C. Malhan

Effects of changes in serum osmolarity on bulk flow of fluid into cerebral ventricles and on brain water content

SummaryThe effects of changes in serum osmolarity on the rate and osmolarity of bulk flow of fluid into the cerebral ventricles and on cortical white and grey matter water content were studied in cats. Bulk flow rates and osmolarities were measured during ventriculocisternal perfusion both before and after intravenous infusion of glucose solutions. Infusions of glucose in concentrations greater than 6% decreased fluid bulk flow rate and its osmolarity. Glucose in concentrations less than 6% increased fluid bulk flow rate and decreased its osmolarity. Bulk flow rate and serum osmolarity were found to be linearly related with a coefficient of osmotic flow of −0.835 μl/min per mOsm/l. At the extremes of induced serum osmolarities, (290 and 360 mOsm/l) bulk flow rate was either increased by 120% or completely inhibited. Effluent osmolarity also increased proportionately to serum osmolarity (0.338 mOsm/l per mOsm/l). When compared to controls, cortical grey and white matter water content increased by 1.9% and 2.9%, respectively, when the infused glucose concentration was 2.5% or less, and decreased by 1.8% and 2.9% when the concentration was 10% or more. The results of these experiments suggest that the increased bulk flow comes from the brain, rather then directly from the blood.

The Rôle of the Skull and Dura in Experimental Feline Hydrocephalus

The skull and dura were removed over one or both cerebral hemispheres of cats with experimental hydrocephalus, and the effects on ventricular volume and csf turnover were measured by ventricular perfusion. This procedure frequently resulted in bilateral massive ventriculomegaly when the calvarium was removed on both sides; when it was removed on one side, ventriculomegaly occurred only on that side. No differences in rates of csf formation and absorption between both groups of animals were noted; however, these rates may be significantly different from those noted in hydrocephalic cats with intact skulls.

The effects of serum osmolarity on cerebrospinal fluid volume flow

Abstract The effects of changes in serum osmolarity on cerebrospinal fluid (CSF) formation were studied in cats. CSF production rates were measured by ventriculocisternal perfusion both before and after intravenous infusion of glucose solutions. Infusion of glucose, hyperosmolar with respect to serum, increased serum osmolarity and caused a decrease in CSF formation rate; conversely, infusion of hypoosmolar solutions lowered serum osmolarity and increased CSF formation. CSF production and serum osmolarity were found to be linearly related. A 1% serum osmolarity change resulted in a 6.7% change in CSF formation. CSF formation increased by 130% with a serum osmolarity of 265 m0sm/1 and was undetectable with serum of 380 m0sm/1.

Kaolin‐induced hydrocephalus impairs CSF secretion by the choroid plexus

CSF volume flow and sodium (Na+)-influx rates in normal and kaolin-induced hydrocephalic cats were measured during ventricular perfusion with anisotonic sucrose solutions. When ventricular fluid osmolality was 120 mOsm, CSF volume flow ceased for both groups of cats. As ventricular fluid osmolality was increased, the CSF volume flow rate of normal cats increased to 70 μl per minute, and in hydrocephalic cats to 40 μl per minute. In normal cats, for ventricular fluid osmolality between 50 and 350 mOsm, Na+-influx was constant and thought to occur by diffusion; while for higher osmolalities, Na+-influx increased. In hydrocephalic cats, Na+-influx increased over the entire range of ventricular osmolality but was less than in normal cats. Acetazolamide decreased the CSF volume flow in normal cats by 40 percent, but was ineffective in hydrocephaiic cats. These results suggest that CSF secretion by the choroid plexus of cats with kaolin-induced hydrocephalus is impaired.

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

SummaryThe 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 osmotic flow using sucrose (0.231 μl/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 μl/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.

Movement of Water Between Blood, Brain and CSF in Cerebral Edema

Movement of water between blood, brain, and cerebrospinal fluid was studied in cats with experimentally induced brain edema. A freeze lesion was used to induce edema characterized by an increase of brain extracellular space fluid. Major blood vessels supplying blood to the head were clamped to produce edema characterized by an increase of brain intracellular space fluid. Serum osmolality was decreased also to induce intracellular edema. Bulk flow of CSF into the cerebral ventricles was measured by the technique of ventriculocisternal perfusion. After perfusion, the water content of cerebral gray and white matter was measured.

Movement of sodium from blood and brain into the cerebral ventricles of cats during altered CSF volume flow rates.

Abstract The movement of Na+ and of volume flow fluid into the ventricles of cats was studied during ventriculocisternal perfusion with anisotonic sucrose solutions. During perfusion with solutions ranging in osmolality from 350 to 10 mOsm, the volume flow of fluid decreased linearly to zero, but Na+ influx remained constant. During perfusion with solutions ranging from 300 to 785 mOsm, both volume flow of fluid and Na+ influx increased linearly without an apparent limit. In some experiments, intraveneous 22Na was used to trace Na+ movement from blood to brain and cerebrospinal fluid. From results of calculations of specific activities of sodium in serum, effluent fluid, and brain, it is concluded that when the cerebral ventricles are perfused with a Na+ free sucrose solution, Na+ diffuses into the ventricular fluid directly from blood flowing in the choroid plexus.

THE RELATIONSHIP BETWEEN SODIUM INFLUX AND VOLUME FLOW INTO THE CEREBRAL VENTRICLES OF CATS

Abstract— The relationship between sodium ion (Na+) influx and vol. flow of fluid into the cerebral ventricles was measured during ventriculocisternal perfusion with sucrose solutions of various concentrations. The vol. flow of fluid into the ventricles of cats varied linearly from 0 to 90 μl/min with sucrose solutions of 6 to 780 mOsm/l. In the vol. flow range of 0 to 35 μl/min, Na+ influx was essentially constant independent of vol. flow rate with a mean value of 6.95 μEq/min. In the vol. flow range of 25 to 90 μl/min, Na+ influx increased linearly with flow rate. Under all conditions, Na+ influx was greater than that corresponding to newly formed fluid with a normal spinal fluid Na+ concentration. The virtual Na+ concentration of nascent fluid was effectively infinite when vol. flow was zero and had an asymptotic minimum value of 109 mEq/l as vol. flow increased above normal. These results demonstrate that Na+ influx into the ventricles may occur by diffusion from the surrounding brain and also with vol. flow of nascent fluid.

On the movement of fluid through the brain of hydrocephalie cats

The effects of changes in serum osmolality on the volume flow of fluid into the cerebral ventricles and on brain water content was examined in cats with kaolin-induced hydrocephalus. Slopes of the regression lines relating volume flow and serum osmolality for both normal and hydrocephalie cats are the same. The constant difference in flow rates between the two lines, 7 μl per minute, is probably due to impaired choroid plexus function of the hydrocephalie cats. The osmotic pressure gradient that causes the flow of fluid is therefore probably between blood and brain. Under these conditions, changes in brain water content of hydrocephalie cats were smaller than in normals and can be related to the edema present in this disorder. Despite the inflammatory response to kaolin, the blood-brain barrier remains intact. From the calculated filtration coefficient, it can be inferred that the flow of water from serum through brain and into cerebrospinal fluid is limited by the resistance of fluid flow through the brain.