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C S Patlak

Publications and source records attributed to C S Patlak.

At least 19 recordsLinked to original sources
PubMed1992

Analysis of in vitro glucose utilization in a circadian pacemaker model.

An in vitro glucose utilization method, based upon 14C-2-deoxyglucose kinetics in brain slices, has been used to study circadian rhythms in hypothalamic slices containing the suprachiasmatic nucleus (SCN). Spontaneous SCN metabolic activity in vitro is similar to that observed in vivo with higher metabolic rates in subjective daytime and lower rates during subjective night. However, in vitro SCN metabolic activity during late subjective day is above that seen when glucose utilization is measured in vivo, suggesting that an inhibitory influence normally active in vivo is lost during slice isolation. Incubation of slices containing SCN in the presence of TTX exposes a TTX-insensitive component of metabolic activity in early subjective day, supporting prior suggestions that glucose utilization by the circadian oscillator continues in the absence of Na(+)-dependent action potentials. Studies with high Mg2+ concentrations are consistent with the hypothesis that most metabolic activity above the basal level observed with the glucose utilization method is related to synaptic activity. Pharmacological studies of the SCN brain slice model with radiotracers offer potential for analysis of both circadian rhythmicity and neural regulation.

Animals↗
PubMed1991

Quantitative measurements of capillary transport in human brain tumors by computed tomography.

The rate at which water-soluble chemotherapeutic drugs enter brain tumors can be extremely variable. The ability to measure or predict the rate of drug entry may have an important role in treatment. We have developed a method that uses information from contrast-enhanced computed tomographic scans to measure quantitatively the rate of transcapillary transport of iodinated compounds in brain tumors. In a group of 10 patients with brain tumors, we obtained serial measurements of tissue (Am) and arterial plasma (Cp) iodine concentration from timed computed tomographic scans done over 30 minutes, after intravenous infusion of meglumine iothalamate (Conray-60). These measurements were analyzed with a two-compartment pharmacokinetic model and nonlinear least-squares regression methods to obtain K1, a blood-to-tissue transfer constant; k2, a tissue-to-blood rate constant; and Vp, tissue plasma vascular volume. Images of K1, k2, and Vp were reconstructed after calculating these values for each 0.8 x 0.8 x 5-mm volume element of the original data. Mean whole tumor K1 values varied from 2.0 mu 1 gm-1 min-1 in a thalamic astrocytoma to 33.9 mu 1 gm-1 min-1 in a glioblastoma multiforme. The value of k2 varied from 0.034 to 0.108 min-1, and Vp varied from 2.4 to 7.9 ml 100 gm-1. In tumor-free brain, the K1 of meglumine iothalamate was 2.9 mu 1 gm-1 min-1; k2 was 0.058 min-1; and Vp was 2.1 ml 100 gm-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

A method to quantitatively measure transcapillary transport of iodinated compounds in canine brain tumors with computed tomography.

We present a quantitative method for determining a blood-to-tissue influx constant (K1), a tissue-to-blood efflux constant (k2), and tissue plasma vascular space (Vp) that uses a computed tomographic (CT) scanner to make tissue and plasma measurements of the concentration of an iodinated compound. Meglumine iothalamate was infused intravenously over time periods of 0.5-5 min, up to 49 CT scans were obtained at one brain level, and arterial plasma was sampled over a 30- to 40-min period. K1, k2, and Vp were calculated for each voxel of the 320 x 320 matrix, using a two-compartment pharmacokinetic model and nonlinear least-squares regression. The method was used in dogs with avian sarcoma virus-induced brain tumors. As many as four studies on different days were done in the same animal. In tumor-free cortex, K1 of meglumine iothalamate was 2.4 +/- 1.7 microliter g-1 min-1 (mean +/- SD) and Vp was 3.4 +/- 0.5 ml 100 g-1. Mean whole-brain tumor K1 values ranged from 3.3 to 97.9 microliters g-1 min-1; k2 ranged from 0.032 to 0.27 min-1; and Vp ranged from 1.1 to 11.4 ml 100 g-1. These values were reproducible in serial experiments in single animals. Independent verification of K1 values was obtained with quantitative autoradiographic measurements of alpha-aminoisobutyric acid, which has similar physicochemical properties to meglumine iothalamate. The CT methodology is capable of demonstrating regional variation of transcapillary transport in brain tumors and may be of value in the study of human brain tumors.

Aminoisobutyric Acids↗
PubMed1991

Kinetic analysis of transport and opioid receptor binding of [3H](-)-cyclofoxy in rat brain in vivo: implications for human studies.

[3H]Cyclofoxy (CF: 17-cyclopropylmethyl-3,14-dihydroxy-4,5-alpha-epoxy-6-beta-fluoromorp hinan) is an opioid antagonist with affinity to both mu and kappa subtypes that was synthesized for quantitative evaluation of opioid receptor binding in vivo. Two sets of experiments in rats were analyzed. The first involved determining the metabolite-corrected blood concentration and tissue distribution of CF in brain 1 to 60 min after i.v. bolus injection. The second involved measuring brain washout for 15 to 120 s following intracarotid artery injection of CF. A physiologically based model (Sawada et al., 1990a) and a classical compartmental pharmacokinetic model (Wong et al., 1986a) were compared. The models included different assumptions for transport across the blood-brain barrier (BBB); estimates of nonspecific tissue binding and specific binding to a single opiate receptor site were found to be essentially the same with both models. The nonspecific binding equilibrium constant varied modestly in different brain structures (Keq = 3-9), whereas the binding potential (BP) varied over a much broader range (BP = 0.6-32). In vivo estimates of the opioid receptor dissociation constant were similar for different brain structures (KD = 2.1-5.2 nM), whereas the apparent receptor density (Bmax) varied between 1 (cerebellum) and 78 (thalamus) pmol/g of brain. The receptor dissociation rate constants in cerebrum (k4 = 0.08-0.16 min-1; koff = 0.16-0.23 min-1) and brain vascular permeability (PS = 1.3-3.4 ml/min/g) are sufficiently high to achieve equilibrium conditions within a reasonable period of time. Graphical analysis (Patlak and Blasberg, 1985) of the data is inappropriate due to the high tissue-loss rate constant (kb = 0.03-0.07 min-1) for CF in brain. From these findings, CF should be a very useful opioid receptor ligand for the estimation of the receptor binding parameters in human subjects using [18F]CF and positron emission tomography.

Animals↗
PubMed1991

Extracellular volume decreases while cell volume is maintained by ion uptake in rat brain during acute hypernatremia.

1. Regulation of brain extracellular and intracellular water content, regarded as volume, and electrolytes in response to 90 min of hypernatremia has been studied in the cerebral cortex of rats under urethane anaesthetic. 2. Total tissue electrolytes and water were partitioned between extracellular and intracellular compartments based on measurements made in two series of experiments. In one, tissue samples were collected and analysed for total water, Na+, K+ and Cl-. In the other, tissue extracellular volume fraction, [Na+] and [K+] were measured in situ using ion-selective microelectrodes. 3. Osmotically induced water loss from cerebral cortex was less than that predicted for ideal osmotic behaviour, revealing a degree of volume regulation, and this regulation was associated with net tissue uptake of Na+, Cl- and K+. 4. Total water content was 3.77 g H2O (g dry weight)-1 in control cortex and this decreased by 7% after 30 min of hypernatremia and then remained relatively stable at this value. Control extracellular water content, based on an extracellular volume fraction of 0.18, was 0.88 g H2O (g dry weight)-1. Control intracellular water content, estimated as the difference between total and extracellular water contents, was 2.89 g H2O (g dry weight)-1. After 30 min of hypernatremia, extracellular water content decreased by an average of 27% but intracellular water did not change. This indicates selective regulation of cell volume. By 90 min the extracellular water content had decreased by 47% and the loss in extracellular water content appeared to be accompanied by a roughly equivalent increase in intracellular water content. The intracellular volume increase, however, was not statistically significant. The tortuosity of the extracellular space averaged 1.57 and increased to 1.65 during the hypernatremia. 5. Brain extracellular fluid and plasma [Na+] were roughly equal in control tissue. Both increased by 30 mu equiv (g H2O)-1 as a result of the hypernatremia, although extracellular [Na+] lagged behind the plasma value during much of the first 60 min of hypernatremia. Extracellular [K+] was homeostatically regulated at 3 mu equiv (g H2O)-1 independent of changes in plasma electrolytes. 6. Estimates of extracellular and intracellular ion content (mu equiv (g dry weight)-1) indicate that extracellular Na+, Cl- and K+ content decreased during hypernatremia, by 32, 21 and 42% respectively, whereas intracellular ion content increased by 100, 169 and 5% respectively. 7. It is concluded that during acute hypernatremia the extracellular space decreases in volume through the loss of water and electrolytes while the intracellular compartment maintains its water content and gains electrolytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Variation in local cerebral blood flow response to high-dose pentobarbital sodium in the rat.

Microvascular bed structure and functions are known to vary throughout the brain. Microvascular responses to high doses of pentobarbital sodium might therefore differ among brain areas. This possibility was examined by measuring local cerebral blood flow (LCBF) with [14C]iodoantipyrine in 52 brain areas at 5, 10, 25, and 60 min after intraperitoneal administration of pentobarbital (50 mg/kg). From 5 to 60 min, LCBF was significantly lowered in 17 of 25 forebrain gray matter areas but in only 1 of 18 hindbrain gray matter structures, the pontine nuclei. Smaller, shorter duration lowering of LCBF was also observed in ten other brain areas. In both control and treated rats, LCBF was found to vary within individual brain structures. The pattern of these LCBF variations was columnar in the cerebral cortex and the hippocampus but was patchy in the caudate-putamen, thalamus, and inferior colliculus. These results indicate that pentobarbital anesthesia more strongly alters LCBF in the forebrain than in the hindbrain and produces different patterns of changes in LCBF than in local cerebral glucose utilization, which was measured with 2-deoxyglucose in a companion study.

Animals↗
PubMed1991

Albumin outflow into deep cervical lymph from different regions of rabbit brain.

Dynamics and pathways of 125I-labeled albumin (RISA) outflow from brain to deep cervical lymph have been studied in anesthetized rabbits between 4 and 25 h after microinjection of 1 microliter RISA into the internal capsule or midbrain. Lymph from the jugular lymph trunks was collected for periods of 2-11 h. RISA was cleared from brain with half-times of disappearance from internal capsule and midbrain of 18.2 and 11.9 h, respectively. RISA was distributed in high concentration to subarachnoid arteries that supplied the tissue injection site; this was consistent with RISA drainage from brain via perivascular spaces. Outflow through lymph rose to a maximum value 15-20 h after tracer injection. Mean recovery of RISA from lymph over the 25-h collection period accounted for 22% of total loss from internal capsule and 18% from midbrain. This result compares with mean recoveries from caudate nucleus and cerebrospinal fluid of 47% and 30%, respectively [M.W.B. Bradbury, H.F. Cserr, and R.J. Westrop, Am. J. Physiol. 240 (Renal Fluid Electrolyte Physiol. 9): F329-F336, 1981]. These are minimal estimates of total outflow to lymph because of the 15- to 20-h delay in RISA passage from brain to lymph.

Animals↗
PubMed1990

Fluid flow rates in human peritumoural oedema.

Five patients with various types of brain tumours were infused with x-ray contrast material in a schedule designed to maintain a constant plasma concentration of tracer over a period of 3 hours. CT scans from an equatorial section of the tumour were taken at frequent intervals the first hour; then at 2 and 3 hours, and when possible up to 14 hours. Two different mathematical models-1. simple diffusion, and 2. transport by bulk flow plus diffusion were used to analyze the changes in tracer amount along profiles placed radially from the tumour center into the oedematous white matter. We found that the simple diffusion model could not account for the spread of contrast material in 3 cases. Adding bulk flow transport gave a very good fit to the measurements, also for the late scans. This model gave bulk flow rates of 0.0005 to 0.005 ml cm-2 min-1 for the extratumoural tissue close to the tumour, and values from 0.25 to 0.55 for the extracellular space in this region. We conclude that the peritumoural tissue is "perfused" by oedema fluid at relatively high flow rates and that this flow transports tracer and other components of plasma into the extracellular space.

Body Fluids↗
PubMed1990

Kinetic analysis of blood-brain barrier transport of D-glucose in man: quantitative evaluation in the presence of tracer backflux and capillary heterogeneity.

The present study deals with the analysis of double-indicator curves for blood-brain barrier studies. Two mathematical models which provide for the estimation of backflux of tracer from brain to blood in conjunction with heterogeneity of the cerebral capillary and large-vessel transit times were used for the analysis of D-glucose transport on the basis of cerebral venous outflow curves. The two models, non-mixed and well mixed, arise from differing assumptions regarding the effective region surrounding the capillary lumen. An approximate solution for the well-mixed model was developed to increase computation speed. Fourteen D-glucose outflow curves and their reference curves were obtained from nine patients and subsequently analyzed by the two models. Further, in five patients data were obtained under different physiological conditions: normal, decreased, and increased cerebral blood flow rates. The results support the appropriateness of the well-mixed model and heterogeneity of the cerebral capillary transit times. The median value for the average extraction was 0.18 and the median distribution space was 0.14. The latter value is similar to the brain extracellular space that has been estimated by other methods. The extraction values calculated from the peak of the venous outflow curves were significantly smaller than the whole-brain average extraction values estimated with the well-mixed model (0.157 vs 0.178, P less than 0.0005). In summary: (a) capillary heterogeneity is present in the human brain and changes with cerebral blood flow; (b) after crossing the blood-brain barrier, D-glucose distributes in the brain extracellular fluid; and (c) the extraction curve is significantly influenced by backflux.

Biological Transport, Active↗
PubMed1990

Asymmetrical transport of amino acids across the blood-brain barrier in humans.

Blood-brain barrier permeability to four large neutral and one basic amino acid was studied in 30 patients with the double indicator technique. The resultant 64 venous outflow curves were analyzed by means of two models that take tracer backflux and capillary heterogeneity into account. The first model considers the blood-brain barrier as a double membrane where amino acids from plasma enter the endothelial cell. When an endothelial cell volume of 0.001 ml/g was assumed, permeability from the blood into the endothelial cell was, for most amino acids, about 10-20 times larger than the permeability for the reverse direction. The second model assumes that the amino acids, after intracarotid injection, cross a single membrane barrier and enter a well-mixed compartment, the brain extracellular fluid, i.e., the endothelial cell is assumed to behave as a single membrane. With this model, for large neutral amino acids, the permeability out of the extracellular fluid space back to the blood was between 8 to 12 times higher than the permeability from the blood into the brain. Such a difference in permeabilities across the blood-brain barrier can almost entirely be ascribed to the effect of a nonlinear transport system combined with a relatively small brain amino acid metabolism. The significance of the possible presence of an energy-dependent A system at the abluminal side of the blood-brain barrier is discussed and related to the present findings. For both models, calculation of brain extraction by simple peak extraction values underestimates true unidirectional brain uptake by 17-40%. This raises methodological problems when estimating blood to brain transfer of amino acids with this traditional in vivo method.

Adult↗
PubMed1990

Kinetic model of 2-deoxyglucose metabolism using brain slices.

A six-compartment, nine-parameter kinetic model of 2-deoxyglucose (2DG) metabolism, which includes bidirectional tissue transport, phosphorylation, two-step dephosphorylation, phosphoisomerization, and conjugation to UDP and macromolecules, has been derived. Data for analysis were obtained from 540- and 1,000-microns-thick hippocampal and hypothalamic brain slices, which were incubated in buffer containing [14C]2DG, frozen, extracted with perchlorate, and separated on anion-exchange columns. Solutions of the equations of the model were fit to the data by means of nonlinear least-squares analysis. These studies suggest that dephosphorylation is adequately described by a single reaction so that the model reduces to eight parameters. The in vitro rate constants for transport, phosphorylation, and dephosphorylation are very similar to prior in vivo results. The phosphoisomerization rate constant is similar to dephosphorylation, so glycosylated macromolecules slowly accumulate and gradually assume larger relative importance as other compounds disappear more rapidly. Rate constants for 540-microns slices from hypothalamus and hippocampus are similar, while 1,000-microns slices have smaller tissue transport constants and larger phosphorylation constants. The rate equation for glucose utilization of this model is relatively insensitive to uncertainties regarding the rate constants. Including later metabolic components in kinetic models improves the calculations of glucose utilization with long isotope exposures.

Algorithms↗
PubMed1990

Cerebrovascular transport of [125I]quinuclidinyl benzilate, [3H]cyclofoxy, and [14C]iodoantipyrine.

The transport rate constants across rat brain capillaries of a muscarinic acetylcholine receptor antagonist, [125I]quinuclidinyl benzilate (IQNB), an opiate receptor antagonist, [3H]cyclofoxy (CF), and a highly diffusible blood flow indicator, [14C]iodoantipyrine (IAP), were determined by the indicator-diffusion technique and a model that includes a distribution of capillary transit times and a homogeneous distribution of the test compound in the tissue parenchyma. The mean influx extraction ratio (E1) of IAP was greater than 0.91, and E1 for CF and IQNB was 0.56-0.79 and 0.34-0.46, respectively. The order of lipid solubility was IQNB greater than IAP greater than CF; the apparent discrepancy (high lipid solubility and low permeability) of IQNB was partly due to intravascular binding to plasma protein and red blood cells. The observed initial tissue distribution volumes (lambda 1, ml/g brain) for IQNB (0.09-0.17), CF (0.51), and IAP (0.71) were compared with those estimated for the unbound free ligand in blood (lambda a, ml/g brain; IQNB = 1.3-2.3, CF = 0.88, and IAP = 1.4). These findings suggest that the binding of lipid-soluble radioligands and drugs to plasma proteins and red blood cells can be a major determinant of transport across the blood-brain barrier and the apparent distribution volume of the ligand in brain tissue.

Animals↗
PubMed1989

Nigrostriatal function in humans studied with positron emission tomography.

The dopamine depletion that is characteristic of Parkinson's disease has been hypothesized to result from the combination of environmentally induced subclinical damage to the substantia nigra and the age-related loss of additional nigral neurons. Essential to this hypothesis is the existence of deteriorating function in the nigrostriatal pathway with advancing age. The present study was undertaken with [18F]6-fluoro-L-dopa and positron emission tomography to determine in vivo the effects of age on the nigrostriatal pathway in a series of 10 asymptomatic subjects (age range, 22-80 years; mean, 49.8 years). A graphical approach was used in the analysis of multiple-time tracer-uptake data to establish the presence of a compartment with unidirectional uptake and to calculate the rate constant, K, for uptake of [18F]6-fluoro-L-dopa from blood to striatum during steady-state, an index of the functional integrity of nigrostriatal nerve endings. There was a significant linear relationship between K and age (r = 0.80, p less than 0.005) with a decrease of 53.3% over the age range studied. These results demonstrate the application of a unidirectional transfer model to the analysis of [18F]6-fluoro-L-dopa and positron emission tomography data and provide in vivo confirmation of an age-related impairment of nigrostriatal function.

Adult↗
PubMed1989

Kinetic analysis of cerebrovascular transport based on indicator diffusion technique.

The indicator diffusion method was used for studies of the blood-brain barrier in rats and [131I]iodoantipyrine (IAP) was used as a highly diffusable model test substance. Interlaminar (Taylor) diffusion and effects of red cell carriage were studied with 57Co-diethylene-triaminepentaacetic acid (DTPA), 125I-human serum albumin, and 46Sc-microspheres (15 microns diameter). Vascular shunting from the pterygopalatine artery (PPA) into the torcula sinus was observed in some animals, and ligation of the PPA was required to obtain reliable data. Dilution curve of the reference compound was corrected to compensate for any difference in interlaminar diffusion and red cell plus protein carriage of the test substance. Apparent extraction ratio of IAP was calculated for each torcula sinus sample and found to increase during the initial phase of the dilution curve, reach a peak of approximately 0.85, and fall during the latter portion of the curve. These results suggest a heterogeneity of intravascular transit times in the cerebral circulation and a rapid efflux of IAP from brain into venous blood. Because of the topography of cerebral capillaries, we developed a modification of the distributed model for intravascular transit and capillary exchange proposed by Goresky et al. (J. Clin. Invest. 52: 991-1009, 1973) and Rose and Goresky (Circ. Res. 34:541-554, 1976); this modification included a well-mixed tissue compartment, as suggested by Johnson and Wilson (Am. J. Physiol. 210: 1299-1303, 1966) and is named the tissue homogeneity model. The experimental data was analyzed by both the tissue homogeneity and Goresky models. The estimated mean extraction E (0.95 and 0.94) and the estimated permeability-surface area product of influx (PS)1 (3.1 and 2.8 ml.min-1.g-1) for IAP in a whole blood injectate were similar using the two different models. The efflux rate constant (k2) for IAP was consistently smaller when the tissue homogeneity model was used (0.13 +/- 0.02 s-1) vs. that obtained with the Goresky model (0.18 +/- 0.02 s-1). Model simulations also indicated that the efflux parameter k2 was most sensitive to the choice of kinetic models, but we could not discriminate between the two model analyses on the basis of the "quality of fit." Nevertheless, from anatomical considerations, we suggest that the tissue homogeneity model may be more appropriate fro brain.

Animals↗
PubMed1989

Brain ion and volume regulation during acute hypernatremia in Brattleboro rats.

Regulation of brain ions and volume in response to 30 min of hypernatremia has been studied in two strains of anesthetized rats, the vasopressin-deficient Brattleboro and its vasopressin-competent parent strain, the Long-Evans. Plasma [Na] was increased by intraperitoneal injection of hyperosmolal NaCl. Brain volume was regulated during hypernatremia associated with tissue uptake of Na and Cl in both strains, but osmotically stimulated uptake of Na was 61% less in the Brattleboro. Blood-to-brain transfer constants for 22Na, measured as a function of plasma osmolality, were similar in the two strains. In contrast, bulk flow of cerebrospinal fluid (CSF) into brain, induced by osmotic dehydration of brain, was 55% less in the Brattleboro. CSF secretion in unstressed animals was also reduced, by 34%, in the Brattleboro compared with the Long-Evans. Reduced Na uptake by the brain of the Brattleboro rat during hypernatremia can be explained on the basis of a three-compartment model of brain volume regulation. Results support a function for vasopressin in brain ion homeostasis.

Acute Disease↗
PubMed1989

[Effects of dehydration of the pituitary microcirculation in rats].

The contiguous three lobe of the pituitary gland have different endocrine functions and vascular bed. This study was designed to investigate the effects of dehydration, which stimulates the secretion of vasopressin, on the pituitary microcirculation. Male Sprague-Dawley rats, weighing 300-380 g, were divided into two groups. Twenty three rats were allowed free access to food and water, and 24 rats had free access to food but were deprived of water for 5 days. Capillary solute transfer (K), plasma volume (Vp) and erythrocyte volume (Ve) in each pituitary lobe were determined for both control and dehydrated rats. Quantitative autoradiographic techniques were used to measure the K with 14C-alpha-aminoisobutyric acid (AIB, a small neutral amino acid), the Vp with 125I-albumin and the Ve with 51Cr-erythrocytes. Body weight was lower (-23%) and the arterial hematocrit was higher (+22%) in the dehydrated rats. In the lobes of the control pituitary gland, the order of K from the highest to the lowest was posterior much greater than anterior greater than intermediate lobe. K was increased by several folds only in the posterior lobe in dehydrated rats (p less than 0.05). Even under normal hydrated conditions, K for AIB in the posterior lobe was several hundreds times greater than in cerebral gray matter structures. The rank of Vp and Ve in each lobe of normal animals was about the same order and anterior greater than posterior much greater than intermediate. Normal microvascular Vp in the anterior and posterior lobes was 5-10 times larger than in cerebral gray matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1988

Dexamethasone effects on vascular volume and tissue hematocrit in experimental RG-2 gliomas and adjacent brain.

We have studied the effects of dexamethasone, a corticosteroid commonly used to treat brain tumors, on vascular volume and tissue hematocrit in RG-2 experimental rat gliomas. 125I-RISA (radioiodinated serum albumin) was used to measure tissue plasma vascular volume (Vp) and 51Cr labeled red cells were used to measure tissue red cell volume (Vrbc). Quantitative autoradiography was used to obtain local measurements of Vp and Vrbc in different brain and tumor regions. From these experimentally measured values, we calculated the tissue vascular volume (Vv), tissue hematocrit (THct) and systemic arterial hematocrit (AHct). The value reported primarily reflect capillary and small vessel volumes since blood drained from larger vessels during tissue processing and large vascular structures were avoided during analysis of the autoradiographic images. A total of 110 tumors were studied in 29 animals. There was a consistent trend for Vp and Vv to be reduced in all tumor regions after dexamethasone treatment, although a significant decrease was seen only in tumor center. Dexamethasone did not affect Vp or Vv in tumor-free brain regions. Dexamethasone appeared to have little effect on Vrbc in any brain or tumor region. THct was consistently, although not significantly, higher in tumors after treatment with dexamethasone; THct in tumor-free brain regions was unaffected by dexamethasone treatment.

Animals↗