recently found in astronauts during flight. Simulation studies showed increased perivascular sympathetic fiber density in the rat brain. HYPOTHESIS: Intracranial microcirculatory adaptations might also occur in astronauts, involving an increase in the turnover rate of catecholamines, i.e., norepinephrine (NE) and its precursor, Dopamine (DA). DA is known to inhibit prolactin (PRL) release and to enhance growth hormone (GH) secretion by the pituitary. Therefore, increased brain dopaminergic activity would result into lower circulating PRL concentrations. At the same time, plasma levels of GH and of its effector insulin-like growth factor-1 (IGF-1) would increase during flight. METHODS: Circulating cortisol (CS), PRL, GH and IGF-1 levels were measured 2 d preflight, inflight (4-5 d after launch) and on different days postflight in four astronauts involved in the Spacelab D-2 mission. RESULTS: No significant changes were found in CS concentrations. PRL decreased while GH and IGF-1 increased inflight (p < 0.05). After flight no statistically relevant hormonal changes were found with respect to preflight. CONCLUSION: The observed hormonal changes were consistent with the original hypothesis that spaceflight might activate CNS adrenergic pathways. They occurred in the absence of two typical markers of stress, namely CS and PRL increase, thus ruling out any non-specific effect of acute stress on the results. In agreement with the most recent results of real and simulated microgravity studies performed in both the experimental animal and in man, these data lend support to the hypothesis that the CNS adrenergic pathways are also activated in the human during spaceflight.

Adaptation, Physiological↗