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At least 163 records · Page 9Linked to original sources
PubMed1995

Influence of high-dose aprotinin on anticoagulation, heparin requirement, and celite- and kaolin-activated clotting time in heparin-pretreated patients undergoing open-heart surgery. A double-blind, placebo-controlled study.

BACKGROUND: Aprotinin causes a prolongation of the celite-activated clotting time (CACT), but not of the kaolin-activated clotting time (KACT). Therefore, concern has been raised regarding the reliability of CACT to monitor anticoagulation in the presence of aprotinin. The current study was designed to test the efficacy of aprotinin to improve anticoagulation, and to investigate whether the prolongation of CACT reflects true anticoagulation or is an in vitro artifact. To elucidate this antithrombotic effect of aprotinin, this study was done in patients prone to reduced intraoperative heparin sensitivity. METHODS: In a prospective, randomized, double-blind clinical trial, 30 male patients scheduled for elective primary coronary revascularization and treated with heparin for at least 10 days preoperatively, received either high-dose aprotinin (group A) or placebo (group C). The CACT and KACT were determined, but only CACT was used to control anticoagulation with heparin. Parameters of coagulation that are indicators of thrombin generation and activity (F1+2 prothrombin fragments, thrombin-antithrombin III complex, and fibrin monomers), parameters of fibrinolysis (D-dimers), aprotinin, and heparin plasma concentrations were measured. Postoperative blood loss and allogeneic blood transfused were recorded. RESULTS: Total heparin administered was 36,200 units (95% confidence interval: 31,400-41,000; group C) compared with 27,700 (25,500-29,800) units (group A; P < 0.05). Hemostatic activation during cardiopulmonary bypass (CPB) was significantly reduced in group A compared with group C. After 60 min of CPB, all parameters were significantly different (P < 0.05) between the groups (group C vs. group A): F1+2 prothrombin fragments, 9.7 (8.9-11.7) ng/ml versus 7.5 (6.2-8.6) ng/ml; thrombin-anti-thrombin III complex (TAT), 53 (42-68) ng/ml versus 29 (23-38) ng/ml; and fibrin monomers, 23 (12-43) ng/ml versus 8 (3-17) ng/ml. Fibrinolysis was also attenuated; D-dimers at the end of operation were 656 (396-1,089) and 2,710 (1,811-4,055) ng/ml for groups A and C, respectively (P < 0.05). The CACT 5 min after the onset of CPB was 552 (485-627) versus 869 (793-955) s for groups C and A, respectively (P < 0.05), whereas the KACT showed no differences between the groups (569 [481-675] vs. 614 [541-697] s for groups C and A, respectively; P = NS). The 24-h blood loss was 1,496 (1,125-1,995) versus 597 (448-794) ml for groups C and A, respectively (P < 0.05). CONCLUSIONS: Aprotinin treatment in combination with heparin leads to less thrombin generation during CPB. Aprotinin has anticoagulant properties. Celite-activated ACT is reliable for monitoring anticoagulation in the presence of aprotinin, because the prolonged CACT in the aprotinin group reflects improved anticoagulation. Kaolin-activated ACT does not reflect this effect of aprotinin.

Adult↗
PubMed2005

Origin of macrophages in a kaolin-induced model of rat syringomyelia: a study using radiation bone marrow chimeras.

STUDY DESIGN: Animal experimental study. OBJECTIVE: To study the origin of macrophages in a rat model of syringomyelia. SUMMARY OF BACKGROUND DATA: Syringomyelia is a clinically important condition in which a cystic cavity forms within the spinal cord. This leads to significant delayed neurologic deterioration, which may be manifested as weakness, numbness, or pain. The pathophysiology and mechanism of syrinx formation remain unclear. Human autopsy findings have demonstrated a prominent accumulation of macrophages in relation to the syrinx. Similar observations have also been made in a previously established rat model of syringomyelia. Little is known about the origin and precise functions of these cells. METHODS: Syrinx formation was induced by intraparenchymal injections of kaolin within the cervical spinal cords of 30 DA rat (RT7.1) radiation bone marrow chimeras reconstituted with bone marrow from RT7.2 congeneic donors. The distribution of macrophages was evaluated at survival times of 3 days, 1 week, and 4 weeks. Immunostaining of fresh-frozen spinal cord tissue was performed using specific antibodies against rat macrophage ED1 antigen and RT7.2 allele of CD45. This allowed donor-derived hematogenous (ED1+, RT7.2+) macrophages to be distinguished from native cells (ED1+, RT7.2-). RESULTS: Central canal dilatation was seen from 1 week. This was associated with extensive accumulation of ED1+ macrophages within the spinal cord parenchyma. A large influx of bone marrow-derived (ED1+, RT7.2+) macrophages was observed. However, a considerable proportion of resident microglia (RT7.2-) also upregulated ED1. These activated microglia demonstrated distinct morphologic features. CONCLUSIONS: Large numbers of macrophages were recruited from the bone marrow in kaolin-induced rat syringomyelia. However, a significant number of resident microglia upregulated their ED1 activity and appear to provide a substantial source of macrophages.

Animals↗
PubMed1985

Plasma total prekallikrein/kallikrein activity in rheumatoid arthritis with and without amyloidosis. Increased kaolin-stimulated activity in patients with amyloidosis.

Following exposure to kaolin, plasma samples were assayed for total prekallikrein/kallikrein activity in 19 patients with rheumatoid arthritis (RA), 39 patients with RA complicated by amyloidosis, 13 patients with nonamyloid nephropathy and 54 healthy subjects. Increased total kallikrein activity was found in RA patients with amyloidosis and in patients with nonamyloid nephropathy. The concentrations of the plasma kallikrein inhibitors C1-inactivator and alpha 2-macroglobulin were normal in RA patients without amyloidosis, whereas they were increased in patients with amyloidosis as well as in patients with nonamyloid nephropathy. The results suggest that the increased activity of plasma kaolin-stimulated kallikrein in RA patients with amyloidosis is due to the nephropathy per se and probably reflects increased levels of prekallikrein.

Adult↗
PubMed1979

Prekallikrein activator and kallikrein in acetone- and kaolin-activated rat plasma.

Activation of plasminogen-free rat citrated plasma (RCPL-P) with acetone/kaolin yielded BAEe-esterase activities of 0.6--0.8 U/ml. Gel filtration demonstrated one single peak of BAEe-esterase activity (mol. wt. approximately 135000) with a kininogenase-esterase ratio (3.3) close to that known for human plasma kallikrein (2.7). Similarly activated rat citrated plasma (RCPL) revealed on gel filtration an additional esterase peak (mol. wt, approximately 47,000) with a low kininogenase-esterase ratio (0.3), and should accordingly not be used for a BAEe-esterase assay of rat plasma kallikrein. Acetone activation of RCPL-P and of RCPL yielded prekallikrein activator (PKA) activities which were about doubled by treatment with kaolin to 1.9--2.1 and 3.5--4.2 PKA-U/ml respectively. Gel filtration of acetone-activated RCPL-P or RCPL revealed two peaks of PKA activity, mol. wt. approximately 110,000 corresponding to activated factor XII (XIIa), and mol. wt. approximately 33,000 corresponding to XII fragments (XIIf). Kaolin-treatment of acetone-activated RCPL-P, but not of RCPL, caused an extensive fragmentation of XIIa to the 4--6 times more active XIIf. The lower yield of PKA-activity in acetone/kaolin-activated RCPL-P, as compared with activated RCPL, seems to be due to the absence of a factor of significance for the activation of factor XII, which is not plasmin, plasma kallikrein, or high molecular weight kininogen.

Acetone↗
PubMed1969

Loss of rubella antibody from immune globulin treated with kaolin.

Sera and immune globulin (IG) preparations are customarily treated with kaolin before titration of their rubella hemagglutination-inhibiting (HI) antibody in order to rid them of nonspecific inhibitors of hemagglutination. The treatment was shown in this investigation to have no adverse effect on the antibody level of the sera but was found to remove considerable amounts of gamma-globulin from IG preparations. Evidence of this removal was obtained by serological tests, by spectrophotometric determination of protein concentration and by disc electrophoresis. In contrast to kaolin, heparin-manganese chloride (MnCl(2)) treatment of IG preparations had essentially no effect on the level of antibody globulin by all the criteria used. Heparin-MnCl(2)-treated IG lots were in these respects similar, if not identical, to their untreated counterparts. Since nonspecific inhibitors associated with the beta-lipoprotein fraction of serum are removed by the method employed to fractionate the IG samples, it seems unnecessary to treat the latter in any way for the HI test. No difficulty was encountered in this investigation with several untreated IG lots.

Adsorption↗
PubMed1989

Differences in lung function and prevalence of pneumoconiosis between two kaolin plants.

To investigate the origin of differences in previously published pulmonary function studies of workers in kaolin plants in Georgia, spirometric and radiographic data collected in a cross sectional survey of two large plants were analysed. As compared with workers in plant 2, workers in plant 1 had a 2.7-fold greater prevalence of pneumoconiosis and a mean 0.361 decrement in adjusted forced vital capacity. Our previous finding that exposure to kaolin was not associated with a decrement in lung function may have resulted from failure to consider differences between the plants.

Adolescent↗
PubMed1987

Severe hypokalaemia from kaolin and morphine abuse.

A 34 year old man, registered disabled as a result of muscle weakness, was admitted to hospital because of increasing weakness. He had profound hypokalaemia and admitted to taking up to 1400 ml of kaolin and morphine mixture daily. After considerable potassium replacement muscle power recovered completely. The hypokalaemia is likely to have been caused by the combination of liquorice extract and sodium bicarbonate in kaolin and morphine.

Adult↗
PubMed1979

Effects of levamisole and D-penicillamine in rat paw oedema induced by carrageenan and by kaolin.

Levamisole potentiated paw oedema induced by carrageenan in the rat whereas penicillamine was without effect. On the other hand, levamisole inhibited paw oedema induced by kaolin, penicillamine again having no effect. The copper complex of penicillamine was inhibitory in the carrageenan test but failed to show inhibition in the kaolin model of inflammation. These results show that levamisole and penicillamine are capable of exerting anti-inflammatory activity in the rat but only under certain conditions.

Animals↗
PubMed1969

Studies on the prekallikrein (kallikreinogen)--kallikrein enzyme system of human plasma. II. Evidence relating the kaolin-activated arginine esterase to plasma kallikrein.

Evidence is presented in this paper that the kaolin-activated arginine esterase of plasma is related to plasma kallikrein activity. Such a relationship is based on studies that (1) establish a constant ratio of esterase activity on various synthetic substrates for the kaolin-activated arginine esterase, purified kallikrein(s), and preparations obtained during the fractionation procedure; (2) exclude other known plasma and tissue arginine esterases; (3) confirm the requirement for factor XII in the activation of the enzyme precursor; and (4) show similarities in behavior between the plasma esterase and purified kallikrein(s) toward a variety of inhibitors. Based on this probable identification, evidence is provided that the concentration of active factor XII determines the rate of activation of plasma kallikreinogen, and that the activation may be blocked by polybrene. Once activated, plasma kallikrein is rapidly inactivated by the naturally occurring plasma inhibitor, but the inhibition is incomplete. Acid or chloroform treatment of plasma rapidly inactivates the plasma inhibitor without affecting the concentration of plasma kallikreinogen. Another plasma arginine esterase with properties suggestive of permeability factor is activated by factor XII in the presence of synthetic substrates, but only at low ionic strength. The data suggest that this enzyme is closely related to plasma kallikrein and that it arises from a common precursor.

Aprotinin↗
PubMed1978

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 microliter per minute, and in hydrocephalic cats to 40 microliter 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 hydrocephalic cats. These results suggest that CSF secretion by the choroid plexus of cats with kaolin-induced hydrocephalus is impaired.

Animals↗
PubMed1990

Pharmacological profile of alminoprofen among four writhing models of mice caused by kaolin, zymosan, acetylcholine and phenylquinone.

The effects of alminoprofen and other non-steroidal antiinflammatory drugs (NSAIDs) on the writhing reaction caused by kaolin, acetylcholine, phenylquinone and zymosan were studied. Aspirin, indomethacin, ibuprofen and diclofenac-Na, as cyclooxygenase inhibitors, showed similar potency ratios on four writhing tests, although, alminoprofen exhibited a somewhat rather higher potency ratio on kaolin- and zymosan-induced writhing models than on acetylcholine- and phenylquinone-induced writhing models. All NSAIDs, cyclooxygenase inhibitors except alminoprofen showed similar shapes in illustrations of potency ratio when the potency of aspirin was expressed as 1.0. The potency of alminoprofen produced a figure unlike those of other cyclooxygenase inhibitors. These results suggest that alminoprofen has a different pharmacological profile from other general NSAIDs in terms of analgesic action. This combination method with potency ratios for writhing reactions caused by the above four inducers could be a simple method for classification of pharmacological profiles of the analgesic actions of NSAIDs.

Acetylcholine↗
PubMed1997

Immunological aspects of kaolin-induced hydrocephalus.

Adult female Sprague Dawley rats were administrated 0.1 ml Kaolin (250 mg/ml) into cisterna magna. One, 4 and 8 weeks later, brains were analyzed using antibodies against MHC class I (OX18), MHC class II (OX6), CD4 (OX38), CD8 (OX8), OX42, ED1, NF, GFAP, AChE and TH. Remarkably high numbers of T lymphocytes, and OX42- and ED1-positive macrophages were found aggregated in subarachnoid spaces, and in the third and fourth ventricles. Marked aggregations of ED1-positive reactive microglial cells were also found in paraventricular structures, medial septum, retrosplenic cortex and commissural structures. However, no such cells were found in hippocampus. ED1-positive areas were also positive for round cells with a rim of MHC I fluorescent cytoplasm as well as for OX42-positive cells and MHC II positive microglial cells. At week 1, in ventro-frontal areas of cortex, CD8-positive cells and MHC I positive astroglial fibers were detected. At week 1, MHC I positive ramified microglial cells were also recognized in almost the entire brain. These positive cells gradually decreased with time and finally remained rounded with a rim of fluorescent cytoplasm. In addition, ED1 positive partly ramified microglial cells could be recognized in corpus callosum, probably representing cells in transition between ramified and reactive microglia. CD8+ cells entered ventral brain structures, and were found in the horizontal diagonal band at week 4, and had disappeared at week 8. Finally in cortex, ED1 positive microglial cells could be identified only in the retrosplenic cortex, and there were also "dark shrunken neurons" in light microscopic stainings. However, there was only a moderate GFAP positive gliosis. In conclusion, kaolin-induced hydrocephalus leads to immune reactions in several defined areas such as cholinergic systems, corpus callosum, circumventricular organs, pontine cerebellar peduncles and the vestibular nucleus.

Animals↗
PubMed2005

[Study on preparation and spectroscopy of silica-alumina hydrogel and silica from kaolin].

In our research, silica-alumina hydrogel was prepared by activation with NaOH and reaction with HCl from kaolin, and silica was obtained from the hydrogel by drying and acidifying with HCl. IR, XRD and XRF were used for testing the results, and better result was obtained. The optimal conditions of processing for kaolin 40 g were 15-20 g of sodium hydroxide and 4-5 mol x L(-1) of hydrochloric acid. Finally, preparation processing to get silica, as well as the structure and purity of the resulting silica were characterized by means of IR, XRD and XRF.

Aluminum Oxide↗
PubMed1987

Role of bradykinin generating and degrading systems in the vascular permeability response induced with kaolin in rats.

We investigated how bradykinin mediates inflammatory reactions in rats, via measurements of bradykinin by enzyme immunoassay method in inflammatory tissue fluids. Vascular permeability was increased markedly during the first 10 min and then declined quickly after the infusion of a kaolin suspension (10 mg/ml) in 0.8% carboxymethl-cellulose solution into an air pouch formed on the back of rats. Bradykinin in the exudate reached a maximum 5 min after the challenge and then decreased quickly. Local treatment with DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid, an inhibitor of kininase I, and captopril, an inhibitor of kininase II in the first 10-min period, each enhanced the vascular permeability increase accompanied by the elevation of the bradykinin level, whereas soybean trypsin inhibitor, a plasma kallikrein inhibitor, lowered both vascular permeability and bradykinin. When applied in the period of 3.5 to 4 hr after the challenge, only the kininase II inhibitor was effective in elevating both vascular permeability and the bradykinin level, whereas soybean trypsin inhibitor was ineffective on vascular permeability. A bradykinin-degrading activity appeared in the exudate as early as 10 min after the challenge. These results suggest that bradykinin plays an essential role for the sudden rise of the vascular permeability observed immediately after the infusion of kaolin suspension. In the later stage (3.5-4 hr), bradykinin level remained below the assay limit of 0.07 ng/ml in spite of its active generation, presumably because of its rapid degradation by the kininases, although it still played a definite role in the vascular permeability increase.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1977

Experimental hydrocephalus of the rat, produced by cisternal injection of kaolin-solution (author's transl).

Experimental hydrocephalus was produced in rats in high percentage, by direct injection of kaolin-solution into the cisterna magna under a operating microscope. Rats with hydrocephalus showed retarded development of the body. The skull enlarged round and became so thin, that the cortical vessels were observed through the skull. The brain showed marked internal hydrocephalus, retaining cerebrospinal fluid passage in the ventricular system, but there was an obstruction at the ambient cistern and the basal cistern. Review of the literature dealing with the methods to produce acquired hydrocephalus showed that this is the first report of experimental hydrocephalus of the rat produced by injecting kaolin-solution.

Animals↗
PubMed1982

The effect of magnesium trisilicate and kaolin on the in vivo absorption of chloroquine.

An in vitro study indicated that certain antacids and adsorbents may decrease the oral availability of th two widely used antimalarial agents chloroquine and pyrimethamine. To determine if this data was applicable to the clinical (in vivo) situation, plasma levels of one of the antimalarial agents (chloroquine) were followed in six Negro--Arab volunteers both when given alone and when taken with separate doses of two of the implicated interactants (magnesium trisilicate and kaolin). This in vivo work confirmed the in vitro findings; chloroquine area under the plasma concentration-time curve data were decreased by both magnesium trisilicate (18.2%) and kaolin (28.6%). Similar results could be expected for pyrimethamine. It is suggested therefore, to avoid loss of drug, that the antimalarials should not be taken with gastrointestinal medications of this type or that their administration should be separated by at least 4 h to reduce the risk of them interacting in the gut, thus preventing drug adsorption to the antacids/adsorbents, and loss of systemic availability.

Adult↗
PubMed1983

Kaolin pneumoconiosis. A case report.

A 35-year-old man who had been occupationally exposed to aerosolized kaolin for 17 years in a Georgia processing plant had diffuse reticulonodular pulmonary infiltrates and an upper lobe mass. Exploratory thoracotomy, performed to evaluate the nature of the mass, revealed an 8 X 12 X 10-cm conglomerate pneumoconiotic lesion containing large amounts of kaolinite. Coincident deposition of silica in the tissue was not demonstrable by either analytic scanning electron microscopy or x-ray diffraction. The case illustrates the effect of chronic kaolin exposure on the human lung and emphasizes the need for periodic evaluation of exposed workers.

Adult↗
PubMed1999

The Detection of Structural Transformations in Kaolin Suspensions by Ultrasound.

Thefractal dimension of kaolin flocs suspended in water was increased by the addition of potassium chloride and indirectly monitored by low-power ultrasonic pulses in a test cell with a "pitch-catch" configuration. The results from these measurements were compared with fractal dimensions obtained from quasi-elastic light-scattering measurements in a kaolin suspension of a much lower solid volume fraction. Further comparison with a coupled phase theory of ultrasound propagation, utilizing measured slope viscosity and particle size distribution, revealed that the observed changes in the ultrasound signature were commensurate with changes in the fractal dimension observed by light scattering over a potassium chloride concentration range of approximately 0-1 mM. Copyright 1999 Academic Press.

Journal Article↗