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Background: Hyperthermia induces vasodilatation that reduces central blood volume (CBV), central venous pressure (CVP) and mean arterial pressure (MAP). Inhibition of atrial natriuretic peptide (ANP) could be a relevant homeostatic defense mechanism during hyperthermia with a decrease in CBV. The present study evaluated how changes in plasma ANP reflect the changes in CBV during hyperthermia., Methods: Ten healthy subjects provided with a water perfused body suit increased body core temperature 1 °C. In situ labeled autologous red blood cells were used to measure the CBV with a gamma camera. Regions of interest were traced manually on the images of the whole body blood pool scans. Two measures of CBV were used: Heart/whole body ratio and thorax/whole body ratio. CVP and MAP were recorded. Arterial (ANP art ) and venous plasma ANP were determined by radioimmunoassay., Results: The ratio thorax/whole body and heart/whole body decreased 7 % and 11 %, respectively (p<0.001). MAP and CVP decreased during hyperthermia by 6.8 and 5.0 mmHg, respectively (p<0.05; p<0.001). Changes in both thorax/whole body (R=0.80; p<0.01) and heart/whole body ratios (R=0.78; p<0.01) were correlated with changes in ANP art . However, there was no correlation between venous ANP and changes in CBV, nor between ANP art and MAP or CVP., Conclusion: Arterial but not venous plasma concentration of ANP, is correlated to changes in CBV, but not to pressures. We suggest that plasma ANP art may be used as a surrogate marker of acute CBV changes.

The aim of the present investigation was to examine how 8 weeks of intense endurance training influenced right and left ventricular volumes and mass in obese untrained subjects. Ten overweight subjects (19-47 years; body mass index of 34+/-5 kg/m(2)) underwent intensive endurance training (rowing) three times 30 min/week for 8 weeks at a relative intensity of 72+/-8% of their maximal heart rate response (mean+/-SD). Before and after 8 weeks of endurance training, the left and the right end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF), stroke volume (SV) and ventricular mass (VM) were measured by Magnetic resonance imaging (MRI). Submaximal heart rate decreased from 126+/-5 to 113+/-3 b.p.m. (10%; P<0.01), and from 155+/-5 to 141+/-4 b.p.m. (9%; P<0.001) at submaximal workloads of 70 and 140 W (110 W for women), respectively (mean+/-SEM). Resting ventricular parameters increased significantly: left ventricular SV, EDV and VM increased by 6%, 7% and 13%, respectively (P<0.01). The right side of the heart showed significant changes in SV, EDV and VM with increase of 4%, 4% and 12%, respectively (P<0.05). Eight weeks of endurance training significantly increased left ventricular SV and right ventricular SV, due to an increase in left ventricular EDV and right ventricular EDV. Furthermore, left VM and right VM increased. We conclude that using MRI and a longitudinal design it was possible to demonstrate similar and balanced changes in the right and left ventricle in response to training.

Background: Cardiotoxity is a side-effect of cancer treatment with anthracycline that is currently monitored by measuring the left ventricular ejection fraction (LVEF) by gated equilibrium radionuclide ventriculography (RNV). We hypothesized that BNP measurements could replace, at least in part, the RNV examinations. Therefore, we studied whether BNP could be used, alone or in combination with RNV, in the monitoring of anthracycline-induced cardiotoxity., Methods: A total of 333 patients undergoing anthracycline treatment had LVEF and BNP concentration measured. Of these, 73 had more than one determination. In the 333 patients we compared the BNP concentration to LVEF, and further, for the 73 patient with more than one examination, we compared the changes in LVEF and BNP. We evaluated different BNP cut-off values for detection of LVEF below 0.50, 0.45 and 0.40, respectively., Results: Using LVEF below 0.50 and a BNP cut-off value of 100 pg ml(-1) it was possible to save 90% of the RNV determinations with the cost of overlooking 68% of the patients with reduced LVEF. Using LVEF below 0.45 and a BNP cut-off value of 30 pg ml(-1) it was possible to save 59% of the RNV determination, with the cost of overlooking 15% of the patients with reduced LVEF., Conclusion: BNP cannot safely be used as an alternative to RNV determination of LVEF in patient undergoing anthracycline treatment if the standard limit of an LVEF of 0.50 was used. However, if only lower LVEF were to be detected BNP could be used to save RNV determinations.

Mixed findings regarding the effects of whole-body heat stress on central blood volume have been reported. This study evaluated the hypothesis that heat stress reduces central blood volume and alters blood volume distribution. Ten healthy experimental and seven healthy time control (i.e. non-heat stressed) subjects participated in this protocol. Changes in regional blood volume during heat stress and time control were estimated using technetium-99m labelled autologous red blood cells and gamma camera imaging. Whole-body heating increased internal temperature (> 1.0 degrees C), cutaneous vascular conductance (approximately fivefold), and heart rate (52 +/- 2 to 93 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg) accompanied by minor decreases in mean arterial pressure (all P < 0.05). The heat stress reduced the blood volume of the heart (18 +/- 2%), heart plus central vasculature (17 +/- 2%), thorax (14 +/- 2%), inferior vena cava (23 +/- 2%) and liver (23 +/- 2%) (all P

Background: Brain natriuretic peptide (BNP) is increased in heart failure; however, the relative contribution of the right and left ventricles is largely unknown., Aim: To investigate if right ventricular function has an independent influence on plasma BNP concentration., Methods: Right (RVEF), left ventricular ejection fraction (LVEF), and left ventricular end-diastolic volume index (LVEDVI) were determined in 105 consecutive patients by first-pass radionuclide ventriculography (FP-RNV) and multiple ECG-gated equilibrium radionuclide ventriculography (ERNV), respectively. BNP was analyzed by immunoassay., Results: Mean LVEF was 0.51 (range 0.10-0.83) with 36% having a reduced LVEF (<0.50). Mean RVEF was 0.50 (range 0.26-0.78) with 43% having a reduced RVEF (<0.50). The mean LVEDVI was 92 ml/m2 with 22% above the upper normal limit (117 ml/m2). Mean BNP was 239 pg/ml range (0.63-2523). In univariate linear regression analysis LVEF, LVEDVI and RVEF all correlated significantly with log BNP (p<0.0001). In a multivariate analysis only RVEF and LVEF remained significant. The parameter estimates of the final adjusted model indicated that RVEF and LVEF influence on log BNP were of the same magnitude., Conclusion: BNP, which is a strong prognostic marker in heart failure, independently depends on both left and right ventricular systolic function. This might, at least in part, explain why BNP holds stronger prognostic value than LVEF alone.

During arm exercise (A), mean arterial pressure (MAP) is higher than during leg exercise (L). We evaluated the effect of central blood volume on the MAP response to exercise by determining plasma atrial natriuretic peptide (ANP) during moderate upright and supine A, L and combined arm and leg exercise (A + L) in 11 male subjects. In the upright position, MAP was higher during A than at rest (102 +/- 6 versus 89 +/- 6 mmHg; mean +/- s.d.) and during L (95 +/- 7 mmHg; P < 0.05), but similar to that during A + L (100 +/- 6 mmHg). There was no significant change in plasma ANP during A, while plasma ANP was higher during L and A + L (42.7 +/- 12.2 and 43.3 +/- 17.1 pg ml(-1), respectively) than at rest (34.6 +/- 14.3 pg ml(-1), P < 0.001). In the supine position, MAP was also higher during A than at rest (100 +/- 7 versus 86 +/- 5 mmHg) and during L (92 +/- 5 mmHg; P < 0.01) but similar to that during A + L (102 +/- 6 mmHg). During supine A, plasma ANP was higher than at rest and during L but lower than during A + L (73.1 +/- 22.5 versus 47.2 +/- 15.9, 67.4 +/- 18.3 and 78.1 +/- 25.0 pg ml(-1), respectively; P < 0.05). Thus, upright A was the exercise mode that did not enhance plasma ANP, suggesting that central blood volume did not increase. The results suggest that the similar blood pressure response to A and to A + L may relate to the enhanced central blood volume following the addition of leg to arm exercise.

Background and Aim: The neurotransmitter histamine is involved in the regulation of appetite and in the development of age-related obesity in mice. Furthermore, histamine is a mediator of the anorexigenic action of leptin. The aim of the present study was to investigate a possible role of histamine in the development of high-fat diet (HFD)-induced obesity., Methods: Histamine-deficient histidine decarboxylase knock-out (HDC-KO) mice and C57BL/6J wild-type (WT) mice were given either a standard diet (STD) or HFD for 8 weeks. Body weight, 24-hour caloric intake, epididymal adipose tissue size, plasma leptin concentration and quantitative expression of leptin receptor (Ob-R) mRNA were measured., Results: Both HDC-KO and WT mice fed an HFD for 8 weeks increased their body weight significantly more than STD-fed mice. A significant difference in body weight gain between HDC-KO mice fed an HFD or an STD was seen after 2 weeks, whereas a significant difference in body weight gain was first observed after 5 weeks in WT mice. After 8 weeks 24-hour caloric intake was significantly lower in HFD- than in STD-fed WT mice. In HDC-KO mice no difference in caloric intake was observed between HFD- and STD-fed mice. After 8 weeks epididymal adipose tissue size and plasma leptin concentration had increased significantly in HFD-fed WT and HDC-KO mice compared to their STD-fed controls. Epididymal adipose tissue size was higher in HDC-KO than WT mice, both in STD- and HFD-fed mice. A significant decrease in Ob-R mRNA in HFD-fed HDC-KO mice compared to STD-fed HDC-KO mice was observed, while no such difference was observed in WT mice., Conclusion: Based on our results, we conclude that histamine plays a role in the development of HFD-induced obesity.