Rubber and plastics hoses. Assessment of ozone resistance under dynamic conditions

Abstract The need for dynamic testing conditions, such as mild flexing, to study the attack of ozone on elastomeric vulcanizates, has become increasingly apparent. Many rubber goods, such as belts, tire sidewalls, and hose, are subjected to intermittent or continuously fluctuating strains in service and to evaluate their ozone resistance under constant stress or strain conditions is unrealistic and often leads to entirely erroneous conclusions. For example, it is well known that under static strain a vulcanizate's ozone resistance is enhanced by compounding with a wax which migrates to its surface and forms a protective film. However, numerous investigators have reported that when a wax film is continuously ruptured by dynamic testing, the vulcanizate is even more vulnerable to ozone attack than if no wax were present. Other surface films also may act detrimentally under dynamic conditions. One such film may form under static exposure by the migration of antiozonants to the surface of a sample where they or their ozone reaction products provide a shield against ozone. Also, diene elastomers, even when not under stress, react with ozone without cracking and it has been postulated that the thin films formed as a result of this reaction are less extensible and consequently more subject to rupture on flexing than the unreacted rubber beneath them. It may well be found that the resistance of any surface barrier to dynamic stresses is the limiting factor for many products in service. Consequently, techniques for testing under dynamic conditions are needed at least to supplement testing under constant stress or strain in ozone. Ozone exposure under dynamic conditions may prove to have analytical advantages over the static method. First, because dynamic tests accelerate ozone attack over that obtained statically even though no increased strain is impressed. This permits the more ozone resistant elastomers to be tested at lower concentrations of ozone than would be possible statically. By testing in more dilute ozone, the correlation between results obtained under atmospheric exposure and the ozone cabinet should be better. Also, it seems likely that compounding ingredients which improve ozone resistance under dynamic conditions should provide improvement under static conditions as well, even though the converse is not necessarily true.

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Ozone Resistance of Natural Rubber Vulcanizates. Part II. Influence of Fillers and Waxes

Rubber Chemistry and Technology ◽

10.5254/1.3542349 ◽

1958 ◽

Vol 31 (4) ◽

pp. 874-881 ◽

Cited By ~ 1

Author(s):

B. I. C. F. van Pul

Keyword(s):

Natural Rubber ◽

Side Chains ◽

Melting Points ◽

Dynamic Conditions ◽

Static Conditions ◽

Natural Rubber Vulcanizates ◽

Ozone Resistance

Abstract Commerical waxes whose melting points, refractive indexes and numbers of side chains are within the ranges described seem likely to give good ozone protection under static conditions. All waxes lead to worse cracking under dynamic conditions than if none had been included and it is clearly better to use no wax if the rubber is likely to be submitted to intermittent stretching.

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Rubber and plastic hoses. Assessment of ozone resistance under dynamic conditions

10.3403/00930321u ◽

2015 ◽

Keyword(s):

Dynamic Conditions ◽

Ozone Resistance

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Ozone Resistance of Natural Rubber Vulcanizates. Part I. Apparatus for Exposure at Low Ozone Concentration

Rubber Chemistry and Technology ◽

10.5254/1.3542348 ◽

1958 ◽

Vol 31 (4) ◽

pp. 866-873

Author(s):

B. I. C. F. van Pul

Keyword(s):

Natural Rubber ◽

Ozone Concentration ◽

Cracking Resistance ◽

Dynamic Conditions ◽

Ozone Concentrations ◽

Natural Rubber Vulcanizates ◽

Ozone Resistance

Abstract An apparatus is described for evaluating the cracking resistance of rubber specimens exposed under static or dynamic conditions to ozone concentrations between 5 and 50×10−8 ml/ml of air. Ozone concentration is kept constant automatically however much is destroyed at the walls of the cabinet or at the surfaces of the rubber testpieces. Temperature can be regulated between 20° and 100° C.

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Neutrophil Derived Cathepsin G Induces Potentially Thrombogenic Changes in Human Endothelial Cells: a Scanning Electron Microscopy Study in Static and Dynamic Conditions

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648825 ◽

1994 ◽

Vol 72 (01) ◽

pp. 140-145 ◽

Cited By ~ 13

Author(s):

Valeri Kolpakov ◽

Maria Cristina D'Adamo ◽

Lorena Salvatore ◽

Concetta Amore ◽

Alexander Mironov ◽

...

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Extracellular Matrix ◽

Endothelial Cells ◽

Thrombus Formation ◽

Cathepsin G ◽

Arterial Segment ◽

Dynamic Conditions ◽

Activated Neutrophils ◽

Scanning Electron

SummaryActivated neutrophils may promote thrombus formation by releasing proteases which may activate platelets, impair the fibrinolytic balance and injure the endothelial monolayer.We have investigated the morphological correlates of damage induced by activated neutrophils on the vascular wall, in particular the vascular injury induced by released cathepsin G in both static and dynamic conditions.Human umbilical vein endothelial cells were studied both in a cell culture system and in a model of perfused umbilical veins. At scanning electron microscopy, progressive alterations of the cell monolayer resulted in cell contraction, disruption of the intercellular contacts, formation of gaps and cell detachment.Contraction was associated with shape change of the endothelial cells, that appeared star-like, while the underlying extracellular matrix, a potentially thrombogenic surface, was exposed. Comparable cellular response was observed in an “in vivo” model of perfused rat arterial segment. Interestingly, cathepsin G was active at lower concentrations in perfused vessels than in culture systems. Restoration of blood flow in the arterial segment previously damaged by cathepsin G caused adhesion and spreading of platelets on the surface of the exposed extracellular matrix. The subsequent deposition of a fibrin network among adherent platelets, could be at least partially ascribed to the inhibition by cathepsin G of the vascular fibrinolytic potential.This study supports the suggestion that the release of cathepsin G by activated neutrophils, f.i. during inflammation, may contribute to thrombus formation by inducing extensive vascular damage.

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