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Biomedical subjects

F Takei

Publications and source records attributed to F Takei.

At least 91 records · Page 5Linked to original sources

Determination of FDP in human plasma by a novel latex immunoassay.

Distribution analyzing latex immunoassay (DALIA), a sensitive method based on the agglutination of latex particles coated with monoclonal antibody, was developed for determination of fibrin degradation products (FDP) in human plasma. The agglutination is measured by using an electric particle counter designed for medical research to determine the volume-ratio of agglutinated to non-agglutinated particles. Interference by serum constituents is avoided by coating the particles with the F(ab')2 fragments of monoclonal antibody and by using suitable latex particles. This assay enabled the determination of FDP in concentrations of 16 to 4000 ng/ml in less than 15 minutes. The mean concentrations of FDP in the plasma of 98 normal subjects and 142 patients with apparent disseminated intravascular coagulation (DIC) were 0.69 and 13.24 micrograms/ml, respectively. Analytical recovery of FDP in plasma samples averaged 104%. The correlation coefficient of DALIA with enzyme immunoassay using two monoclonal antibodies, was 0.809. The results obtained by analyzing the cross-reactivity with related components of FDP and the inhibitory effect of D monomer indicated that the present method can effectively detect the high molecular weight (HMW) fragments of FDP produced in the early stage of plasmin digestion.

Antibodies, Monoclonal↗

Characterization of a murine T cell surface disulfide-linked dimer of 45-kDa glycopeptides (YE1/48 antigen). Comparison with T cell receptor, purification, and partial amino acid sequences.

The YE1/48 antigen, defined by two rat monoclonal antibodies YE1/48 and YE1/32, is a disulfide-linked dimer of 45- to 50-kDa subunits expressed on murine T cells. It has previously been described as a T cell receptor alpha/beta-like molecule because of its similar m.w., dimeric structure, and isoelectric points comparable to those of the murine T cell receptor. We have now further characterized this antigen, directly compared it with the T cell receptor, and obtained internal amino acid sequences from the purified and trypsin-digested antigen. Endoglycosidase F treatment revealed the peptide cores of the antigen to be approximately 32 to 38kDa under reducing conditions and they possess at least three glycosylation side-chains. On diagonal gel analysis (nonreducing vs reducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis), the YE1/48 antigen and the T cell antigen receptor alpha/beta immunoprecipitated from thymocytes are indistinguishable. However, the two molecules can be distinguished on EL-4 cells by sequential immunoprecipitation using the YE1/48 monoclonal antibody and a rabbit antiserum reactive with the murine T cell receptor. Furthermore, two MBL-2 variant clones, which differ in the level of YE1/48 antigen expression by more than 200-fold, express comparable level of the T cell receptor. Therefore, the YE1/48 antigen and the T cell antigen receptor alpha/beta seem to be different molecules. The YE1/48 antigen was purified from MBL-2(4.1) cells by affinity chromatography and preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis, digested with trypsin and the resultant peptides were separated by reverse phase high performance liquid chromatography. The amino acid sequences of several of the YE1/48 tryptic peptides were determined. Upon comparison with the protein sequences in the data base, no identical sequences were detected. These results demonstrated that the YE1/48 antigen is clearly different from the T cell receptor alpha-, beta-, or gamma- chain gene products, and it is a novel T cell antigen not previously described. However, the possibility of homology with other proteins remains undetermined because the tryptic peptides are too short to yield meaningful statistical comparison with the data base.

Amino Acid Sequence↗

Murine T lymphoma cells express a novel membrane-associated antigen with unique features.

A novel membrane-associated antigen expressed on various murine T lymphoma cells has been detected by a rat monoclonal antibody. The antibody YE6/6 initially produced against Moloney leukemia virus-transformed T lymphoma line MBL-2, reacted with several other lymphoma lines including non-T lymphoma lines as well as thymocytes from leukemic AKR mice, but it did not show significant reactivities with resting or mitogen-activated normal lymphocytes by flow cytometric analysis. The antibody did not bind to some Abelson leukemia-transformed cells, which express Moloney virus antigens, suggesting that the antigen is unlikely to be encoded by Moloney virus genome. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of the antigen molecules immunoprecipitated by the antibody revealed three major polypeptides. Two of the polypeptides, with approximate m.w. of 95,000 and 35,000, can be labeled by the cell surface iodination and, therefore, seem to be exposed on the cell surface. The third polypeptide, with approximate m.w. of 65,000, is not labeled by the surface iodination but it is readily detected by [35S]methionine labeling. The third polypeptide was labeled with [32P]orthophosphate indicating that it is a phosphoprotein. Western blot analysis showed that YE6/6 antibody primarily reacts with 35,000 m.w. polypeptide. Furthermore, the same 35,000 m.w. protein was also detected in concanavalin A-activated spleen cells at a low level by Western blot, but normal resting lymphocytes were negative. These results suggest that the antigen detected by YE6/6 antibody may be a cell proliferation-associated antigen and its expression is highly elevated on transformed lymphoma cells as compared to normal mitogen-activated lymphocytes.

Animals↗

Novel technique for isolation of human lung mast cells.

A novel technique for isolation of human lung mast cells is developed. Human lung tissue was enzymatically digested and the cells were partially purified by centrifugation on Percoll density gradient. Cells obtained at the Percoll density of 1.05-1.09 g/ml were then subjected to a cell sorter equipped with a single argon laser beam (FACS 440). Using four criteria as density, granularity, size and autofluorescence, four major cell populations were identified. One of the major populations contained 70-95% mast cells with a mean and SE values of 88 +/- 11% purity, n = 18 as determined by the measurement of total histamine content, light microscopic observation of stained cells with toluidine blue and estrase, and surface-stained IgE fluorescence antibody. Approximately less than 10% mast cells were identified in the three other major cell populations. Mast cells isolated by FACS were found to be intact, viable (approximately equal to 90%) and functionally normal as determined by the release of histamine evoked after stimulation with ionophone A23187, or challenged with anti-human IgE.

Cell Separation↗

New ultrastructural changes of the ependyma in experimental hydrocephalus.

New ultrastructural alterations of the ependymal cells in the altered container model of experimental feline hydrocephalus are described. These include half desmosomes and a basal lamina on the apical surface of the ependymal cells, punctate adhesion-like structures between intraventricular mononuclear cells and the apical surface of the ependymal cells and unusual distortion of the ependymal cells. The significance of these previously unreported morphological alterations is unknown.

Animals↗

Further evidence for importance of the subunit combination of silk fibroin in its efficient secretion from the posterior silk gland cells.

A locus responsible for the Nd-s mutation of the silkworm, Bombyx mori, has been mapped very close to or within the fibroin light (L) chain gene on the 14th chromosome (Takei, F., K. Kimura, S. Mizuno, T. Yamamoto, and K. Shimura, 1984, Jpn. J. Genet., 59:307-313). A strain of B. mori carrying the homozygous Nd-sD mutation (Nd-sD/Nd-sD; Nd-sD is allelic to Nd-s) secretes less than 0.3% of fibroin into the lumen of the posterior silk gland compared with a strain carrying the homozygous wild-type alleles (+/+). The small amount of fibroin that is secreted in the Nd-sD/Nd-sD strain consists of the heavy (H) chain only and lacks the L chain, although the L chain mRNA and the proteins that are cross-reactable with the anti-L chain serum are present in the posterior silk gland cells. In the hybrid silkworm, Nd-sD/+, the H chain derived from either the Nd-sD or + allele forms disulfide linkage with the L chain derived from the + allele and these fibroins are secreted into the lumen with an equal efficiency, but the L chain derived from the Nd-sD allele remains in the cell unbound to the H chain. Some evidence suggesting structural abnormality of the L chain derived from the Nd-sD allele is presented. These results, together with the previous results on the effect of the H chain gene-linked Nd(2) mutation (Takei, F., F. Oyama, K. Kimura, A. Hyodo, S. Mizuno, and K. Shimura, 1984, J. Cell Biol., 99:2005-2010), strongly suggest that the H-L subunit combination of silk fibroin is important for its efficient secretion.

Alleles↗

Influence of the rate of ventricular enlargement on the ultrastructural morphology of the white matter in experimental hydrocephalus.

The influence of the rate of ventricular enlargement on the morphology of hydrocephalic white matter was studied and correlated with previous studies of water content. Different rates of ventricular enlargement were obtained in two groups of cats by opening either the calvaria or the calvaria and the dura mater before injecting kaolin into the cisterna magna. Animals from each group underwent in vivo fixation of brain 2, 3, and 6 weeks after hydrocephalus was induced. Specimens of white matter were taken 1, 2, and 3 mm lateral to the ependymal surface of the lateral ventricles, imbedded, and examined using transmission electron microscopy. The ultrastructural changes associated with ventricular enlargement varied with the model used and the duration of hydrocephalus. Marked expansion of the extracellular space extending 2 mm lateral from the ependyma was found in the craniectomy-durectomy preparations examined 2 to 3 weeks after kaolin injection. Time-matched craniectomy preparations had less enlargement of the extracellular space that was confined to the white matter immediately adjacent to the ventricle. Marked glial reaction was observed in these areas in the early craniectomy preparations. When studied 6 weeks after hydrocephalus induction, both models had less expansion of the extracellular spaces compared to early observations. Glial reaction was found in both models, but was greater in the craniectomy model. The correlation of these morphological findings with the rate of ventricular enlargement and earlier studies of water content are discussed.

Animals↗

Influence of the rate of ventricular enlargement on the white matter water content in progressive feline hydrocephalus.

The effectiveness of transependymal absorption of cerebrospinal fluid in hydrocephalus was studied by correlating the measured water content of feline hydrocephalic white matter with the rate of enlargement of the ventricles. Two groups of cats were subjected to opening of either the calvaria or the calvaria and dura before the intracisternal injection of kaolin to obtain two profiles of ventricular enlargement. The water content 1, 2, and 3 mm from the lateral ventricles was measured in each group using the dry/wet weight and microgravimetric techniques after sacrificing the animals in each group at 2, 3, or 6 weeks after inducing hydrocephalus. In the animals with both calvarial and dural opening, the ventricles enlarged rapidly in the first 2 to 3 weeks and then continued to increase but at a slower rate. Concomitant with this early increase of ventricular size was a progressive increase in white matter water content both adjacent to and remote from the ventricles, which continued through 6 weeks. When only the calvaria was opened, ventricular size increased gradually, but continued to increase at a constant rate throughout the 6 weeks. Water content adjacent to the ventricle did not increase until the 3rd week, with little spread to adjacent areas by the 6th week. The central canals of the spinal cord were enlarged in both groups at all sampling levels. Neither increased periventricular water nor dilatation of the central canal was associated with stabilization of ventricular size in these studies. The authors conclude that these pathways are not sufficient to arrest the hydrocephalic process in these models.

Animals↗

A laboratory model of shunt-dependent hydrocephalus. Development and biomechanical characterization.

This study was designed to determine whether implanting shunts in hydrocephalic cats produced the same biomechanical changes as have previously been found in children with shunts. Neuraxis volume-buffering capacity (pressure-volume index: PVI) and the resistance to the absorption of cerebrospinal fluid (CSF) were determined before and 3 weeks after placing shunts in 16 hydrocephalic cats. Intracranial pressure (ICP) was monitored for at least 6 hours after the shunts were occluded. The brains were perfused in vivo and removed to assess the size of the ventricles. The mean PVI of the hydrocephalic cats was 3.6 +/- 0.2 ml (+/- standard error of the mean) before the shunts were placed. Three weeks after adequate shunt function was first established, the mean PVI decreased to 1.1 +/- 0.1 ml and was similar to values determined in control animals. Prior to shunt placement, the resistance to the absorption of CSF was 28.4 +/- 4.5 mm Hg/ml/min and did not vary with ICP. This parameter changed after shunting and increased as a function of ICP (r = 0.87, p less than 0.001). At ICP's below 20 mm Hg, the resistance to the absorption of CSF was 65.0 +/- 18.0 mm Hg/ml/min but increased to 220.0 +/- 40.5 mm Hg/ml/min when determined at ICP's above 20 mm Hg. Corroborating evidence for this linkage of resistance to the absorption of CSF to ICP was found in the inexorable rise of ICP during the 6 hours of monitoring after the shunts were occluded. After shunt placement, the ventricles were normal in size in 12 cats and slightly enlarged in four. The biomechanical profile and pressure response to shunt occlusion in this laboratory model resembles that previously described in shunt-dependent children. As in humans, shunt placement in hydrocephalic cats results in normalization of the PVI and a linkage of the resistance to the absorption of CSF to ICP. The significance of these changes as they relate to shunt dependency is discussed.

Animals↗

Progressive ventricular enlargement in cats in the absence of transmantle pressure gradients.

Intracranial pressure (ICP) was measured simultaneously at multiple sites in cats to determine if transmantle pressure gradients were present in progressive hydrocephalus. The cats underwent craniectomy and intracisternal injection of kaolin; 4 to 9 weeks later ICP was measured at the ventricle, cisterna magna, and convexity subarachnoid space, and in the brain tissue and the sagittal sinus. In 13 cats in which ventricular size conformed to previously established norms for duration of hydrocephalus, there were no demonstrable gradients of pressure at any of the sites of measurement according to one-way analysis of variance (p greater than 0.05). The mean (+/- standard error of the mean) peak and trough pressures (in mm Hg) at each site were: ventricle, 12.7 +/- 0.7 and 12.0 +/- 0.6; cisterna magna, 12.9 +/- 0.8 and 12.3 +/- 0.7; subarachnoid space, 12.7 +/- 0.8 and 12.1 +/- 0.7; brain tissue, 12.9 +/- 0.9 and 12.4 +/- 0.9; and sagittal sinus, 13.1 +/- 0.8 and 11.9 +/- 0.8. These results indicate that ventricular expansion can progress without measurable transmantle pressure gradients.

Animals↗

Lymphocyte function-associated antigen (LFA-1) is involved in B cell activation.

Human LFA-1 is a widely expressed leukocyte antigen present on cells of myeloid and lymphoid lineage. Monoclonal antibodies to LFA-1 have been shown to inhibit in vitro T cell immune functions. However, a role for LFA-1 in B cell activation has not been documented. To investigate this possibility, we examined the distribution of LFA-1 on normal, neoplastic, and EBV-transformed B cells as well as the ability of a monoclonal anti-LFA-1 antibody (NB-107) to inhibit B cell mitogenesis. NB-107 immunoprecipitates a noncovalently linked heterodimer of approximately 170,000 and 95,000 daltons. Sequential immunoprecipitation and cross-blocking studies showed that NB-107 identified a distinct epitope on the LFA-1 molecule. NB-107-defined LFA-1 was present on peripheral blood mononuclear cells (PBMC) from all normal individuals (N = 27) and on EBV-transformed cell lines (N = 9), but was absent from four of seven neoplastic B lymphoma lines. NB-107 was observed to profoundly inhibit the response of PBMC to the B cell mitogens anti-IgM (mean 71% inhibition) and lipopolysaccharide (mean 80% inhibition). In order to investigate the mechanism of inhibition, B cells were sequentially purified from PBMC by using a combination of E rosette depletion of T cells, monocyte removal by glass adherence, and finally cell sorting. These extensively enriched populations of B cells, although still responding to anti-mu, showed no evidence of inhibition by NB-107. Growth of EBV-transformed cell lines, cultured in the presence of NB-107, also was not inhibited by this antibody. When tested in assays for T cell function, NB-107 was shown to inhibit the mixed lymphocyte response, but had no effect on phytohemagglutinin stimulation of PBMC nor on the clonal growth and differentiation of granulopoietic, erythropoietic, and pluripotent progenitor cells. We conclude that anti-LFA-1 monoclonal antibody inhibits B cell mitogens via indirect effects on monocytes and/or T cells, rather than by a direct antiproliferative effect on B cells.

Animals↗

Expression of a T cell receptor-like molecule on normal and malignant murine T cells detected by rat monoclonal antibodies to nonclonotypic determinants.

A T cell receptor-like molecule with a dimer structure of 45 kilodaltons (Kd) under reducing and 90 Kd under nonreducing conditions was detected on the surface of two murine T lymphoma lines, EL-4 and MBL-2, by two rat monoclonal antibodies. The two antibodies seemed to react with different determinants on the same molecule. The antibodies did not react with the surface of normal T cells as tested by flow cytometric analysis of cell surface staining. Two-dimensional gel electrophoresis (IEF vs SDS-PAGE) and tryptic peptide analysis revealed the molecule to consist of two chains with different isoelectric points and different tryptic peptides. A conventional antiserum was raised against the heterodimer purified from EL-4 cells. The immune serum did not bind to the surface of normal T cells. However, the immune serum as well as the monoclonal antibodies immunoprecipitated the dimer molecules from detergent-solubilized normal thymocytes and spleen cells. The dimer molecule was detected on both immature and mature thymocytes. These results suggest that the antibodies detect non-clonotypic determinants on a T cell receptor-like protein. The determinants are masked on the surface of normal T cells, whereas they are exposed on the surface of at least two T lymphoma cell lines. Three polypeptides of 30 Kd, 25 Kd, and 15 Kd were also coprecipitated with the heterodimer from MBL-2 cells. These proteins may associate with the heterodimer and may be masking the antigenic determinants on normal T cells. The relationship between the heterodimer molecule described here and the T cell antigen receptor or the human T cell antigen 9.3 is still unknown.

Animals↗

Monoclonal antibodies to HLA-DP, DQ, and DR determinants: functional effects on the activation and proliferation of normal and EBV-transformed B cells.

To investigate the function of HLA class II molecules in B-cell activation, we generated three new anti-HLA class II monoclonal antibodies with differing specificities for DP, DQ, and DR determinants. These were tested for their ability to inhibit various B- and T-lymphocyte responses. Each of these antibodies (NB-29, DH-84, and DH-224) immunoprecipitates a heterodimer of approximately 35,000 and 28,000 mol wt from 125I-surface-labeled B-lymphoma cells, as shown by SDS-PAGE. NB-29 (IgG1) detects a polymorphic DQ determinant, while DH-224 (IgG1) is reactive with monomorphic DR determinants, and DH-84 (IgG2a) has specificity for DP, DQ, and DR. Both DH-224 and DH-84, but not NB-29, were found to inhibit significantly the stimulation of peripheral blood mononuclear cells (PBMC) by anti-mu (70%-90% inhibition) and by lipopolysaccharide (80%-90% inhibition), as measured by incorporation of tritiated thymidine. When added to highly purified populations of peripheral blood B cells, none of these anti-class II monoclonal antibodies inhibited anti-mu-induced stimulation. This suggests that the inhibitory effect that DH-224 and DH-84 have on the stimulation of unfractionated PBMC may be due to their ability to interfere with the action of accessory cells. Epstein-Barr-virus (EBV)-transformed B-cell lines, in contrast, showed substantial inhibition of growth when cultured in the presence of any of the three antibodies. With respect to T cells, DH-84 and DH-224 strongly inhibited the mixed lymphocyte response; NB-29 did not. None of these antibodies inhibited stimulation of PBMC by phytohemagglutinin (PHA). These findings suggest that DQ and DR HLA class II molecules have differing roles in B-cell activation and document a direct antiproliferative effect of anti-HLA class II monoclonal antibodies on the growth of EBV-transformed cell lines.

Animals↗

Restricted expression of a new acute myelogenous leukemia-associated antigen (NHL-30.5) on normal hemopoietic progenitor cells.

We have previously reported the isolation of a monoclonal antibody (NHL-30.5) that reacts with an antigen expressed on a substantial proportion of marrow and blood cells of most patients with newly diagnosed or relapsing acute myeloid leukemia. This antigen is also found on several cell lines derived from myeloid malignancies of human origin. It is not present on mature hemopoietic cells or on the majority of differentiating bone marrow cells. In order to determine whether the NHL-30.5 antigen may, nevertheless, be expressed on low-frequency primitive normal hemopoietic cells, not detected in standard antibody screening procedures, its expression was studied on clonogenic erythropoietic and granulopoietic cells. Light-density (less than 1.077 g/mL) suspensions of normal or chronic myelogenous leukemia bone marrow and peripheral blood cells were stained with NHL-30.5 and fluorescein isothiocyanate labeled second antibody and then sorted into two fractions using the fluorescence-activated cell sorter. The first contained the top 5% of cells with the highest fluorescence intensity. The remainder were collected in the second fraction. Colony assays of both fractions showed the first to be enriched in CFU-E, BFU-E, and CFU-C content (fourfold to 17-fold). The second fraction was correspondingly depleted of these progenitors. These findings reveal NHL-30.5 antigen expression to be a transient event during normal hemopoiesis that characterizes primitive hemopoietic cells on several pathways. Subsequent experiments showed that the presence of up to 10 micrograms/mL of purified NHL-30.5 antibody in colony assay cultures neither inhibited nor stimulated colony formation. Marrow fibroblasts (subcultured marrow adherent cells) were NHL-30.5 negative. Immunoprecipitation studies showed that the antigen detected by NHL-30.5 is clearly distinct from that identified by My-10, another monoclonal antibody that has previously shown some similarities to NHL-30.5. It thus appears that the NHL-30.5 antibody reacts with a new myeloid differentiation antigen of as yet unidentified function that is normally restricted in its expression to early stages of hemopoiesis.

Antibodies, Monoclonal↗

NHL-30.5: a monoclonal antibody reactive with an acute myeloid leukemia (AML)-associated antigen.

The reactivity of a murine IgG1 monoclonal antibody, NHL-30.5, that detects a surface antigen expressed on acute myeloid leukemia (AML) cells has been studied. Initially raised against the HL-60 cell line, NHL-30.5 has subsequently reacted with blood and/or bone marrow cells from 15 of 19 AML patients studied at presentation or in relapse, 1 patient with chronic myelomonocytic leukemia (CMML), 1 patient with myelofibrosis (MF) who subsequently developed AML, and 1 of 5 patients with acute lymphoblastic leukemia (ALL). It has shown no detectable binding to cells from AML patients in remission (0/3), patients with chronic myelogenous leukemia in chronic phase (CML) (0/7), normal bone marrow (0/9), normal peripheral blood mononuclear cells, granulocytes, platelets, erythrocytes, monocytes, or splenocytes by radioimmunoassay or fluorescence analysis using flow cytometry. HL-60 cells induced to differentiate following incubation in the presence of dimethylsulfoxide (DMSO) lost their ability to bind NHL-30.5. Immunoprecipitation of iodinated HL-60 cell surface components showed the antigen to have an apparent mol./wt of 180,000 under reducing conditions. These results suggest that the antigen is different from any other myeloid antigens reported to date, and may be useful in further studies of leukemic cell phenotypes.

Adult↗

Effect of the skull and dura on neural axis pressure-volume relationships and CSF hydrodynamics.

The pressure-volume index (PVI) technique of bolus manipulation of cerebrospinal fluid (CSF) was used to measure changes of neural axis volume buffering-capacity and CSF dynamics produced by different conditions of the skull and dura. Twenty-eight cats were studied in the intact state, after bilateral craniectomy, and with the dura opened. At each stage of altering the container of the brain, the following parameters were obtained: steady-state intracranial pressure (ICP), sagittal sinus venous pressure, PVI, and the resistance to the absorption of CSF. The resistance to absorption of CSF was determined using both the bolus injection and the continuous infusion of fluid. After craniectomy, PVI increased from 0.76 +/- 0.04 to 1.3 +/- 0.07 ml (+/- standard error of the mean) (p less than 0.001) and increased further to 3.6 +/- 0.17 ml (p less than 0.001) after opening the dura. The resistance to absorption of CSF (Ro), determined by bolus injection, decreased after craniectomy from 91.3 +/- 7.5 to 56.3 +/- 6.2 mm Hg/ml/min (p less than 0.001) and decreased further to 8.9 +/- 0.66 mm Hg/ml/min (p less than 0.001) after opening the dura. Although resistance determined by constant infusion was similar, results were dependent on the rate of infusion. Despite these changes of resistance and PVI, steady-state ICP and sagittal sinus venous pressure were similar in all three conditions of the skull and dura. These studies indicate that changes of the container of the brain affect pressure-volume relationships within the neural axis. However, the changes of resistance to absorption of CSF are in a direction that preserves a steady-state hydrodynamic equilibrium.

Absorption↗

Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats.

In a craniectomy-durectomy model of kaolin-induced feline hydrocephalus, the pressure-volume index (PVI) technique of bolus manipulations of cerebrospinal fluid (CSF) was used to study the biomechanical changes associated with hydrocephalus. Steady-state intracranial pressure (ICP), PVI, and the resistance to the absorption of CSF were determined acutely and 3 to 5 weeks later in hydrocephalic cats and time-matched control cats. Steady-state ICP was 11.0 +/- 2.1 mm Hg (+/- standard deviation) in the hydrocephalic cats, compared to 10.8 +/- 2.2 mm Hg in the chronic control group (p greater than 0.1). The ICP in both the chronic hydrocephalic and chronic control groups was significantly higher (p less than 0.001) than after acute durectomy (mean ICP 8.5 +/- 1.2 mm Hg). Immediately after dural opening, the mean PVI was 3.6 +/- 0.2 ml (+/- standard error of the mean); over time, it decreased to 1.3 +/- 0.1 ml in the chronic control group (p less than 0.001), but remained elevated in the hydrocephalic group at 3.5 +/- 0.4 ml (p less than 0.001). Resistance to CSF absorption was 9.1 +/- 1.4 mm Hg/ml/min immediately after dural opening and increased to 28.8 +/- 4.5 mm Hg/ml/min (p less than 0.001) in the hydrocephalic cats; it increased even further in the chronic measurements in control cats, to 82.3 +/- 9.2 mm Hg/ml/min (p less than 0.001). Ventricular size was moderate to severely enlarged in all hydrocephalic cats, and normal in the control group. These results indicate that the biomechanical profile of the altered brain container model of kaolin-induced feline hydrocephalus resembles that described in hydrocephalic infants. As shown in the control subjects, an absorptive defect alone is not sufficient to cause progressive ventricular enlargement. Increased volume-buffering capacity coupled with a moderate increase of CSF absorption resistance facilitates volume storage in the ventricles.

Absorption↗