Modulating the efficiency of Ru(II) luminescence via ion binding-induced conformational restriction of bipyridyl ligands.

Conformational restriction imposed upon Ru(bpy)32+ crown ether complexes by metal ion binding leads to enhanced luminescence.

Effects of isoproterenol treatment of isolated perfused rat hearts on myofibrillar phosphorylation and ATPase activity.

Perfusion of isolated rat hearts with isoproterenol resulted in increases in the level of protein-bound phosphate of the myofibrils. After perfusion of the hearts with 32P, followed by SDS-polyacrylamide gel electrophoresis of the purified myofibrils, four major 32P-containing protein bands were identified. Most of the increased 32P incorporation produced by isoproterenol was localized on the troponin I and myosin light chain bands, and, to lesser extent, on the M-protein band. ATPase activity was tested in the purified myofibrils. No changes in Ca2+ requirement for activation were found after isoproterenol perfusion. However, maximal ATPase activity was markedly reduced in the myofibrils obtained from isoproterenol-treated hearts. It would appear that the myofibrillar protein phosphorylation induced by isoproterenol perfusion results in a decrease in actomyosin ATPase activity.

Structure activity relationships of selected benzodiazepines as anticonvulsants to local anesthetics.

Diazepam, oxazepam, N-methyloxazepam, nitrazepam and N-desmethyldiazepam prevented seizures in mice produced by lidocaine, mepivacaine, and prilocaine, and in rats by lidocaine when administered IP five minutes before IP local anesthetic. ED50 values for antagonism of lidocaine tremors ranged from 0.7 to 5.2 mg/kg for N-methyloxazepam and N-desmethyldiazepam respectively in mice, and 0.08 to 0.54 mg/kg for N-desmethyldiazepam and oxazepam respectively, and for antagonism of prilocaine convulsions, 0.2 to 0.6 mg/kg for N-methyloxazepam and N-desmethyldiazepam respectively. All compounds tested terminated ongoing lidocaine tremors when injected IV in mice with ED50 values ranging from 1.7 x 10(-3) to 3.0 x 10(-3) mg/kg for N-desmethyldiazepam and N-methyloxazepam respectively, N-methyloxazepam was significantly more potent after IP injection than nitrazepam, oxazepam and N-desmethyldiazepam against lidocaine in mice and more potent than N-desmethyldiazepam and oxazepam against mepivacaine; it was more potent than diazepam and oxazepam against lidocaine in rats. N-desmethyldiazepam was most potent against lidocaine in rats and lest potent in mice. There were no significant differences in ED50 values preventing prilocaine convulsions in mice or after IV injection to terminate ongoing lidocaine seizures. The presence of a methyl and hydroxyl group at position N-1 and C-3 respectively (N-methyloxazepam) was apparently responsible for the higher potency relative to some of the other compounds in preventing lidocaine and mepivacaine tremors in mice and lidocaine tremors in rats. It is concluded however that the magnitudes of differences in potencies of the compounds in antagonizing local anesthetic seizures in mice and rats were not so large as to prefer any single agent over diazepam.

Relationship between theophylline-induced relaxation and excitation-contraction coupling in intestinal smooth muscle.

The effects of 1.0 to 10.0 mM theophylline on excitation-contraction (E-C) coupling in the taenia coli of the guinea-pig were observed with the sucrose-gap technique. Theophylline at all concentrations simultaneously inhibited spontaneous, calcium-dependent action potentials and muscle contractions. At the higher doses, theophylline depolarized the membrane in spontaneously active preparations. In the presence of high potassium (60 mM) the spike activity was blocked only by 10.0 mM theophylline. High potassium made the spikes more resistant to the drug than were those in spontaneously active preparations. The phasic and tonic components of the potassium-contracture were progressively decreased by increasing concentrations of theophylline and were completely blocked by the 10.0 mM concentration. The drug had no effect on the potassium-induced membrane depolarization observed during the potassium-contracture. On the basis of these observations, it is proposed that theophylline inhibits spike and contractile activity in taenia coli by interfering with the availability of calcium which has been postulated to be necessary for maintenance of these functions.