Data were presented showing that I1-imidazoline sites show a unique ligand specificity that differs markedly from that of any of the alpha 2-adrenergic subtypes or the I2-imidazoline sites labeled by [3H]idazoxan. On the other hand, the ligand specificity of I1-imidazoline sites is maintained across mammalian species (cow, rat, dog, and human) and between different tissues and cell types. I1-Imidazoline sites can be further distinguished from I2 sites because the latter, unlike I1 sites, were not present in RVLM membranes from bovine brain stem. Furthermore, I1-imidazoline sites were modulated by guanine nucleotides with a specificity appropriate for a receptor coupled to G-protein and were mainly localized to plasma membranes. I1-Imidazoline sites show a unique pattern of distribution between diverse tissues and cell types and appear to be a neuroepithelial marker as well as being present in secretory cells of the pancreatic islets. The widespread distribution of I1-imidazoline sites implies that the functional significance of this putative receptor may have been underestimated. The signaling pathway associated with the I1-imidazoline receptor remains to be fully elucidated, but is likely that activation of phospholipase A2 leading to release of arachidonic acid and subsequent generation of prostaglandins plays a major role.

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The fatigue behavior and fracture toughness of injection molded shortglass-fiber-reinforced poly(viny1 chloride) (sgfr-PVC) were investigated using the Crack Layer approach and fractography. Fatigue crack propagation (FCP) experiments in single-edge-notched (SEN) specimens were conducted concurrently with microscopic observations. Fracture was observed to propagate as a main crack surrounded by a layer of damage. The magnitude of damage was controlled by the content of glass fiber, which in turn controlled crack reduced acceleration and fracture toughness. FCP behavior was successfully described by the Crack Layer theory, which accounts for the damage associated with crack propagation. In absence of significant interfacial bonding, mechanical fiber/matrix interlocking provided the main resistance to crack propagation. Fiber-induced matrix deformation and fiber pull-out appeared to be the dominant energy absorbing mechanisms.

Fatigue crack propagation (FCP) of injection‐molded glass‐fiber‐reinforced poly(vinyl chloride) was examined as a function of fiber‐matrix adhesion (coupling) and fiber content at different load levels. Considering the entire FCP history, from crack initiation to critical propagation, it is shown that fatigue lifetime and fracture toughness of coupled composites increase with fiber weight fraction. Uncoupled material exhibits the highest fracture toughness at 10 wt% fiber, yet its fatigue life is considerably shorter. Damage analysis indicates that fiber debonding, pullout, and particularly fiber fracture seem to contribute to the higher fatigue lifetime noted in coupled composites. The Crack Layer Theory is employed to describe the observed FCP behavior. The effective enthalpy of damage parameterizes the resistance of the composite to FCP in terms of the observed mechanisms.

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