We evaluated regional electrical impedance (Z degree) at 2.5 and 100 kHz to separate intra- and extracellular fluid changes and correlated Z degree over the thorax (TI) to relative changes in the central blood volume (CBV) induced by head-up tilt. In nine experiments head-up tilt resulted in normotensive central hypovolaemia associated with a 3.7 +/- 0.4 Ohm (mean +/- SE) increase in TI100 kHz after 60 min. In 24 experiments pre-syncopal symptoms were induced after 43 +/- 2 min, when TI100 kHz had increased 4.2 +/- 0.2 Ohm. Head-up tilt instantly decreased the activity of technetium labelled erythrocytes (99Tcm) over the thorax by 24 +/- 2%, and increased 99Tcm over the thigh by 68 +/- 10% (P less than 0.01, n = 8) with no further changes during the sustained tilt. Haematocrite increased during head-up tilt from 43.1 +/- 0.3 to 47.9 +/- 0.6% (P less than 0.01, n = 8). Accordingly, the increase in TI (6.3 +/- 0.6 vs. 4.5 +/- 0.4 Ohm, n = 6) and the decrease in Z degree through one leg (7.2 +/- 1.2 vs. 2.8 +/- 0.5 Ohm, n = 6) at 2.5 kHz was more pronounced than at 100 kHz. Also the changes in TI were correlated to CBV as calculated from 99Tcm and haematocrite (r = 0.90, P less than 0.01). The results suggest that: (1) Hypovolaemic shock is associated with a faster increase of TI than normotensive head-up tilt. (2) Head-up tilt is characterized by an initial decrease in CBV followed by a further decrease in plasma volume, which eventually leads to hypovolaemic shock. (3) Blood volume changes during head-up tilt are reflected in regional Z degree.

Because of the lack of agreement on when rectus diastasis (RD) is pathologic, the aim was to investigate indications for surgical repair. This study presents classifications of RD, current knowledge on the relation to pregnancy, and conservative and surgical management. A systematic search in Pubmed, Embase, Cochrane, and Cinahl revealed 437 studies. Inclusion criteria were applied according to the above mentioned subjects of interest. In total 28 studies were included, representing 3725 patients, 11 of these by assessing reference lists of included studies. Only one RCT was found; most studies were case-series lacking statistical analysis. RD was common in post-partum women. Antepartum activity level may have a protective effect on RD and exercise may improve post-partum symptoms of RD. Repair was done during abdominoplasty or laparoscopically. The patient-satisfaction was high and long-term recurrence was reported by one study, while five reported no recurrence. Overall major complications were few, while minor complications were primarily seroma and wound complications. RD is by itself not a true hernia and, therefore, not associated with the risk of strangulation. Repair is mostly done due to cosmetic reasons. The condition does not necessarily require repair, and conservative management may be an alternative. If done, the protrusion of the abdomen, rather than the diastasis itself should influence the decision of repair. It is recommended that future studies use the established classifications (e.g. Beer, Rath, or Nahas) when reporting RD and long-term outcome of treatment. Comparison of surgical techniques and studies that address and compare conservative management with surgery are needed.

To evaluate the importance of right atrial filling pressure versus central blood volume for the plasma concentration of atrial natriuretic peptide in man, head-up tilt to 50 degrees maintained until the appearance of presyncopal symptoms was carried out in six healthy males. Head-up tilt increased thoracic electrical impedance from 35.4 +/- 0.9 (mean and SE) to 39.2 +/- 0.9 ohm, mean arterial pressure from 64.5 +/- 3.6 to 76.6 +/- 3.0 mmHg and heart rate from 51 +/- 3 to 85 +/- 4 beats min-1 (P less than 0.01). After 35 +/- 7 min presyncopal symptoms appeared, together with a decrease in mean arterial pressure to 51 +/- 4 mmHg and in heart rate to 59 +/- 7 beats min-1 (P less than 0.01). Central venous pressure (2.1 +/- 1.0 mmHg) did not change significantly, but atrial natriuretic peptide decreased from 9.4 +/- 1.6 to 4.2 +/- 1.3 pmol l-1 (P less than 0.01) and was inversely related to thoracic impedance (r = -0.65, n = 44, P less than 0.001). The results indicate that changes in the central blood volume rather than in central venous pressure determine the secretion of atrial natriuretic peptide in man.

In conscious male rats intracerebroventricular infusion of histamine increased the plasma concentrations of ACTH and \g=b\-endorphinimmunoreactivity 2.5-fold (P < 0.01). Gel filtration of plasma revealed two peaks of \g=b\-endorphinimmunoreactivity corresponding to \g=b\-endorphin and \g=b\-lipotropin. The two fractions increased almost equally in histamine-stimulated animals, whereas most of the circulating \g=b\-endorphin immunoreactivity in control animals corresponded to \g=b\-endorphin. Central infusion of the H1\ x=r eq-\ receptor agonist 2-thiazolylethylamine and of the H2\ x=r eq-\ receptor agonists dimaprit or 4-methylhistamine increased the plasma ACTH and \g=b\-endorphin immunoreactivity concentrations 2-and 3-fold, respectively (P < 0.01). Infused intracerebroventricularly, the H2\ x=r eq-\ receptor antagonists cimetidine or ranitidine prevented the histamine-induced increase in plasma ACTH and \g=b\-endorphinimmunoreactivity (P < 0.01), whereas the H1-receptor antagonist mepyramine inhibited the peptide responses by 70% (P < 0.01). Infused intra-arterially cimetidine or ranitidine inhibited the histamine\x=req-\ induced increase in plasma ACTH by 80% (P < 0.01) and plasma \g=b\-endorphinimmunoreactivity by 45% (P < 0.05), whereas mepyramine or the other H1-receptor antagonist SKF-93944 inhibited the ACTH response by 50% (P < 0.05), but had no effect on the \g=b\-endorphinimmunoreactivity. The results indicate that histamine increases the release of the pro-opiomelanocortin derived peptides ACTH, \g=b\-lipotropin and \g=b\-endorphin from the anterior pituitary lobe, whereas an effect of histamine on the release of \g=b\-endorphin from the neurointermediate lobe is possible. The effect of histamine seems primarily mediated by H2-receptors, whereas H 1-receptors appear to play a minor role.