Biomedical subjects

B Pump

Publications and source records attributed to B Pump.

8 recordsLinked to original sources

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

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↗

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

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↗

PubMed1997

Left atrial distension and antiorthostatic decrease in arterial pressure and heart rate in humans.

It was investigated to what degree left atrial distension augments the hypotensive effects of a 15-min moderate antiorthostatic maneuver in humans. Ten healthy males underwent a posture change from upright seated (Seat, legs horizontal) to supine (Sup) or to supine with simultaneous lower body negative pressure (Sup + LBNP) to keep left atrial diameter (LAD) unchanged. After 2.5 min of Sup, mean arterial pressure (MAP) decreased from 94 +/- 3 to 86 +/- 3 mmHg (P < 0.05), whereas a similar decrease was delayed 7.5 min into Sup + LBNP. Heart rate (HR) decreased within 2.5 min of Sup from 68 +/- 2 to 60 +/- 3 beats/min (P < 0.05) and remained significantly decreased for at least 2.5 min longer than during Sup + LBNP. Aortic systolic distension (ASD) increased by 59 +/- 17% during Sup (P < 0.05) but was unchanged during Sup + LBNP. The 29 +/- 4% decrease in plasma norepinephrine (NE) during Sup (P < 0.05) was abolished during Sup + LBNP. In conclusion, the increases in LAD and ASD seem important stimuli for the prompt decrease in MAP, the 2.5-min longer-lasting decrease in HR, and the sustained decrease in NE during a 15-min moderate antiorthostatic posture change in humans.

Adult↗

PubMed1997

Contribution of abdomen and legs to central blood volume expansion in humans during immersion.

The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 +/- 1 to 64 +/- 1 g/l and from 46.7 +/- 0.3 to 45.5 +/- 0.4% (P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 +/- 2 to 36 +/- 1 mm (P < 0.05) during WI and increased similarly during WI+Occl from 27 +/- 2 to 35 +/- 1 mm (P < 0.05). Central venous pressure increased from -3.7 +/- 1.0 to 10.4 +/- 0.8 mmHg during WI (P < 0.05) but only increased to 7.0 +/- 0.8 mmHg during WI+Occl (P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

Abdomen↗

PubMed1996

Preoperative lymph-node staining with liposomes containing patent blue violet. A clinical case report.

A case study is reported using patent blue violet entrapped in liposomes to localize lymph nodes before surgery. Liposomes containing 44 mg patent blue violet were injected into foot lymphatics of a patient due to undergo retroperitoneal staging-lymphonodectomy. Lymph nodes were readily visualized and removed, and urine and serum was collected for assay of the dye. The maximum concentration of patent blue violet in serum was 2.7 micrograms mL-1, 1.5 h after the termination of the injection, almost no dye was detectable by the time of the operation 24 h later. In the first urine sample (2 h after the termination of the injection) the concentration of patent blue violet was 1.3 micrograms mL-1, and subsequently diminished, with the last urine sample to contain detectable dye being collected 20 h later. A total of 0.8 mg dye (2% of the injected amount) was excreted in the urine suggesting 10% of the circulating amount of dye was renally excreted. Endolymphatic injection of patent blue violet simplifies the often difficult process of finding the lymph nodes and additionally reduces side-effects. All surgery cases demanding a radical lymphonodectomy may profit, including testicular or bladder cancers and many gynaecological tumours.

Adult↗