The effects of ventricular fluid osmolality on bulk flow of nascent fluid into the cerebral ventricles of cats

Abstract

The effects of ventricular fluid osmolality on the bulk flow of nascent fluid into the cerebral ventricles of anesthetized cats was measured during ventriculocisternal perfusion. This nascent fluid consists of both cerebrospinal fluid (CSF) and fluid which results from an osmotic gradient between ventricular fluid and the blood and/or brain. Perfusions were carried out with both mock CSF and with solutions containing either sucrose, urea, or NaCl. Differences between the normal bulk flow rate of nascent CSF and bulk flow rate measured during perfusion with anisotonic solutions were linearly related to corresponding differences in osmolality of the effluent fluid from the ventricles. The coefficients of somotic flow using sucrose (0.231 mul/min per mOsm) and NaCl (0.224) were similar, and greater than that using urea (0.156). During perfusion with sucrose when effluent osmolality increased by 200 mOsm (63% of normal), bulk flow rate of nascent fluid increased by 50 mul/min (200% of normal). Flow was undetectable when the effluent osmolality was 190 mOsm (decrease of 135 mOsm), although osmotically active particles continued to enter the ventricular system. Intravenous injection of acetazolamide reduced these coefficients to similar values of 0.0963 for NaCl, and 0.0955 for urea. In all experimental conditions no changes were found in cerebral water content. These results suggest that the increased bulk flow which occurs during perfusion with hypertonic solutions originates from the choroid plexus.

“Compensated hyperosmolarity” of cerebrospinal fluid and the development of hydrocephalus

“…Therefore, it is necessary to point out that a change in CSF osmolarity does not affect CSF formation/secretion (Orešković et al, 2002), as was believed during earlier investigations (Hochwald et al, 1974;Wald et al, 1976). Just as it was clearly demonstrated in our previous publications that net CSF formation does not exist (Orešković et al, 2002;Klarica et al, 2009;Maraković et al, 2010;Orešković and Klarica, 2010), so in this work on dogs by following the water from the bloodstream into the CSF system in iso-osmolar and osmotically loaded CSF (Fig.…”

“…water) in the CSF system. It has recently been proposed that development of hydrocephalus (Krishnamurthy et al, 2009;Orešković and Klarica, 2011) and the change in CSF volume is caused by changes in blood or CSF osmolarity (Hochwald et al, 1974;Wald et al, 1976;Orešković et al, 2002;Maraković et al, 2010;Jurjević et al, 2012) and that elevated CSF osmolarity should be considered as one of the most important factors in excessive CSF/water accumulation. We have also presumed that the greatest responsibility for the maintenance of CSF iso-osmolarity is the rapid extraction of water from the bloodstream into the osmotically loaded CSF space, and that extracted water would consequently cause an accumulation of fluid, increase in ICP and the development of hydrocephalus.…”

“…As there are almost no obstacles/barriers for water within the CNS, and as water quickly and easily crosses from one compartment to another (blood, CSF, ISF, intracellular fluid), the cause of excessive fluid accumulation should be searched for in pathophysiological conditions leading to the displacement of water into the CSF space, and its accumulation within the CSF system. It is well documented that osmotic gradients play a significant part in the regulation of brain water and CSF volume (Hochwald et al, 1974;Wald et al, 1976;Orešković et al, 2002;Maraković et al, 2010;Jurjević et al, 2012). Because of this, it has been presumed that without significant obstruction or stenosis of the CSF system, all pathological processes in which an increase of CSF osmolarity (the osmotic load of CSF) takes place should lead to an increase in CSF volume, and consequently should cause hydrocephalus (Krishnamurthy et al, 2009;Orešković and Klarica 2010; what speaks in favor the most recent multiinstitutional studies of hydrocephalus as a consequence of hemispherectomy surgery for medically intractable epilepsy treatment (Lew et al, 2013).…”

Development of hydrocephalus and classical hypothesis of cerebrospinal fluid hydrodynamics: Facts and illusions

“…It was shown on cats that an increase in ventricular CSF osmolarity leads to an increase in CSF volume (Marlin et al, 1978;Orešković et al, 2002;Wald et al, 1976). The volume flow rate was inhibited completely with ventricular fluid osmolarity of 127 mOsm/l, and it increased without an apparent limit to more than 70 µl/min with a ventricular CSF osmolarity of 550 mOsm/l (Marlin et al, 1978).…”

“…In experiments in which the choroid plexuses (main site of CSF secretion) have been removed, no changes in the volume and composition of the newly formed CSF have been observed (Milhorat, 1969;Milhorat et al, 1976). Furthermore, it has been shown that there is no net formation of CSF in isolated brain ventricles, and that CSF does not circulate along the CSF system, but rather that permanent CSF changes happen within the surrounding tissue, depending on the fluid osmolarity (Bulat et al, 2008;Maraković et al, 2010;Orešković et al, 2001;Orešković et al, 2002;Wald et al, 1976). By monitoring the behavior of different substances in the CSF of some patients, it was also concluded that CSF is formed everywhere and absorbed everywhere inside the CSF cavities (Di Chiro, 1964;1966).…”