The frequency of thermal windows increased with increasing ambient temperature and body weight. We assume that the restriction of an enhanced cutaneous blood ACY-738 price flow to thermal windows might enable the animal to react more flexibly to its needs with regard to heat loss. With this
understanding, the use of thermal windows in heat loss might be seen as a fine-tuning mechanism under thermoneutral conditions. (C) 2010 Elsevier Ltd. All rights reserved.”
“The effect of cerebrospinal fluid (CSF) osmolarity on the CSF volume has been studied on different CSF/brain tissue contact areas. It has been shown, on anesthetized cats under normal CSF pressure, that the perfusion of CSF system (12.96 mu l/min) by hyperosmolar CSF (400 mOsml/l) leads to significantly higher outflow volume (mu l/min) during ventriculo-cisternal perfusion (29.36 +/- 1.17 and 33.50 +/- 2.78) than the ventriculo-aqueductal perfusion (19.58 +/- 1.57 and 22.10 +/- 2.31) in experimental period of 30 or 60 min. Both of these hyperosmolar perfusions resulted in significantly higher outflow volume than the perfusions by isoosmolar artificial CSF (12.86 +/- 0.96 and 13.58 +/- 1.64).
These results suggest that the volume of the CSF depends on both the CSF osmolarity and the size of the contact area Selleckchem OTX015 between CSF system and surrounding tissue exposed to hyperosmolar CSF. However, all of these facts imply that the control of the CSF volume is not in accordance with the classical hypothesis of cerebrospinal fluid hydrodynamic. According to this hypothesis, the CSF volume should be regulated by active formation of CSF (secretion) inside the brain ventricles and passive CSF absorption outside of the brain. learn more Obtained results correspond to the new hypothesis which claims that the volume of CSF depends on the gradients of hydrostatic and osmotic forces between the blood on one side and extracellular fluid and CSF on the
other. The CSF exchange between the entire CSF system and the surrounding tissue should, therefore, be determined by (patho)physiological conditions that predominate within those compartments. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“The purpose of this study was to determine if mild hypothermia alters mitotic activity in normal and post-ischemic hippocampal slices. (1) Normothermic oxygen-glucose deprivation (OGD 60 min) increased mitotic activity in the hippocampus up to 4d post-OGD. (2) Mild hypothermia (33 degrees C for 24 h) initiated after OGD stress reduced mitotic activity compared to normothermic controls up to 8 d post-OGD. (3) Mild hypothermia stimulated mitotic activity in normal (no OGD stress) hippocampus up to 24 h post-hypothermia.