The Effect of ω-Substituted Acceptors in 4-Dimethylamino-trans-Styrenes on the Polarity in the Ground and Excited Singlet State
ABSTRACT The electric dipole moment in the ground (μg) and in the first excited singlet state (μe) of co-substituted acceptors in 4-dimethylamino-trans-styrenes (Z = P(S)Ph2 , P(O)Ph2 , SO2CH3 ) were determined by solvatochromic and thermochromic methods. The obtained values of μe and μg and the values for Z = CN and Z = NO 2 known from the literature [2] fulfill the linear relation between the dipole moments (μe or μg and the Hammett constants σp of the substituents. On pincreasing the electron-acceptor power of Z, μe grows faster than μg
Molecular Relaxation Processes During Film Formation
Traditionally many coatings and polymer chemists and physicists who follow the increase in viscosity of coating materials as changes occur during drying, use only one-point or steady-state methods for monitoring the ‘cure’. Insight can be gained by determining a flow curve at various shear rates for coating binders and formulations. However, as a proper formulated coating begins the process of changing from a liquid which generally flows readily to a solid coating, all are viscoelastic in nature. Such is the case with industrial, architectural or special protective coatings manufactured by the paint industry and printing inks, adhesives, paper coatings or other similar types. Only a few materials of commercial importance are not viscoelastic in normal usage, e.g. some Newtonian oils. Since this is the case, it is important for scientists not only to measure the viscosity of a coating but also to know something about the elastic response of the material.
Mechanism of the depressor response to dopamine in the rat treated with phenoxybenzamine.
Alterations of hypotensive responses to dopamine by antagonists were characterized in alpha-blocked, anaesthetized rats. Responses were not affected by d-propranolol (0.1 mg/kg) whereas d,1-propranolol (0.1 mg/kg) or haloperidol (1.0 mg/kg) attenuated them; higher doses of inhibitors (1.0 mg/kg; 5.0 mg/kg, respectively) failed to produce a higher inhibition, but combinations of low doses abolished the depressor responses. In adrenalectomized rats, hypotensive responses decreased; haloperidol always attenuated the responses while d,1-propranolol became ineffective. Dopamine produced an enhancement of plasma adrenaline and noradrenaline levels, which was decreased by d,1-propranolol and increased by haloperidol. The data suggest that in rats the depressor component of dopamine is due to activation of both dopaminergic and beta-adrenoceptors. The beta component appears to be due to the release of adrenaline. The results also support the concept of the existence in sympathetic nerve endings and adrenal glands of stimulatory beta-adrenergic and inhibitory dopaminergic prejunctional receptors.