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At least 451 records · Page 25Linked to original sources
PubMed2005

Temporal representation of the delay of iterated rippled noise in the dorsal cochlear nucleus.

It has been suggested that the dorsal cochlear nucleus (DCN) is involved in the temporal representation of both envelope periodicity and pitch. This hypothesis is tested using iterated rippled noise (IRN), which is generated by a cascade of delay and add [IRN(+)] or delay and subtract [IRN(-)] operations. The autocorrelation functions (ACFs) of the waveform and the envelope of IRN(+) have a first peak at the delay, which corresponds to the perceived pitch of the IRN. With the same delay, the pitch of IRN(-) is generally an octave lower than for IRN(+). This is reflected in a first peak at twice the delay in the ACF of the waveform for IRN(-). In contrast, for identical delays, the ACF of the envelope for both IRN(-) and IRN(+) is the same. Thus the use of IRN allows the distinction between envelope- or fine-structure sensitivity. Recordings were made from 135 single units (BFs <5 kHz) in the DCN of the anesthetized guinea pig using IRN with delays ranging from 1 to 32 ms. In our sample 42% were sensitive to the periodicity of IRN(+) and were tuned to a particular delay in their first-order interspike interval histograms (ISIHs). This tuning was highly correlated with their response to white noise. Most units with best frequencies (BFs) <500 Hz show a different all-order ISIH for IRN(+) and IRN(-), which corresponds to the perceived pitch difference, whereas units with higher BFs show a similar response to IRN(+) and IRN(-). The results indicate that low-frequency units (BF <500 Hz) in the DCN may be involved in the representation of the waveform fine structure, although units with BFs >500 Hz are able to encode only the envelope periodicity of broadband IRN in their temporal discharge characteristics.

Acoustic Stimulation↗
PubMed2005

Cholesterol targeting alters lipid raft composition and cell survival in prostate cancer cells and xenografts.

Lipid rafts are cholesterol- and sphingolipid-enriched microdomains in cell membranes that regulate phosphorylation cascades originating from membrane-bound proteins. In this study, we tested whether alteration of the cholesterol content of lipid rafts in prostate cancer (PCa) cell membranes affects cell survival mechanisms in vitro and in vivo. Simvastatin, a cholesterol synthesis inhibitor, lowered raft cholesterol content, inhibited Akt1 serine-threonine kinase (protein kinase Balpha)/protein kinase B (Akt/PKB) pathway signaling, and induced apoptosis in caveolin- and PTEN-negative LNCaP PCa cells. Replenishing cell membranes with cholesterol reversed these inhibitory and apoptotic effects. Cholesterol also potentiated Akt activation in normal prostate epithelial cells, which were resistant to the apoptotic effects of simvastatin. Elevation of circulating cholesterol in SCID mice increased the cholesterol content and the extent of protein tyrosine phosphorylation in lipid rafts isolated from LNCaP/sHB xenograft tumors. Cholesterol elevation also promoted tumor growth, increased phosphorylation of Akt, and reduced apoptosis in the xenografts. Our results implicate membrane cholesterol in Akt signaling in both normal and malignant cells and provide evidence that PCa cells can become dependent on a cholesterol-regulated Akt pathway for cell survival.

Animals↗
PubMed1997

Sebum and water content in the skin of aged immobilized patients.

In the present study we investigated the sebum content and hydration of the skin in aged immobilized patients. Healthy aged as well as young and aged immobilized patients were evaluated by photometry, using a sebum tester and capacitance meter to detect sebum and hydration, respectively, in various skin areas. Sebum content was significantly higher in the young groups as compared to the aged ones, including those of the immobilized patients. Similar values of water content were observed in the healthy young and aged volunteers. However, surprisingly, a significantly marked decrease was detected in each tested area of the immobilized patients. We may assume that a cascade of events caused by the immobilization status of the patients leads to a significant decrease in water content within the dermis.

Adult↗
PubMed1999

Modulation of biological phenotypes for tumor growth and metastasis by target-specific biological inhibitors in gastric cancer.

For tumor progression, a cascade of linked sequential biological events is essential. We tried to test whether biological therapy can modulate specific biological phenotypes and increase the anti-tumor effect when combined with chemotherapy. Five human gastric cancer cell lines (YCC-1, YCC-2, YCC-3, YCC-7, AGS) were used in these studies. Pentosan polysulfate (PPS) as a heparin-binding growth factor inhibitor, Tranexamic acid as a plasmin inhibitor, Lovastatin as an adhesion inhibitor and Adriamycin as a chemotherapeutic agent were selected. The effects of each drug on colony formation and tumor cell proliferation were evaluated by soft agar assay and cell proliferation assay, respectively to test direct anti-tumor effect. The expression of uPA, PAI-1 was determined by ELISA, while MMPs activity was evaluated by zymography. PPS suppressed the colony-forming activity as much as Adriamycin did, but it showed only cytostatic effects in cell proliferation assay. Migration capacity using Boyden chamber assay was more closely correlated with adhesive capacity than uPA or MMP-2 expression. The motility inhibitory effect of Tranexamic acid was observed in the YCC-7 cell line, which expressed all the required biological phenotypes for migration. In AGS, with high cell motility and adhesiveness, the adhesion was inhibited by Lovastatin and most of the inhibitory effect was recovered by Mevalonate. When PPS was combined with Adriamycin on the Adriamycin-resistant, midkine (MK) gene expressing YCC-7 cell line, the growth inhibition rate increased up to 84%, while that for a single treatment of PPS or Adriamycin was 40% and 22%, respectively (p=0.001). When we combined Tranexamic acid and Adriamycin, we observed the synergistic effect in YCC-3 and YCC-7, while no combined effect was found in YCC-1. The combination of Lovastatin and Adriamycin did not show any combined effects in any of the cell lines. In conclusion, a synergistic anti-proliferative effect (chemo-sensitization) with combined chemo-biotherapy was found in cancer cells with specific biological target, MK. The anti-motility effect was the greatest when the gastric cancer cells expressed all the specific biological phenotypes.

Anticoagulants↗
PubMed2002

Effects of leptin administration and feed restriction on thecal leucocytes in the preovulatory rat ovary and the effects of leptin on meiotic maturation, granulosa cell proliferation, steroid hormone and PGE2 release in cultured rat ovarian follicles.

Leptin is expressed by adipocytes and is thought to play a role in regulating food intake and in reproduction. It has been demonstrated that acute leptin administration to immature gonadotrophin-primed rats in vivo inhibits ovulation and causes a decline in food intake. However, feed restriction alone does not inhibit ovulation. Two experiments were designed to investigate the mechanism of leptin-induced inhibition of ovulation. In the first experiment, which was prompted by the importance of ovarian leucocytes in ovulation, the role of leucocytes in leptin-induced inhibition of ovulation was investigated. The second experiment investigated whether high leptin concentrations could inhibit other factors important to ovulation, such as meiotic competence of oocytes, granulosa cell proliferation, steroid or PGE(2) release, and interleukin 1beta production, in vitro. In the first experiment, the populations of neutrophils and monocytes-macrophages in the preovulatory follicles of gonadotrophin-primed, leptin-treated and -untreated rats were examined. A decrease in food intake, as a result of either leptin treatment or feed restriction, specifically reduced the numbers of neutrophils and monocytes-macrophages infiltrating the theca interna of preovulatory follicles without affecting the numbers found in the stroma. The findings show that reduced infiltration of thecal neutrophils and macrophages into preovulatory follicles is a response to reduced food intake. Furthermore, this reduction is not the direct cause of the leptin-induced inhibition of ovulation. In the second experiment, ovarian follicles were cultured for 4 or 12 h in the presence or absence of the following hormones: FSH (500 miu), insulin-like growth factor I (IGF-I) (50 ng ml(-1)), LH (100 ng ml(-1)) and leptin (300 ng ml(-1)). The results demonstrated that high concentrations of leptin in follicle culture do not affect meiotic maturation or steroid release, but tend to inhibit release of PGE 2 (although this result was not significant). DNA synthesis in granulosa cells was not inhibited by leptin in FSH- and IGF-I-supplemented culture media. These results are in agreement with previous studies that have shown that leptin inhibits the stimulatory effects of IGF-I on FSH-stimulated oestradiol production in rat granulosa cells without affecting progesterone production. In summary, leptin does not appear to have an adverse effect on the components of ovulation tested in this study, and therefore must impact on the ovulatory cascade in a way that remains to be defined.

Animals↗
PubMed1994

Use of response surface statistical designs to detect effects of biologic response modifiers such as IL-2.

Recently many biologic response modifiers have been discovered or produced, but their effects are incompletely understood. The effects of these agents are complicated by their dependence not merely upon the administered dose, nor even the interval of time between administration and observation of effect, but also because of the cascade of interactions that can be invoked. Conventional experimental designs that test a specific combination looking for statistical significance, and that involve doing a series of studies varying one parameter at a time, are likely to require large numbers of animals or patients to answer the question of possible effect, and have a high likelihood of missing the effect altogether because of not selecting the correct combination of parameter levels. Response surface designs are intended for simultaneous multiparameter evaluation and so are less likely to miss an effect. However, if fixed sample designs are employed, the number of subjects required may still be quite large. Sequential designs based on response surface models have been used in other fields but are only now being applied in the fields of biology and medicine. We have explored the use of these designs to evaluate the potential usefulness of interleukin-2 (IL-2) to increase tumor uptake of subsequently administered antibody in nude mice. We found that these methods enabled us to efficiently determine optimal combinations of dose of IL-2 and interval of time between IL-2 and antibody administration for enhancement. Enhancement of tumor uptake of the antibody by IL-2 was substantial in amount and sufficient to stimulate studies in patients where we will use similar sequential methodology for trial design.

Animals↗
PubMed1995

c-fos is not essential for v-abl-induced lymphomagenesis.

Recent studies have suggested that cellular transformation by abl oncoproteins may be mediated by the ras signaling pathway. One of the main nuclear targets of this signal transduction cascade is the Fos and Jun family of transcription factors. To test the relevance of the c-fos proto-oncogene for v-abl-induced cancer development, we inoculated c-fos-deficient mice with the Abelson murine leukemia virus. Neonatal c-fos-deficient mice infected with the Abelson complex are able to develop the pre-B-cell lymphoma that characterizes Abelson disease. c-fos-deficient animals succumb to the disease with similar kinetics as their wild-type and heterozygous littermates. Moreover, the transformed cell that brings about the malignancy in mutant mice is the same pre-B-cell lymphoblast that is seen in control animals. These results demonstrate that c-fos is not required for in vivo transformation by v-abl.

Abelson murine leukemia virus↗
PubMed1988

Arachidonic acid reversal of phenytoin-induced neural tube and craniofacial defects in vitro in mice.

Diphenylhydantoin (DPH), a common anticonvulsant drug, is known to produce anomalies in the craniofacial region of animals and humans. We hypothesize that phenytoin disrupts craniofacial morphogenesis by inhibiting the arachidonic acid cascade; a pathogenesis already demonstrated for glucocorticoids and hyperglycemia. This hypothesis was tested in vitro by administering DPH, with and without the addition of exogenous arachidonic acid (AA), to murine embryos. Forty-five 8.7-day-old embryos were randomly assigned to one of three groups: control, DPH, or DPH plus AA. After 48 hours in culture, all specimens were examined at 6x magnification for defects in the facial arches, head fold, and neural tube fusion. The DPH-treated specimens had a significantly greater (P less than or equal to .05) number of anomalies in each of the three anatomical areas than did the controls. Specimens cultured in DPH plus AA had significantly fewer defects in each of the three features than those treated with DPH alone. These data support the hypothesis that phenytoin disrupts normal embryonic development through interruption of the arachidonic acid cascade. Furthermore, removal of the visceral yolk sac from 50% of the specimens in control and treatment groups provided evidence that the drug had a direct effect on the embryos rather than secondary to yolk sac involvement as has been suggested in the literature.

Animals↗
PubMed1990

Sex determination and the Y chromosome: the application of molecular genetic technique to behavioral genetics.

In mammals, the Y chromosome mediates both gonadogenesis and spermatogenesis. It is also known to influence such traits as histocompatibility, sperm head morphology, pubertal (but not adult) testosterone level, sexual behavior, and aggressive behavior. An immediate goal in my laboratory is the isolation and characterization of the Y chromosomal gene responsible for initiating differentiation of the primitive bipotential gonads to become testes: the Y chromosomal gonadogenesis gene. Function of this gene initiates a cascade of events involving large numbers of other genes scattered throughout the genome, but it is not responsible for initiating development of all of the male phenotype; where : is XXSxr karyotype males, bearing the Sxr region of the Y chromosome which includes this gene, are sterile. It is not known if this gene influences those behaviors known to be influenced by the Y chromosome. If animals with an XXSxr karyotype, transgenic for specific Y chromosomal genes, could be produced, questions such as this could be answered. The developmental biology of the testis, molecular genetics of the Sxr region of the Y chromosome, and isolation of the testis determination gene from DNA of XXSxr males are discussed. Also discussed are the production of transgenic mice and the prospects for using such animals as coisogenic strains, differing by precisely known DNA sequences, in behavior genetic analysis. Such animals could be used both to test for behavioral phenotype and to dissect out biochemical and neurological mechanisms responsible for the behavior.

Animals↗
PubMed2003

Colchicine down-regulates cytochrome P450 2B6, 2C8, 2C9, and 3A4 in human hepatocytes by affecting their glucocorticoid receptor-mediated regulation.

The xenobiotic-mediated induction of three major human liver cytochrome P450 genes, CYP2B6, CYP2C9, and CYP3A4, is known to be regulated by the constitutive androstane receptor (CAR) and the pregnane X receptor (PXR). CAR and PXR are regulated, at least in part, by the glucocorticoid receptor (GR) and the hypothesis of a signal transduction cascade GR-[CAR/PXR]-P450 has been proposed. This study was aimed at testing this hypothesis in primary human hepatocytes by using the tubulin network disrupting agent colchicine. Colchicine (COL) decreased both basal and rifampicin- and phenobarbital-inducible expression of CYP2B6, CYP2C8/9, and CYP3A4. A parallel down-regulation of mRNA expression of CAR, PXR, and tyrosine aminotransferase, a prototypic gene directly regulated by GR, was observed. COL affected neither the level of GR mRNA nor ligand binding to GR. To evaluate the effect of colchicine on GR-mediated gene transactivation, HeLa cells stably or transiently transfected with a GR-responsive element-dependent luciferase reporter gene were used. COL decreased the dexamethasone-induced luciferase expression in stably transfected cell line by 50%, whereas GR transactivation in transiently transfected cells was not affected by COL. In contrast, ligand-dependent GR translocation in the human embryonic kidney 293 cell line transiently transfected with GFP-GR was inhibited by COL. We conclude that alteration of the signal transduction mediated through the GR-[CAR/PXR]-P450 cascade by colchicine is responsible for the down-regulation of CYP2C9 and CYP3A4, implicating cytoskeleton as necessary for correct functioning of this cascade under physiological conditions.

Animals↗
PubMed1991

[Inhibition of arachidonic acid cascade by extract of rye pollen].

A standardized extract mainly from rye pollen (Cernilton N) was tested in vitro on the inhibition of prostaglandin and leukotrien synthesis. The determination of the prostaglandin and leukotrien synthesis from labelled arachidonic acid was done in microsomes of ram seminal vesicles resp. in rat basophilic leukemia cells (RBL-1 cells). The water soluble resp. the fat soluble extract fraction from the whole pollen extract were tested separately. The radio-TLC separation of the reaction metabolites showed a dose dependent inhibition of the cyclo-oxygenase and the 5-lipoxygenase activity by the fat soluble pollen extract fraction. The IC50-values are 0.005 mg/ml resp. 0.08 mg/ml and similar to those of the also tested diclofenac. The water soluble fractions showed no effect in this test system. According to these in vitro results and the clinical experience so far with the pollen extract its therapeutic efficacy on benign prostate diseases is best explainable by the anticongestive resp. anti-inflammatory effect of the fat soluble fraction. Due to the different actions of prostaglandins and leucotrienes also relaxant and antiproliferative effects were conceivable.

Animals↗
PubMed2005

Mutational analysis in UK patients with a clinical diagnosis of familial hypercholesterolaemia: relationship with plasma lipid traits, heart disease risk and utility in relative tracing.

As part of a randomised trial [Genetic Risk Assessment for Familial Hypercholesterolaemia (FH) Trial] of the psychological consequences of DNA-based and non-DNA-based diagnosis of FH, 338 probands with a clinical diagnosis of FH (46% with tendon xanthomas) were recruited. In the DNA-based testing arm (245 probands), using single-strand conformation polymorphism of all exons of the low-density lipoprotein receptor (LDLR) gene, 48 different pathogenic mutations were found in 62 probands (25%), while 7 (2.9%) of the patients had the R3500Q mutation in the apolipoprotein B (APOB) gene. Compared to those with no detected mutation, mean untreated cholesterol levels in those with the APOB mutation were similar, while in those with an LDLR mutation levels were significantly higher (None=9.15+/-1.62 vs LDLR=9.13+/-1.16 vs APOB=10.26+/-2.07 mmol/l p<0.001, respectively). Thirty seven percent of the detected mutations were in exon 3/4 of LDLR, and this group had significantly higher untreated cholesterol than those with other LDLR mutations (11.71+/-2.39 mmol/l vs 9.88+/-2.44 mmol/l, p=0.03), and more evidence of coronary disease compared to those with other LDLR or APOB mutations (36 vs 13% p=0.04). Of the probands with a detected mutation, 54 first-degree relatives were identified, of whom 27 (50%) had a mutation. Of these, 18 had untreated cholesterol above the 95th percentile for their age and gender, but there was overlap with levels in the non-carrier relatives such that 12% of subjects would have been incorrectly diagnosed on lipid levels alone. In the non-DNA-based testing arm (82 probands) only 19 of the 74 relatives identified had untreated cholesterol above the 95th percentile for their age and gender, which was significantly lower (p<0.0005) than the 50% expected for monogenic inheritance. These data confirm the genetic heterogeneity of LDLR mutations in the UK and the deleterious effect of mutations in exon 3 or 4 of LDLR on receptor function, lipids and severity of coronary heart disease. In patients with a clinical diagnosis of FH but no detectable mutation, there is weaker evidence for a monogenic cause compared with relatives of probands with LDLR mutations. This supports the usefulness of DNA testing to confirm diagnosis of FH for the treatment of hyperlipidaemia and for further cascade screening.

Cardiovascular Diseases↗
PubMed2003

Compromised DNA repair enhances sensitivity of the yeast RNR3-lacZ genotoxicity testing system.

The RNR3-lacZ genotoxicity testing system was developed based on the induction of a Saccharomyces cerevisiae RNR3-lacZ reporter gene in response to a broad range of DNA-damaging agents. In order to enhance the sensitivity of the RNR3-lacZ system, several deletion mutant strains representing different repair pathways were created and examined for their effects on RNR3-lacZ expression. It was found that inactivation of different DNA repair pathways has profound effects on the DNA damage induction of RNR3 expression. Although deletion of MAG1 in the base excision repair pathway enhances the detection sensitivity to DNA-alkylating agents, and deletion of RAD2 in the nucleotide excision repair pathway enhances the detection sensitivity to ultraviolet and agents that produce bulky lesions, inactivation of genes involved in the recombination repair and postreplication repair variably reduces RNR3-lacZ induction. This study not only helps to establish a more sensitive genotoxicity testing system but also suggests that certain eukaryotic DNA repair pathways are required for gene regulation in response to DNA damage and probably serve as sensors in the signal transduction cascade.

DNA Repair↗
PubMed1984

[Demonstration of C3-binding circulating immune complexes using Raji, conglutinin and anti-C3 assays--a critical review].

There remains no doubt at the present time, that the appearance of circulating immune complexes in illness accompanying vasculitis and for glomerulonephritis correlates with the severity of disease. Moreover, immune complexes are of diagnostic importance where infections with a chronic development or neoplastic diseases are concerned. The choice of IC test system should incorporate their essential biological functions and identify those IC that activate the complement cascade both by the classical and the alternative route. The detection of IC bound C3 cleavage products (C3b, C3bi, C3d) represents the key to identification of a wide range of IC. Of the presently available methods Raji cell test, conglutinin- and anti C3-IC assay, on critical appraisal, the anti C3-IC assay represents the most applicable way of defining complement binding IC. The advantage of this system is that appreciable disturbances and limitations that influence other systems do not affect the antigen-antibody reaction which is the core of the anti C3 assay.

Antigen-Antibody Complex↗
PubMed1995

G alpha-16 complements the signal transduction cascade of chemotactic receptors for complement factor C5a (C5a-R) and N-formylated peptides (fMLF-R) in Xenopus laevis oocytes: G alpha-16 couples to chemotactic receptors in Xenopus oocytes.

The human leukocyte chemoattractant receptors for complement factor C5a (C5a-R) and N-formylated peptides (fMLF-R) are important members of the superfamily of G-protein coupled receptors (GPCR). Uniquely among the GPCR, these two receptors cannot be expressed in a functionally active form in the oocytes of the frog Xenopus laevis, but require substitution of total RNA of the myelomonocytic U-937 or HL-60 cell lines, respectively. Recently, it was reported that the C5a-R may couple to the alpha subunit of G-16. We have tested this G-protein for its ability to complement the signal transduction cascade of the C5a-R and fMLF-R in Xenopus oocytes. Injection of cRNA for the C5a-R in combination with G alpha-16 led to expression of a functional C5a-R as measured by ligand-induced whole cell current. In contrast to a previous report, the fMLF-R exhibited some residual functional activity when transiently expressed in Xenopus oocytes the extent of which could, however, substantially be increased by coexpression of G alpha-16. Thus, G alpha-16 complements the signal transduction cascade of both receptors in Xenopus laevis oocytes and is most likely the complementing factor present in the U-937 and HL-60 cell lines.

Animals↗
PubMed2005

Activation of the p38 MAPK pathway by follicle-stimulating hormone regulates steroidogenesis in granulosa cells differentially.

In the present study, we started out to test whether the follicle-stimulating hormone (FSH)-activated p38 MAPK signaling cascade was involved in the regulation of steroidogenesis in granulosa cells (GCs). GCs were prepared from the ovaries of DES-treated immature rats and cultured in serum-free medium. Treatment of GCs with FSH (50 ng/ml) induced the phosphorylation of p38 MAPK rapidly with the phosphorylation being observed within 5 min and reaching the highest level at 30 min. Such activation was protein kinase A-dependent as indicated by the results using specific inhibitors. FSH stimulated the production of progesterone and estradiol as well as the expression of the steroidogenic acute regulatory protein (StAR) in a time-dependent manner, with a maximum level being observed in the production of progesterone and StAR at 48 h. Moreover, the potent p38 MAPK inhibitor SB203580 (20 microM) augmented FSH-induced progesterone and StAR production, while reduced FSH-induced estradiol production at the same time (P<0.01). RT-PCR data showed that inclusion of SB203580 in the media enhanced FSH-stimulated StAR mRNA production, while decreased the FSH-stimulated P450arom mRNA expression (P<0.05). Immunocytochemical studies showed that FSH treatment together with the inhibition of p38 MAPK activity resulted in a higher expression of StAR in mitochondria than FSH treatment alone. FSH also significantly up-regulated the protein level of LRH-1, a member of the orphan receptor family that activates the expression of P450arom in ovaries and testes. p38 MAPK inactivation down-regulated the basal and FSH-induced LRH-1 expression significantly. The intra-cellular level of DAX-1, another orphan receptor that inhibits StAR expression, also decreased upon p38 MAPK being inactivated. For the first time, the present study suggests that FSH-activated p38 MAPK signal pathway regulates progesterone and estrogen production in GCs differentially, and that the transcription factors LRH-1 and DAX-1 might play important roles in the process.

Animals↗
PubMed2005

Particle size distribution of polycyclic aromatic hydrocarbons in motorcycle exhaust emissions.

The size distribution of polycyclic aromatic hydrocarbons (PAHs) in emission of a two-stroke carburetor motorcycle was studied. The exhaust gas from the test motorcycle was passed to a dilution tunnel and collected using a 10 cascade micro-orifice uniform deposit impactor (MOUDI) of 0.056-10 microm aerodynamic diameter fitted with aluminum substrates. All MOUDI substrates were analyzed for particulate mass and for PAHs by GC/MS. Most of the 21 analyzed PAHs have two significant modes that peak at <0.1 and 0.18-0.32 microm. For some PAHs, a third peak appears around 1.8 microm. MOUDI impactor samples show that 88.9% particulate and 89.6% PAH mass distributed smaller than 2.5 microm. Mass median diameters of PAHs are about 0.2 microm. Total benzo[a]pyrene toxic equivalency emission factor was 440+/-13.8 ng/km for the test motorcycle. An average of 90.3% of carcinogenicity is observed in particulate smaller than 1.0 microm. The results suggest that submicron particulates predominate in the exhaust from motorcycle and exhibit high carcinogenic potency for these particulate.

Air Pollutants↗
PubMed2003

The influence of induced hypothermia for hemostatic function on temperature-adjusted measurements in rabbits.

UNLABELLED: In hypothermic patients, a tendency to bleed may be observed even when hemostatic tests seem to be normal. Coagulation and platelet function tests are usually performed at 37 degrees C. We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function testing using Sonoclot Analyzer (Sonoclot) and Thromboelastography (TEG). Anesthesia was induced and maintained with IV ketamine and fentanyl on 15 male New-Zealand White rabbits. A water blanket was used to induce hypothermia to 30 degrees C and to rewarm to 37 degrees C. Blood samples were obtained at four points: before hypothermia, at 34 degrees C, at 30 degrees C, and after rewarming. Standard coagulation tests were performed at 37 degrees C (C method), and simultaneously, real temperature hemostasis function tests (R method) were run. In Sonoclot(R), activated clotting time and time to peak increased and clot rate decreased significantly at 30 degrees C in the R method compared with those in the C method. In TEG(R), reaction time and clot formation time were prolonged and clot formation rate was diminished at 30 degrees C in the R method compared with those in the C method. Induced hypothermia delayed the coagulation cascade and reduced platelet function. During hypothermia, hemostatic measurements should be performed at real temperature to avoid overestimating patient hemostatic function based on results measured at the standard 37 degrees C. IMPLICATIONS: We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function tests in rabbits using Sonoclot Analyzer and Thromboelastography. Induced hypothermia delayed the coagulation cascade and reduced platelet function. The conventional coagulation tests performed at 37 degrees C failed to detect these hypothermia-induced degradations in hemostasis performance.

Anesthesia↗