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PubMed1985

[Mechanism of systolic anterior motion and left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy].

Two-dimensional echocardiographic studies were performed for 22 patients with asymmetric septal hypertrophy and systolic anterior motion (SAM) of the mitral valve to clarify the mechanism of SAM and left ventricular outflow obstruction. The long-axis view of the left ventricle showed that a distal portion of the anterior mitral leaflet became surplus when the mitral valve was closed in 15 of 16 patients with SAM-septal contact and in four of six patients without it. In these patients, the mitral leaflet coaptation was displaced anteriorly, and/or the anterior leaflet was elongated, showing an anterior motion. In an unusual patient with SAM-septal contact, a distal portion of the long posterior mitral leaflet was surplus. The remaining two patients without SAM-septal contact had a rather widely coapted portion of the mitral leaflets. The distal surplus portion and the coapted portion of the mitral valve were displaced anteriorly prior to the onset of ejection, and moved forward and protruded into the outflow tract more rapidly and more excessively than the papillary muscles during early to mid systole in all patients. Then, the distal mitral valve and the chordae tendineae adopted the configuration of an inverted V in mid systole. The tip of the surplus leaflet contacted the interventricular septum in patients with SAM-septal contacts. In the short-axis view of the left ventricle, the central portion of the distal mitral valve moved forward excessively and bent like an inverted U during early to mid systole. Therefore, SAM of the distal mitral valve is thought to be caused by the hydrodynamic force generated by the ejection flow. This force is supposed to be not only due to the Venturi effect, but is more properly understood as a "pushing force". Left ventricular outflow obstruction is considered to be formed by the protruding distal mitral valve and the hypertrophied septum.

Adolescent↗
PubMed1985

Independent regulation of ornithine decarboxylase and S-adenosylmethionine decarboxylase in methylthioadenosine phosphorylase-deficient malignant murine lymphoblasts.

The control of polyamine synthesis in neoplastic cells is complex and incompletely understood. Using murine lymphoma cells deficient in methylthioadenosine (MTA) phosphorylase, we have analyzed the role of MTA in the regulation of ornithine decarboxylase and S-adenosylmethionine (SAM) decarboxylase, the two rate-limiting enzymes in the polyamine-biosynthetic pathway. The addition of MTA to the enzyme-deficient lymphoblasts induced within 1 to 3 h an increase in the activities of both decarboxylases and an accompanying rise in putrescine and decarboxylated SAM levels. The ornithine decarboxylase inhibitor alpha-difluoromethylornithine blocked the MTA-triggered accumulation of putrescine but not decarboxylated SAM. In a reciprocal manner, the SAM decarboxylase inhibitor methylglyoxal bis(guanylhydrazone) prevented the accretion of decarboxylated SAM but not putrescine. The MTA-induced rise in SAM decarboxylase and ornithine decarboxylase activities preceded by several hours changes in spermidine or spermine pools. However, MTA decreased the flux through the polyamine-synthetic pathway, as estimated by the incorporation of radioactive ornithine into spermine. Similar changes in polyamine metabolism were observed in a secondary mutant deficient in MTA phosphorylase, but resistant to MTA toxicity. These results suggest that the velocity of polyamine synthesis, or the concentration of MTA itself, may regulate ornithine decarboxylase and SAM decarboxylase activities through separate, growth-independent mechanisms.

Adenosine↗
PubMed1985

Dose-dependent sulfoconjugation of salicylamide in dogs: effect of sulfate depletion or administration.

The effects of plasma inorganic sulfate concentrations on the dose-dependent kinetics of salicylamide (SAM) were examined in the dog. Decreasing plasma sulfate concentrations from 0.9 mM to less than 0.3 mM significantly decreased clearance of a small dose of SAM (5 mg/kg) to the sulfate conjugate. Infusing sodium sulfate to prevent the decrease in plasma inorganic sulfate concentration that follows a p.o. 20-mg/kg dose of SAM did not increase SAM elimination. However, sodium sulfate given p.o. decreased SAM bioavailability, which suggests a local effect of sulfate on intestinal first-pass metabolism of SAM. These data show some dependence of SAM metabolism on plasma inorganic sulfate concentrations, but only when they are markedly reduced.

Animals↗
PubMedDate not supplied

[Comparative S-adenosyl-L-methionine and S-adenosyl-L-homocysteine content in the tissues of experimental tumors in the process of their growth].

Content of S-adenosyl-l-methionine (SAM) in rat tissues of Pliss lymphosarcoma, of sarcoma 180 and in adenocarcinoma 755 of mice varied within the limits of 27-57 nM/g, 60-64 nM/g and 32-40 nM/g of wet tissue, respectively, content of S-adenosyl-l-homocysteine (SAH) varied in the tumors studied within the limits of 19-28, 16-21 and 11-20 nM/g, respectively. In the tumor bearing mice the content of SAM was unaltered in liver tissue during the growth of sarcoma 180 or adenocarcinoma 755. Development of Pliss lymphosarcoma in rats was accompanied by a decrease in content of SAM in liver tissue. When the rate of Pliss lymphosarcoma growth was decreased, the content of SAH in the tumor was unaltered but the level of SAM was decreased about 2-fold and the ratio SAH/SAM was increased, correspondingly, approximately 2-fold. If the rate of growth of mice adenocarcinoma 755 was elevated, content of SAM in the tumor was increased but the SAH level was markedly decreased and the ratio SAH/SAM was decreased about 2-fold. Concentrations of SAH and SAM were unaltered in mice sarcoma 180 with the linear rate of growth from 0.15 to 1.6 g. The data obtained suggest that the rate of growth of the tumors studied correlated with relative and absolute content of SAM and SAH.

Adenocarcinoma↗
PubMed1981

Decreased cerebral catabolism of [3H]histamine in vivo after S-adenosylmethionine administration.

Administration of S-adenosyl-L-methionine (SAM) (200 mg/kg) to adult mice significantly elevated its cerebral levels while the steady-state levels of histamine (HA) and S-adenosyl-L-homocysteine remained unaltered. [3H]HA (1 microCi/10 microliters) was injected intraventricularly (i.vt.) 20 sec, 2, 5, 10 or 20 min prior to sacrifice (1 hr after SAM) and brains were analyzed for [3H]HA, [3H]methylhistamine (MeHA) and [3H]methylimidazoleacetic acid. Brains of SAM-treated mice contained more [3H]HA than vehicle-treated controls at 20 sec, 2, 5 and 10 min (22, 35, 52 and 25%, respectively). [3H]MeHA levels were lower than controls at 20 sec, but higher at 2 and 5 min. Fifteen minutes after i.vt. [3H]histidine, brains of SAM-treated mice contained 47% more [3H]HA and 39% more [3H]MeHA (compared to controls) while [3H]histidine and [3H]methylimidazoleacetic acid levels remained unchanged. SAM treatment had no effect on the activity of cerebral histamine-N-methyltransferase, S-adenosyl-L-homocysteine hydrolase and monoamine oxidase type A (substrate 5-hydroxytryptamine) when tested in vitro, while monoamine oxidase B (substrate phenylethylamine) activity was significantly decreased. In vitro, SAM had no effect on monoamine oxidase A or B. The findings demonstrate that, unexpectedly, the rate of catabolism of HA to MeHA is significantly decelerated in brains containing elevated levels of SAM.

Animals↗
PubMed1994

Age-associated decreases in the messenger ribonucleic acid level and the rate of synthesis of apolipoprotein A-II in murine senile amyloidosis.

BACKGROUND: Apolipoprotein A-II (apoA-II), an apoprotein of serum high density lipoprotein, is the serum precursor of murine senile amyloid protein fibril. Three types of apoA-II protein variants (type A, B, and C) were found among inbred strains of mice. We reported the decreased concentration and the accelerated clearance of serum apoA-II with advancing age in the senescence-accelerated mouse-prone (SAM-P/1) mice, a strain with a high incidence of severe senile systemic amyloidosis and type C apoA-II. EXPERIMENTAL DESIGN: Age-related changes in hepatic mRNA levels and rates of synthesis of apoA-II were investigated in SAM-P/1 and SAM-R/1, the latter of which has a low incidence of amyloidosis and type B apoA-II. RESULTS: At age 2 months, both strains had the same levels of hepatic apoA-II mRNA. However, in SAM-P/1 after age 4 months, we observed a remarkable age-associated decrease in apoA-II mRNA levels and the level at age 14 months was about 50% of that seen at age 2 months. On the other hand, in SAM-R/1, the level at age 17 months was still 77.4% of the level at age 2 months. No age-related decrease in mRNA levels of apoA-I, another major apolipoprotein of high density lipoprotein, was observed in either strain. Slight age-associated decreases in ApoE mRNA levels and age-associated changes in apoB mRNA levels were observed, with the same profiles for both strains. The rates of hepatic synthesis of apoA-II protein decreased significantly in SAM-P/1 and decreased slightly in SAM-R/1, with advancing age. The parallel changes observed between mRNA levels and rates of synthesis of apoA-II indicate that decrease in the rate of apoA-II synthesis reflects age-associated decreases in mRNA levels. CONCLUSIONS: These findings suggest that the decreased concentration of serum apoA-II protein with advancing age may be caused by a decrease in the level of its mRNA.

Aging↗
PubMed1996

Sequestered endoplasmic reticulum space for sequential metabolism of salicylamide. Coupling of hydroxylation and glucuronidation.

The metabolic disposition of simultaneously delivered [14C]salicylamide (SAM) (100 microM) and a tracer concentration of its hydroxylated metabolite [3H]gentisamide (GAM) was studied with single-pass followed by recirculating rat liver perfusion (10 ml/min). The use of dual radiolabeling of precursor-product pairs in single-pass and recirculating perfusions allowed for characterization of the differential metabolism of preformed [3H]GAM and formed [14C]GAM, which arose in situ in the liver with [14C]SAM single-pass perfusion, and the behavior of circulating [14C]GAM, which behaved as a preformed species in recirculation. In both modes of perfusion, [14C]SAM was mainly sequentially metabolized to [14C]GAM-5-glucuronide, whereas [3H]GAM predominantly formed [3H]GAM-5-sulfate. The steady-state and time-averaged clearances of SAM were identical and approached the value of flow, yielding a high hepatic extraction ratio (E = 0.98). The apparent extraction ratio of formed GAM [E(mi) = 0.96] was greater than that of the preformed species [E(pmi) approximately 0.7]. Because the coupling of (SAM) oxidation and (GAM) glucuronidation was a plausible explanation for the observation, a novel physiological pharmacokinetic model was developed to interpret the data. In this model, the liver was divided into three zonal units, within which acinar distribution of enzymatic activities was considered, namely periportal sulfation, evenly distributed glucuronidation, and perivenous hydroxylation. Each zonal region was subdivided into extracellular, cytosolic, and endoplasmic reticulum compartments, with cytosolic (sulfotransferases) and microsomal (cytochromes P-450 and UDP-glucuronosyltransferase) enzymes being segregated intracellularly into the cytosolic compartment and endoplasmic reticulum compartment, respectively. The simulations provided a good prediction of the present experimental data as well as previously obtained data with increasing SAM concentration and retrograde flow and supported the contention that SAM oxidation and GAM glucuronidation are coupled.

Animals↗
PubMed2000

Gene sam1 encoding adenosylmethionine synthetase: effects of its expression in the fission yeast Schizosaccharomyces pombe.

By screening gene libraries of Schizosaccharomyces pombe with a DNA fragment encoding part of the Saccharomyces cerevisiae S-adenosylmethionine synthetase (SAMS), we isolated the fission yeast sam1 gene. Its sequence exhibits good homology to SAMSs of other organisms and reveals the motifs characteristic for SAMSs. SAMS activity and sam1 mRNA levels decrease when cells enter stationary phase. In haploid strains, gene sam1 is essential for growth; if weakly expressed, cells mate and sporulate at a reduced rate. Strains overexpressing sam1 exhibit methionine-sensitive growth. This methionine-induced growth inhibition is partially relieved by adenine. We assume that methionine reduces the level of one or several adenine nucleotides by a SAMS-mediated mechanism. Intracellular SAM levels increase drastically by exogenously added methionine. This increase predicts that mutants exhibiting methionine revertible phenotypes can be indicative for mutations in proteins exhibiting SAM-dependent functions. In agreement with this prediction, we show that mutant pmt2-5 has this phenotype and that gene pmt2 encodes a potential SAM-dependent enzyme.

Amino Acid Sequence↗
PubMed1999

Methyl donor for 1-methyladenine biosynthesis in starfish ovarian follicle cells.

1-Methyladenine (1-MeAde), the oocyte maturation-inducing substance of starfish, is produced by ovarian follicle cells upon stimulation with a gonad-stimulating substance (GSS) released from radial nerves. It has been reported that a process of methylation is involved in GSS-induced 1-MeAde production by starfish ovarian follicle cells. The present study sought to identify a possible methyl donor for 1-MeAde biosynthesis in follicle cells of the starfish Asterina pectinifera. When isolated follicle cells were incubated with [methyl-(14)C]methionine (Met), there was an increase in the level of radiolabeled S-adenosylmethionine (SAM). After further incubation with GSS, the [methyl-(14)C]SAM level decreased, concomitant with a marked increase in radiolabeled 1-MeAde production. The amount of [methyl-(14)C]SAM consumed under the influence of GSS was similar to the amount of [methyl-(14)C]1-MeAde produced. Therefore, it is concluded that SAM is a methyl donor for 1-MeAde biosynthesis in starfish ovarian follicle cells. On the other hand, it is likely that the purine molecule of 1-MeAde is not derived from SAM but from ATP. 3-Isobutyl-1-methylxanthine, a potent inhibitor of cyclic AMP phosphodiesterase, also caused a reduction in the level of radiolabeled SAM following 1-MeAde production. This suggests that the methylation process of 1-MeAde biosynthesis in starfish ovarian follicle cells upon stimulation with GSS is mediated by a second messenger, cyclic AMP.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Adhesion and proliferation of corneal epithelial cells on self-assembled monolayers.

The effect of surface chemistry on the proliferation and adhesion of SV-40 human corneal epithelial cells was investigated. The surface chemistry of substrates was controlled by the deposition of self-assembled monolayers (SAMs) terminated with the following functional groups: -CF3, -CH3, -CO(2)H, and -NH(2). SAMs of alkanethiols on gold and of alkylsiloxanes on SiOx were included in the study. Comparisons are made between different types and functionalities of SAMs and between SAM-covered substrates and tissue culture polystyrene. Adhesion assays were performed after incubation of the cells for 1 h in 10% fetal bovine serum and in serum-free conditions. The cellular response was found to be a function of surface chemistry and the presence of exogenous proteins. The number of cells that adhered to most of the SAMs in 10% serum and in serum-free conditions was not significantly different from the number of cells that adhered to TCPS. Proliferation assays were carried out in 10% serum and in 0.5% serum. Cell behavior was influenced by surface chemistry but did not deviate significantly from the behavior on TCPS for most of the SAMs. Serum level did not play a major role in cell proliferation. Our data establish the expected behaviors for a corneal epithelial cell line under defined conditions on specific surfaces.

Adhesiveness↗
PubMed2001

Surface characterization and platelet adhesion studies of self-assembled monolayer with phosphonate ester and phosphonic acid functionalities.

Because of its well-defined surface configuration and creative chemical structure, an alkanethiol self-assembled monolayer (SAM) on gold is a model surface for a blood compatibility investigation. In this study two laboratory-synthesized long-chain alkanethiols, HS(CH(2))(10)PO(3)-(C(2)H(5))(2) and HS(CH(2))(10)PO(3)H(2), were employed for the direct preparation of SAMs with nonionic and ionic functional groups. Various instrumental analyses confirmed the high purity of the phosphonate ester and phosphonic acid terminated alkanethiols. The surface characterization results showed the -PO(3)H(2) terminated SAM was more hydrophilic than the -PO(3)(C(2)H(5))(2) one. Higher hysteresis values for the -PO(3)(C(2)H(5))(2) and -PO(3)H(2) terminated SAMs were noted, which were possibly due to the steric hindrance of the bulky terminal groups. In addition, the O(2) plasma + EtOH-rinse pretreated Au sample was hydrophilic because of the residual gold oxide on the surface. This finding was supported by electron spectroscopy for chemical analysis (ESCA) as well. The ESCA analysis also indicated bulky and polar terminal groups [-PO(3)(C(2)H(5))(2) and -PO(3)H(2)] were situated in the outermost layer of its monolayer. The platelet reactivity on the SAM with the nonionic group -PO(3)(C(2)H(5))(2) was less than those of the ionic terminated SAMs -COOH and -PO(3)H(2). The O(2) plasma + EtOH-rinse pretreated gold substrate exhibited the least platelet-activating surface among the different pretreated Au substrates studied.

Biocompatible Materials↗
PubMed1988

Fluorescence microscopy study of polymorphonuclear leukocyte substrate attached materials.

We describe a technique to visualize substrate-attached materials (SAM) of polymorphonuclear leukocytes (PMN) using the fluorescent lipid analog 1,1'-dioctadecyl-3,3,3',3',-tetramethylindocarbocyanine-perchlorate (DiC18Icc). DiC18Icc was incorporated into the membranes of living cells or SAMs. Since cell preparation does not require fixation, SAMs can be rapidly visualized by fluorescence microscopy. SAMs are generated by subjecting attached cells to a shearing force by rinsing with phosphate-buffered saline (PBS). The SAM-labeling protocol identified a membrane compartment as shown by detergent extraction. The SAMs of PMN leukocytes observed with this technique display complex patterns of interconnecting filaments, foci with radiating filaments, and smooth membranous areas with interconnecting filaments. The sensitivity and nondestructive nature of the DiC18Icc-labeling procedure have allowed us to observe filopodia of motile cells. The results are consistent with the hypothesis that locomotion involves a series of attachment and detachment steps. After 60 minutes of locomotion, these trailing filopodia have been measured at lengths up to 100 micron. The amount of membrane associated with these filopodia accounts for roughly 10% of the total membrane area of resting cells. These data set limits for models of membrane flow during chemotaxis.

Carbocyanines↗
PubMed2003

Simultaneous detection of S-adenosylmethionine and S-adenosylhomocysteine in mouse and rat tissues by capillary electrophoresis.

A capillary electrophoresis method for the determination of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) in rat liver and kidney and mouse liver is described. The method can also be used to determine SAM in whole blood. The method provides rapid (approximately 16 min sample to sample) resolution of both compounds in perchloric extracts of tissues. Separation was performed by using an uncoated 50 microm ID capillary with 60 cm total length (50 cm to the detector window). Samples were separated at 22.5 kV and the separation running buffer was 200 mM glycine pH 1.8 (with HCl). The method compares favorably to HPLC methods (r (2) = 0.994 for SAM, r (2) = 0.998 for SAH) and has a mass detection limit of about 10 fmol for both SAM and SAH at a signal-to-noise ratio of 3. The method is linear over ranges of 1-100 microM SAM and 1-250 microM SAH. This method can be used to determine tissue concentrations of SAM and SAH, two metabolites that can provide insight into many biological processes.

Animals↗
PubMed1996

Differential expression pattern of S-adenosylmethionine synthetase isoenzymes during rat liver development.

The pattern of expression of liver-specific and extrahepatic S-adenosylmethionine (SAM) synthetase in developing rat liver was established by determining steady-state levels of the respective messenger RNAs (mRNAs) and protein content. Levels of liver-specific SAM synthetase mRNA increased progressively from day 20 of gestation, increased 10-fold immediately after birth, and reached a peak at 10 days of age, decreasing slightly by adulthood. Conversely, mRNA levels of extrahepatic isoenzyme decreased toward birth, increased threefold in the newborn, and decreased further in the postnatal life, reaching a minimum in the adult. Similar expression profiles were observed in isolated hepatocytes, indicating that both mRNAs are differentially regulated in the same cell type. Western blot analysis showed that levels of immunoreactive liver-specific isoenzyme followed a trend similar to the mRNA, indicating that developmental regulation of this enzyme is mediated at the mRNA level. Developmental patterns of expression of albumin and alpha-fetoprotein (AFP) mRNAs were closely related to those for liver-specific and extrahepatic isoenzymes, respectively. Therefore, it is suggested that liver-specific SAM synthetase may be a marker for hepatocyte differentiation. Incubation of primary cultures of hepatocytes from 21-day-old fetuses with permeant cyclic adenosine monophosphate (cAMP) analogues elicited an up-regulation of the mRNA for the liver-specific isoenzyme with a concomitant down-regulation of the extrahepatic message, suggesting a physiological role for the increased postnatal glucagonemia in the control of this isoenzyme switching. In contrast with the isoenzyme expression profiles, the levels of SAM, the product of SAM synthetase reaction, were determined to be greater during gestation than in immediate postnatal periods. These results indicate that synthesis and utilization of SAM may be regulated differentially in fetal and adult hepatocytes.

Albumins↗
PubMed1997

Regulation of rat liver S-adenosylmethionine synthetase during septic shock: role of nitric oxide.

We investigated the modulation of rat liver S-adenosylmethionine (SAM) synthetase in a model of acute sepsis. Our results show that animals treated with bacterial lipopolysaccharide experience a marked decrease in liver SAM synthetase activity. No changes were detected in the hepatic levels of SAM synthetase protein, suggesting that inactivation of the existing enzyme was the cause of the observed activity loss. Lipopolysaccharide treatment resulted in the expression of calcium-independent/cytokine-inducible nitric oxide (NO) synthase in liver and the accumulation in plasma of the NO-derived species nitrite and nitrate. NO implication in the in vivo regulation of SAM synthetase was evaluated in animals treated with the NO donor molecule 3-morpholinosydnonimine. The analysis of liver enzymatic activity, along with protein and messenger RNA levels yielded results similar to those obtained with lipopolysaccharide treatment. To assess directly the sensitivity of SAM synthetase to NO, the rat liver-purified high- and low-molecular weight forms of the enzyme were exposed to various doses of 3-morpholinosydnonimine and other NO donors such as S-nitroso-N-acetylpenicillamine, resulting in a dose-dependent inhibition of enzymatic activity. This effect was reversed by addition of the reducing agents beta-mercaptoethanol and glutathione. Finally, cysteine 121 was identified as the site of molecular interaction between NO and rat liver SAM synthetase that is responsible for the inhibition of the enzyme. To reach this conclusion, the 10 cysteine residues of the enzyme were changed to serine by site-directed mutagenesis, and the effect of NO on the various recombinant enzymes was measured.

Animals↗
PubMed2004

Proteomic profiling of platelet proteins by trypsin immobilized self-assembled monolayers digestion chip and protein identification using electrospray ionization tandem mass spectrometry.

Self-assembled monolayers (SAMs) on coinage metal provide versatile modeling systems for studies of interfacial electron transfer, biological interactions, molecular recognition, and other interfacial phenomena. Recently, the bonding of enzyme to SAMs of alkanethiols onto Au electrode surfaces was exploited to produce a bio-sensing system. In this work, the attachment of trypsin to a SAMs surface of 11-mercaptoundecanoic acid was achieved using water soluble 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide and N-hydroxysulfosuccinimide as coupling agent. Experimental results have revealed that the X-ray Photoelectron Spectroscopy (XPS) C1s core levels at 286.3 and 286.5 eV (C with N), 288.1 eV (amide bond), and 289.3 eV (carboxyl) illustrate the immobilization of trypsin. These data were also in good agreement with Fourier-Transformed Infrared Reflection-Attenuated Total Reflection (FTIR-ATR) spectra for the peaks valued at 1659.4 cm(-1) (amide I) and 1546.6 cm(-1) (amide II). Using electrospray ionization tandem mass spectrometry (ESI-MS/MS) observations, analytical results have demonstrated the platelet proteins digestion of the immobilized trypsin on the functionalized SAMs surface. For such surfaces, platelet proteins were digested on the trypsin-immobilized SAMs surface, which shows the enzyme digestion ability of the immobilized trypsin. The terminal groups of the SAMs structure can be further functionalized with biomolecules or antibodies to develop surface-base diagnostics, biosensors, or biomaterials.

Blood Platelets↗
PubMed2007

Stability of and inflammatory response to silicon coated with a fluoroalkyl self-assembled monolayer in the central nervous system.

A self-assembled monolayer (SAM) of fluoroalkyl silane (FAS) (CF(3)(CF(2))(5)(CH(2))(2)SiCl(3)) was deposited on the surface of silicon wafers, aiming to enhance its stability and to reduce the inflammatory response in the central nervous system. Following implantation of the FAS SAM coated silicon in rat brains, the FAS SAM coating failed to reduce the inflammatory response of silicon, because it could not prevent the corrosion of the underlying silicon. The corrosion was hindered for the initial 10 days by the FAS SAM coating, but there was nearly no difference when compared to the uncoated silicon when the implantation periods were extended to 28 and 90 days. The FAS SAM coating was completely removed within 28 and 90 days. Meanwhile, on all the extracted uncoated and FAS SAM coated silicon wafers, there were proteinaceous substances deposited on the surfaces, and the amount of the deposits increased with exposure time.

Animals↗
PubMed1995

Impaired alveolar macrophage function in smoke inhalation injury.

The high incidence of both bacterial pneumonia and the adult respiratory distress syndrome (ARDS) associated with smoke inhalation injury (SII) may result, at least in part, from smoke-induced injury to the alveolar macrophage (AM). Specifically, we hypothesized that AM antimicrobial function, ability to phagocytose apoptotic PMNs, and capacity to prevent apoptosis in PMNs are impaired by smoke. To test these hypotheses, AMs were harvested by bronchoalveolar lavage from sheep before and after the animal was exposed to cotton smoke. The two populations of AMs were incubated with Pseudomonas aeruginosa (PSA) in vitro. Normal AMs (NAMs) phagocytosed a mean of 99 +/- 11% of the PSA placed in their wells, whereas smoke-exposed AMs (SAMs) ingested only 60 +/- 8%. NAMs killed 80 +/- 8% of PSA ingested, whereas SAMs killed only 56 +/- 16% (P < 0.05). When sheep PMNs, allowed to undergo apoptosis, were incubated with the two AM populations, 66 +/- 3% of the NAMs and 40 +/- 6% of the SAMs demonstrated phagocytosis of these apoptotic PMNs (P < 0.05). Fresh sheep PMNs were incubated in unconditioned media, NAM and SAM-conditioned media, and followed over 48 hr for the development of apoptosis and maintenance of viability. The NAM-conditioned media markedly prevented apoptosis and augmented PMN survival relative to the unconditioned and SAM-conditioned media (P < 0.05). The poor antimicrobial function known to be characteristic of apoptotic PMNs, together with the directly impaired antimicrobial function of AMs, may contribute to the infectious complications of SII. If the PMNs recruited to the lung in SII are not properly supported by the AMs following smoke injury, large numbers may undergo apoptosis. If not properly disposed of by these SAMs, the apoptotic PMNs could eventually lyse, releasing tissue toxins, resulting in escalation of lung injury and leading to ARDS.

Animals↗