Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Research highlights from the literature

Item Type:Article
Title:Research highlights from the literature
Creators Name:Jordan, J.
Abstract:Never a dull moment in perusing the literature! In one study, the investigators tested an artificial baroreflex system in patients undergoing orthopedic surgery. Beat-by-beat blood pressure data was inserted into a computer system that served as an artificial vasomotor center. The vasomotor center regulated epidural catheter electrodes at the level of the lower thoracic spinal chord. The resulting constriction of splanchnic blood vessels attenuated experimental hypotension. In another study, the hypothesis that the sympathetic nervous system modulates granulocyte-colony stimulating factor (G-CSF)-induced release of hematopoetic stem cells from bone marrow was tested. The authors showed that G-CSF induces a bone-specific activation of the sympathetic nervous system. The sympathetic activation improves stem cell release through beta-adrenoreceptor stimulation. A third study tested the hypothesis that disordered sympathetic regulation at the tissue level may contribute to lipodystrophy in HIV patients on highly active antiretroviral therapies. Systemic sympathetic activity was not increased in these patients. However, interstitial norepinephrine was increased, particularly in adipose tissue. Excessive local sympathetic activity might redistribute fat from subcutaneous adipose tissue to other organs and other adipose tissue reservoirs. We can conclude that a machine can operate the baroreflex and that the immune system and adipose tissue will have to react accordingly.
Keywords:Autonomic, Baroreflex, Hypotension, Bone marrow, Hematopoetic stem cells, Granulocyte-colony stimulating factor (G-CSF), Human immunodeficiency virus (HIV), Antiretroviral therapy, Lipodystrophy
Source:Clinical Autonomic Research
ISSN:0959-9851
Publisher:Springer
Volume:16
Page Range:83-85
Date:April 2006
Official Publication:https://doi.org/10.1007/s10286-006-0343-6
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library