CO-induced ring-slippage reactions of molybdenocene and tungstenocene carbonyl complexes. Electrochemical and elevated-pressure infrared evidence for an electron-transfer catalysis
Abstract Infrared studies at a CO pressure of 120 bar show (η 5 -C 5 H 5 ) 2 W(CO) to be completely resistant to an excess of CO in the absence of oxidants, but cyclovoltammetric measurements with this complex and with (η 3 -C 5 H 5 )(η 5 -C 5 H 5 )W(CO) 2 in THF solution at 0°C indicate that the ring-slipped dicarbonyl complex is catalytically generated by a one-electron oxidation of the tungstenocene monocarbonyl under CO at ambient pressure. Similar results are found for the reaction of (η 5 -C 5 H 5 ) 2 Mo(CO) with CO.
Electrophilic addition of CCl4 to a cyclopentadienyl ligand in the tungstenocene carbonyl [W(η5-C5H5)2(CO)] to give [W(η5-C5H5)(η4-C5H5-exo-CCl3)(CO) Cl]
Abstract Reaction of the tungstenocene monocarbonyl complex [W( η 5 -C 5 H 5 ) 2 (CO)] with an excess of CCL 4 at room temperature gives a 50% yield of an adduct which crystallizes in the monoclinic space group P 2 1 / n with a = 12.938(2) A , b = 6.724 (1) A , c = 16.226(3) A , β = 93.29(1)° . A single crystal X-ray diffraction study ( R F = 3.36%, R w = 3.32%) has established that the adduct is [W( η 5 -C 5 H 5 )( η 4 -C 5 H 5 -exo-CCl 3 )(CO)Cl], with a trichloromethyl group bonded exo to the saturated carbon of an η 4 -cyclopentadiene ligand and a dihedral angle between the plane containing this carbon and the mean plane of the butadiene residue of 35.3°. The 1 J C-H coupling constants of the four carbon atoms of the butadiene residue indicate an average hybridization of sp 1.9 . The first step in the addition is proposed to involve electron transfer from the metal to fragment the CCl 4 into the trichloromethyl radical and the chloride anion. Exo addition of the trichloromethyl radical to an η 5 -C 5 H 5 ligand would then be followed by trapping of the 16-electron cationic intermediate by the Cl − anion.
Neuronal uptake inhibitors, nisoxetine and fluoxetine on rat vascular contractions.
The importance of neuronal uptake processes in rat arteries and veins was compared using nisoxetine and fluoxetine, selective inhibitors for neuronal uptake of norepinephrine and serotonin, respectively. Nisoxetine (10(-7) - 10(-5) M) increased the sensitivity to exogenous norepinephrine in the portal and mesenteric veins (10-fold) and in the mesenteric artery (2.5-fold). Responses to field stimulation were also increased afternisoxetine in all three vessels. After nisoxetine, aortic responses to norepinephrine were unaltered and in all tissues, serotonin-induced contractions were reduced. Fluoxetine did not potentiate responses to norepinephrine or to field stimulation except in the mesenteric vein where sensitivity to norepinephrine was increased and the relaxation rate after field stimulation was prolonged. Although serotonin has been detected in blood vessels, fluoxetine did not increase vascular responses to serotonin. These studies suggest that rat mesenteric veins have a highly sensitive neuronal uptake mechanism of norepinephrine. Furthermore, these data provide indirect evidence against a functionally important serotonergic uptake process in rat blood vessels and suggest that neuronal uptake of serotonin does not exert a major role in terminating the vascular action of this biogenic amine.