Tunable polymer lens.

A new type of solid-state variable focal length lens is described. It is based on shape changes in an elastomeric membrane driven by compression of a reservoir of a polymer gel. A novel fabrication process based on individual lens components allows for customization of lens power based on the desired application. The lens shape as a function of applied compressive strain is measured using direct surface profile measurements. The focal length of a solid state lens was reversibly changed by a factor of 1.9. Calculated back focal lengths of the lens were consistent with experimental measurements.

Optical properties of a bio-inspired gradient refractive index polymer lens.

The design, fabrication, and properties of one of a new class of gradient-index lenses are reported. The lens is an f/2.25 GRIN singlet based on a nanolayered polymer composite material, designed to correct for spherical aberration. The light gathering and focusing properties of the polymer lens are compared to a homogeneous BK7 glass singlet with a similar f-number. The modulation transfer function of the polymer GRIN lens exceeded that of the homogeneous glass lens at all spatial frequencies and was as much as 3 times better at 5 cyc/mm. The weight of the polymer lens was approximately an order of magnitude less than the homogeneous glass lens.

Phonon dispersion and nanomechanical properties of periodic 1D multilayer polymer films.

We report on the first systematic study of phonon propagation in nanostructured composite polymer multilayer films as a function of periodicity and composition using Brillouin light scattering and numerical simulations. The high sensitivity of phonon dispersion to structure and composition allows the probing of the mechanical properties down to the single-layer level. We observe a strikingly different dependence of the longitudinal and shear moduli on confinement effects in the polymer nanolayers. In addition, temperature dependent measurements of sound velocities reveal the presence of distinct glass transition temperatures, indicative of phonon localization in films with large layer thicknesses in agreement with theoretical predictions.

In vivo biocompatibility and biodegradation of poly(ethylene carbonate).

Biodegradation and biocompatibility of poly(ethylene carbonate) (PEC) was examined using an in vivo cage implant system. Exudate analysis showed that PEC and PEC degradation products were biocompatible and induced minimal inflammatory and wound healing responses. Adherent foreign body giant cells (FBGCs) caused pitting on the PEC surface, which led to extensive degradation over time. Data obtained from molecular weight and examination of film cross-sections in the scanning electron microscope (SEM) indicated that PEC underwent surface erosion with no change to the remaining bulk. Attenuated total reflectance infrared (ATR-FTIR) spectroscopy was used to characterize the chemical degradation. Superoxide anion released from inflammatory cells appeared to initiate an "unzipping" mechanism of degradation by deprotonation of PEC hydroxyl end groups. The resulting alkoxide ion participated in a concerted mechanism involving water and the carbonate carbonyl, leading to elimination of ethylene glycol. Carbonate ions decomposed further with release of carbon dioxide to regenerate alkoxide ion.

Biodegradation of polyether polyurethane inner insulation in bipolar pacemaker leads.

Several bipolar coaxial pacemaker leads, composed of an outer silicone rubber insulation and an inner polyether polyurethane (PEU) insulation, which were explanted due to clinical evidence of electrical dysfunction, were analyzed in this study. Optical microscopy (OM) and scanning electron microscopy (SEM) were used to determine the cause of failure. Attenuated total reflectance-Fourier transform infrared microscopy (ATR-FTIR) was used to analyze the PEU insulation for chemical degradation. In all leads, the silicone rubber outer insulation showed no signs of physical damage. Physical damage to the inner PEU insulation was the source of electrical dysfunction. Cracks through the PEU compromised the insulation between the inner and outer conductor coils in the lead. It was observed with SEM that these cracks originated on the outer surface of the inner insulation and progressed inward. ATR-FTIR analysis showed that the PEU had chemically degraded via oxidation of the ether soft segment. Furthermore, it was revealed that chemical degradation was more advanced on the outer surface of the PEU. It was hypothesized that hydrogen peroxide permeated through the outer silicone insulation and decomposed into hydroxyl radicals that caused the chemical degradation of PEU. The metal in the outer conductor coil catalyzed the decomposition of the hydrogen peroxide. Chemical degradation of the PEU could also have been catalyzed by metal ions created from the corrosion of the metal in the outer conductor coil by hydrogen peroxide. Physical damage probably occurred in regions of the leads that were subjected to a higher hydrogen peroxide concentration from inflammatory cells and high degrees and rates of strain due to intercorporeal movement, including, but not limited to, cardiac movement. Chemical degradation and physical damage probably had a synergistic affect on failure of the insulation, in that as chemical degradation proceeded, the polymer surface became brittle and more susceptible to physical damage. As physical damage proceeded, cracks propagated into the unaffected bulk, exposing it to oxidants.

Biocompatibility of poly(etherurethane urea) containing dehydroepiandrosterone.

Poly(etherurethane urea) (PEUU) elastomers, with their broad range of mechanical properties and high biocompatibility, are used clinically for medical applications. However, the possibility exists for the ether soft segment of PEUU to degrade in long-term uses. To retard degradation, antioxidants that scavenge reactive oxygen intermediates are added. In this study, we incorporated dehydroepiandrosterone (DHEA), which functions by the alternate mechanism of modulating or down-regulating adherent macrophage activity, to retard the biodegradation of PEUUs. Biocompatibility of PEUU samples containing 1% DHEA, 5% DHEA, and 5% vitamin E (alpha-tocopherol) by weight were studied in vivo and in vitro. The biocompatibility was initially evaluated by examination of the inflammatory cellular exudate. Compared to PEUU without additives and PEUU with 5% vitamin E, the addition of 5% DHEA to PEUU caused a decrease in the total leukocyte exudate concentration at 4 days. The addition of 5% DHEA also caused lower macrophage adhesion and FBGC formation compared to the other materials at 7 days. Despite these short-term effects, the biocompatibility at later time points (14, 21, and 70 days) was similar for all materials. Transmission infrared analysis of the materials revealed that more than 70% of the DHEA had leached out of the samples by 3 days implantation. Furthermore, through attenuated total reflectance Fourier transform analysis and scanning electron microscopy, it was determined that unlike vitamin E, DHEA did not enhance long-term PEUU biostability. The effect of DHEA on inflammatory cell activity appeared to be dose dependent, with improved biocompatibility in vivo for higher loading levels of DHEA, but the overall effect was limited owing to the rapid diffusion of the water-soluble DHEA from the PEUU.

In vivo biocompatibility and biostability of modified polyurethanes.

Modified segmented polyurethanes were examined for biostability and biocompatibility using an in vivo cage implant system for time intervals of 1, 2, 3, 5, and 10 weeks. Two types of materials were used: polyether polyurethanes and polycarbonate polyurethanes. Two unmodified polyether polyurethanes (PEUU A' and SPU-PRM), one PDMS endcapped polyether polyurethane (SPU-S), and two polycarbonate polyurethanes (SPU-PCU and SPU-C) were investigated in this study. Techniques used to characterize untreated materials were dynamic water contact angle, stress-strain analysis, and gel permeation chromatography. Cellular response was measured by exudate analysis and by macrophage and foreign body giant cell (FBGC) densities. Material characterization, postimplantation, was done by attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR) in order to quantify biodegradation and scanning electron microscopy (SEM) to qualitatively describe the cellular response and biodegradation. The exudate analysis showed that the acute and chronic inflammatory responses for all materials were similar. Lower FBGC densities and cell coverage on SPU-S were attributed to the hydrophobic surface provided by the PDMS endgroups. The polycarbonate polyurethanes did not show any significant differences in cell coverage or FBGC densities even though the macrophage densities were slightly lower compared to polyether polyurethanes. By 10 weeks, biodegradation in the case of PEUU A' and SPU-PRM was extensive as compared to SPU-S because the PDMS endcaps of SPU-S provided a shield against the oxygen radicals secreted by macrophages and FBGCs and lowered the rate of biodegradation. In the case of polycarbonate polyurethanes, the oxidative stability of the carbonate linkage lowered the rate of biodegradation tremendously as compared to the polyether polyurethanes (including SPU-S). The minor amount of biodegradation seen in polycarbonate polyurethanes at 10 weeks was attributed to hydrolysis of the carbonate linkage.

The effect of strain state on the biostability of a poly(etherurethane urea) elastomer.

The effect of deformation state on degradation of a PEUU without added stabilizers was examined in an oxidative environment that simulates the in vivo biodegradation of the polymer. Polymer tubes were stressed uniaxially and biaxially over glass mandrels and treated in 20% hydrogen peroxide/0.1 M cobalt chloride solution for 12 days at 37 degrees C. The amount of degradation was determined from the ATR-FTIR peak height of the amorphous aliphatic ether absorbance at 1110 cm-1. If a uniaxial stress was applied, degradation was inhibited and the amount of surface ether remaining after treatment increased linearly with strain. If the stress was biaxial, the amount of degradation was not reduced unless the strain was greater than 200%. Decreased degradation correlated with the amount of soft-segment orientation. The decreased degradation rate was attributed to compaction of the polyether phase by orientation, which resulted in lower permeability to oxidative agents, particularly oxygen. Macroscopic damage was confined to a thin peeling surface layer if the stress was uniaxial. In comparison, biaxially stressed PEUU ruptured.

Comparison of two antioxidants for poly(etherurethane urea) in an accelerated in vitro biodegradation system.

Vitamin E (+/-alpha-tocopherol) was recently investigated as an antioxidant for implanted poly(etherurethane urea) (PEUU) elastomers. In that work, vitamin E prevented chemical degradation of biaxially strained PEUU up to 5 weeks implantation, and prevented pitting and cracking of the PEUU surface for the duration of the 10-week cage implant study. The promising results of the in vivo studies motivated a detailed comparison of vitamin E with Santowhite, the standard antioxidant used in PEUU elastomers. To evaluate vitamin E and Santowhite as antioxidants in PEUU, an accelerated in vitro treatment system was used that mimics the in vivo degradation of PEUUs. Vitamin E was even more effective than Santowhite in preventing pitting and cracking to the biaxially strained PEUU elastomers. The inhibition of ether oxidation was greater with vitamin E than with Santowhite when compared by equivalent concentrations and molar concentrations, respectively. It is hypothesized that the increased effectiveness of vitamin E in this system, compared to Santowhite, is due to differences in antioxidant mechanism(s). Vitamin E is more efficient in preventing PEUU oxidation than Santowhite because its phenoxy radical is more stable and it can terminate more than one chain per vitamin E molecule.

Role of oxygen in biodegradation of poly(etherurethane urea) elastomers.

It is generally accepted that biodegradation of poly(etheruethane urea) (PEUU) involves oxidation of the polyether segments on the surface where leukocytes are adhered. The influence of dissolved oxygen, which is known to control oxidation of polymers in more traditional environments, was explored in this study. Specimens treated in vitro with hydrogen peroxide-cobalt chloride for 12 days exhibited a brittle, degraded surface layer about 10 microm thick. Attenuated total reflectance-Fourier transform infrared spectroscopy of the surface revealed that the ether absorbance at 1110 cm(-1) gradually decreased with in vitro treatment time to 30% of its initial value after 12 days. In contrast, 6 days in vitro followed by 6 days in air produced a decrease to 12% of the initial volume. Therefore, removing a specimen from the in vitro solution after 6 days and exposing it to air for the remainder of the 12 days actually resulted in more oxidation than leaving it in the in vitro solution for the entire 12 days. These results suggest that PEUU degrades by an autooxidation mechanism sustained by oxygen. By successfully modeling the depth of the surface degraded layer with a diffusion-reaction model, it was demonstrated that PEUU biodegradation is controlled by diffusion of oxygen into the polymer.

Vitamin E as an antioxidant for poly(etherurethane urea): in vivo studies. Student Research Award in the Doctoral Degree Candidate Category, Fifth World Biomaterials Congress (22nd Annual Meeting of the Society for Biomaterials), Toronto, Canada, May 29-June 2, 1996.

Poly(etherurethane) elastomers are useful materials in medical devices because of their mechanical properties and biocompatibility. However, it is necessary to stabilize these elastomers against the oxidation of their ether soft segments. Synthetic antioxidants such as Santowhite and Irganox are often satisfactory; however, particularly for biomedical applications, it was of interest to test the natural antioxidant vitamin E in poly(etherurethane urea) (PEUU) elastomers in vivo. The alpha-tocopherol form of vitamin E was added to PEUU at 5% by weight. Biaxially strained PEUU specimens with and without vitamin E were tested in vivo in the cage implant system. The influence of vitamin E on PEUU biostability was analyzed by attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy and scanning electron microscopic (SEM) characterization of the PEUU surface. ATR-FTIR results showed that vitamin E prevented chemical degradation of the PEUU surface up to 5 weeks implantation, and at 10 weeks 82% of the ether remained. In contrast, without an antioxidant, only 18% of the ether remained after 10 weeks. No surface pitting or cracking was observed by SEM on PEUU with vitamin E; PEUU without antioxidant ruptured owing to extensive pitting and cracking. It was concluded that the antioxidant properties of vitamin E prevented oxidation of strained PEUU elastomers in vivo. The influence of vitamin E on PEUU biocompatibility was characterized by exudate leukocyte counts, density of leukocytes adherent to the PEUU, and morphology of adherent leukocytes. These results indicated decreased leukocyte counts in the exudate and less active adherent cells on the PEUU with vitamin E compared to PEUU without antioxidant. A proposed cell-polymer feedback system demonstrates how vitamin E improves both biostability and biocompatibility of PEUU elastomers in vivo.

Complement-mediated leukocyte adhesion on poly(etherurethane ureas) under shear stress in vitro.

Blood-contacting biomaterials may activate the complement cascade, thus promoting leukocyte adhesion to the biomaterial surface. We hypothesize that the extent of complement activation is modulated by biomaterial formulation and the presence of fluid shear stress. To investigate this hypothesis, we tested base poly(etherurethane ureas) formulated with or without Santowhite antioxidant, a nucleophilic additive. We found that adherent leukocyte densities decreased with increasing shear stress. Moreover, leukocyte adhesion was decreased significantly further by Santowhite additive under shear stress but not under static conditions. Monocytes showed a higher propensity for adhesion than did neutrophils under shear and static conditions. Under static conditions, adherent cells on the Santowhite-containing polyurethane had a slightly more activated morphology than those on the base polyurethane. Cell adhesion under shear stress was significantly decreased when C3 or fibronectin was depleted from the suspension medium. Santowhite additive increased Factor B adsorption to the test surface while shear stress increased Factor H adsorption. The combination of Santowhite additive and shear stress increased the adsorption of both Factor B and Factor H and the serum protein S-terminal complement complex levels, but it did not further increase the state of activation of adherent cells. We conclude that leukocyte adhesion on poly(etherurethane urea) surfaces is sensitive to the levels of shear stress and that both C3 and fibronectin are required to maintain adhesion in the presence of shear stress. The low state of cellular activation and increased Factor H adsorption may explain the decreased adherent leukocyte density on the Santowhite-containing polyurethane.

Role for interleukin-4 in foreign-body giant cell formation on a poly(etherurethane urea) in vivo.

Interleukin-4 (IL-4) was previously shown to induce extensive macrophage fusion to form foreign-body giant cells (FBGCs) in vitro. In the present study, our goal was to extend these findings to an in vivo test environment on biomaterials. The subcutaneous cage-implant system was modified for mice to elucidate IL-4 participation in mediating FBGC formation in vivo. Exudate leukocyte concentrations from cages containing poly(etherurethane urea) (PEUU A') and empty cage controls indicated a similar inflammatory response that turned toward resolution by 14 days postimplantation, thus confirming the applicability of the cage-implant system in mice. FBGC kinetic analysis showed that the formation of mouse FBGCs occurs through the fusion of adherent macrophages at a constant rate up to 14 days of implantation. Purified goat anti-mouse IL-4 neutralizing antibody (IL4Ab) or normal goat nonspecific control IgG (gtIgG) at various concentrations, or recombinant murine IL-4 (muIL4) was injected into the implanted cages containing PEUU A' every 2 days for 7 days. The injection of IL4Ab significantly decreased the FBGC density on PEUU A' cage-implanted in mice, when compared with the nonspecific IgG or PBS injection controls. Conversely, the FBGC density was significantly increased by the injection of muIL4 when compared with nonspecific IgG and PBS injection controls. Adherent macrophage density, FBGC morphology, FBGC average size, and size distribution were not significantly different among IL4Ab, nonspecific control gtIgG, muIL4, and PBS control groups. Our data suggest that IL-4 participates in FBGC formation on biomaterials in vivo.

Oxidative biodegradation mechanisms of biaxially strained poly(etherurethane urea) elastomers.

As part of ongoing studies in polyurethane biostability and biodegradation, we have investigated an in vitro system to test strained poly(etherurethane urea) (PEUU). Recently, we utilized this system to reproduce in vivo stress cracking in strained Pellethane. In this study, strained PEUU was tested to determine whether it degrades through a common mechanism with Pellethane and to further examine the steps involved in this degradation. Biaxially strained PEUU elastomers were treated with an alpha 2-macroglobulin (alpha 2-Mac) protein solution followed by an oxidative H2O2/CoCl2 treatment. Characterization of the strained PEUU specimens was performed with attenuated total reflectance-Fourier transform infrared spectroscopy, scanning electron microscopy (SEM), electron spectroscopy for chemical analysis, and contact angle analysis. The results from these characterization techniques provide conclusive evidence that biodegradation of PEUU and Pellethane occurs through a common mechanism. Chemical changes to the PEUU include cleavage of the polyether soft segments and urethane linkages, leaving the hard segment domains unaffected. SEM analysis shows that this chain cleavage leads to the development of severe pitting and cracking of the PEUU surface. In addition, the in vitro degradation accurately reproduces the in vivo degradation chemically and physically. This result verifies that the primary species responsible for biodegradation of PEUUs, in vivo, are hydroxyl and/or hydroperoxide radicals. alpha 2-Mac pretreatment increases the rate of degradation compared to direct treatment in H2O2/CoCl2. As the PEUU soft segment chains are cleaved, the degradation products are extracted into the treatment solution or environment. Finally, a new biodegradation mechanism of PEUUs is presented that involves crosslinking of the polyether soft segments.

Theoretical analysis of in vivo macrophage adhesion and foreign body giant cell formation on strained poly(etherurethane urea) elastomers.

Quantitative description of foreign body giant cell (FBGC) formation on poly(etherurethane urea) (PEUU) surfaces as a function of time can conceivably predict the effects of polymer characteristics on cellular responses in vivo. In the present study, the formation of FBGCs on strained and unstrained PEUUs was quantified with two parameters: the density of adherent macrophages present initially that participate in FBGC formation (d(o)) and the rate constant for cell fusion (k); both kinetic parameters were used to calculate the time-dependent FBGC density (dfc). Relationships were sought between results of the cellular analysis and the extent of environmental stress cracking (ESC), as characterized by scanning electron microscopy. Surface degradation was semiquantified with percent light transmittance. The materials used were: base PEUU, base PEUU with 1% Santowhite antioxidant powder, base PEUU with 5% Methacrol 2138F antifume agent, and base PEUU with both 1% Santowhite and 5% Methacrol 2138F. A comparison of unstrained base PEUU with base PEUU strained to 400% elongation indicated that the rate of cell fusion, but not d(o) and dfc, increased in the presence of strain. In all strained samples, additives that strongly affected the ESC also influenced FBGC kinetic parameters. Strained PEUU containing Santowhite had the lowest d(o), the slowest rate of cell fusion, and lowest dfc, and the least incidence of ESC. The results suggest that the incidence of ESC in PEUU was decreased in the presence of Santowhite, which also lowered the number of adherent macrophages participating in FBGC formation, the rate of FBGC formation and the subsequent FBGC density. These studies also indicate that strain in PEUUs does not directly modulate the adherent macrophage and FBGC density. Further studies are necessary to delineate the relationship between PEUU strain and adherent macrophage and FBGC activation, which leads to the exocytosis of degrading agents and the observed incidence of biodegradation.

Creep of a poly(etherurethane urea) in an oxidative environment.

The creep behavior of a PEUU without added stabilizers was examined in H2O2/CoCl2, an environment that simulates the biodegradation of this polymer. Creep in the control environments, air, water, and H2O2, was logarithmic with time as is characteristic of primary or viscoelastic creep. At short times, creep in H2O2/CoCl2 followed the same time dependency as creep in H2O2; however, at longer times an acceleration in the creep rate was observed. Creep in H2O2/CoCl2 was satisfactorily described by addition of a linear time term to the creep equation with an induction time, ti. The induction time was extended by stress-induced crystallization of the soft segments, but was reduced by an increase in H2O2 concentration. Oxidative degradation of the PEUU soft segments was detected by infrared and GPC analysis at times less than ti. This led to the speculation that an initial "precursor" layer was created at the surface by chain cleavage. Microcracking in a subsequent stage was postulated to be responsible for the observed effect on the creep behavior.

Characterization of extractable species from poly(etherurethane urea) (PEUU) elastomers.

Methanol extracts of four poly(etherurethane urea) (PEUU) materials were analyzed using Gel Permeation Chromatography (GPC). The additives in the materials were Santowhite powder at 1 wt% and Methacrol 2138 F at 5 wt% loading levels. One-to-two wt% of the original PEUU films was extractable with methanol. The extractables consisted of a low molecular weight (Mw) PEUU polymer, an MDI-rich oligomer, the additives Santowhite (SW) powder and Methacrol 2138 F, and aniline. The low Mw PEUU polymer had a Mw of 12,000 relative to polystyrene, and the MDI-rich oligomer had a Mw of 1000 relative to polystyrene. Quantitation of all extracted species was achieved using GPC; the use of dual-detectors on the GPC made it possible to determine the soft-to-hard composition of the PEUU extracts as a function of molecular weight.

Theoretical analysis of in vivo macrophage adhesion and foreign body giant cell formation on polydimethylsiloxane, low density polyethylene, and polyetherurethanes.

Quantitative description of foreign body giant cell (FBGC) formation on implanted polymer surfaces as a function of time can conceivably correlate cell adhesion with polymer properties and possibly predict the behavior of the polymer in vivo. In the present study, the formation of FBGCs on various biomedical polymers was quantified by two parameters: the density of adherent macrophages present initially that participate in FBGC formation (d0) and the rate constant for cell fusion (k); both kinetic parameters were used to calculate the time-dependent FBGC density (dfc). The materials used were: three Pellethane poly(etherurethanes) (PEUs) varying in weight percent of hard segment, one poly(etherurethane urea) (PEUU), and NHLBI-DTB primary reference materials: low density polyethylene (LDPE), silica-free polydimethylsiloxane (PDMS). The results indicated that up to 5 weeks of implantation, FBGCs were formed from the fusion of one population of adherent macrophages present by 3 days post-implantation. Furthermore, only a small fraction (< 8%) of this initial adherent macrophage population participated in FBGC formation. Based on the results of previous studies and the current study, it was concluded that increase in PEU hard segment weight percent, surface hardness and hydrophobicity increased total protein adsorption and effectively increased d0 and dfc. No further correlations between the material properties of all polymers and the cell kinetics can be made at this time. However, this study demonstrated that macrophage adhesion and FBGC formation can be quantified with the cell fusion model, and are modulated by various polymer properties.

Relationship between arterial thrombosis and neutralization of a polyethylene ionomer.

The influence of three levels of sodium neutralization of an ethylene/methacrylic acid copolymer on in vivo blood compatibility was studied in a canine arterial model. Effects due to sample fabrication methods (thermal pressing versus solution casting) were also monitored. Sodium content, sodium release, hydrogen dissociation, and localization of anionic groups were noted. Polymer surface energy, surface morphology, water uptake, and thermal properties were characterized. Material characterization and in vivo implantation disclose the following: 1) Thermal pressing generated oxidation degradation products that decreased in vivo blood compatibility. Solution-cast samples adhered and activated fewer blood elements. 2) Platelets and leukocytes were sensitive to differences in shear rate in the carotid and femoral arteries, with the femoral site tending toward higher shear, more platelet deposition and fewer leukocytes. 3) The surface properties of the polyethylene control, 0% Na, and 50% Na samples tended to be similar. These properties were different from the 100% Na sample. The 100% Na ionomer was more hydrophilic, had a higher polar component for its surface energy, and was unique in exhibiting discrete ionic clusters 1-10 microns in diameter on its surface. 4) These differences were manifested in vivo by platelet activation and thrombus development on the polyethylene, 0% Na, and 50% Na implants, while the 100% Na implant surfaces were predominantly covered by singly adherent, unactivated platelets. 5) It is proposed that the improvement in biocompatibility for the 100% Na ionomer is due to the cluster development in the neutralized methacrylic component and that either directly, or through appropriate protein adsorption and/or conformational adjustment to the cluster regions, platelets are not activated and do not initiate the coagulation mechanism.

Human plasma alpha 2-macroglobulin promotes in vitro oxidative stress cracking of Pellethane 2363-80A: in vivo and in vitro correlations.

It is hypothesized in this study that the phenomenon of environmental stress cracking (ESC) in polyetherurethane is caused by a synergistic action of biological components in the body fluids, oxidative agents, and stress. An in vitro system is designed to mimic the in vivo system; human plasma contains certain biological components that can act as a stress cracking promoter, while H2O2 (Co) solution provides an oxidative reaction comparable to that observed in the respiratory burst of adherent macrophages and foreign-body giant cells. It is demonstrated that the phenomenon of in vivo stress cracking in Pellethane 2363-80A is duplicated by an in vitro system that involves a pretreatment of prestressed specimens with human plasma at 37 degrees C for 7 days followed by oxidation in 10% hydrogen peroxide with 0.10M cobalt chloride at 50 degrees C for 10 days. The pretreatment with plasma has a synergistic effect with the oxidation by H2O2 (Co) treatment to produce ESC. A plasma component responsible for promoting stress cracking in Pellethane polyurethane is identified to be alpha 2-macroglobulin (alpha 2M).