Syntheses of chromium pentacarbonyl derivatives of arsenic(V) and antimony(V). contrasting chemical reactivity with organic halogen derivatives.

We have synthesized a new series of chromium-group 15 dihydride and hydride complexes [H(2)As(Cr(CO)(5))(2)](-) (1) and [HE(Cr(CO)(5))(3)](2)(-) (E = As, 2a; E = Sb, 2b), which represent the first examples of group 6 complexes containing E-H fragments. The contrasting chemical reactivity of 2a and 2b with organic halogen derivatives is demonstrated. The reaction of 2a with RBr (R = PhCH(2), HC triple bond CCH(2)) produces the RX addition products [(R)(Br)As(Cr(CO)(5))(2)](-) (R = PhCH(2), 3; R = C(3)H(3), 4), while the treatment of 2b with RX (RX = PhCH(2)Br or HC triple bond CCH(2)Br, CH(3)(CH(2))(5)C(O)Cl) forms the halo-substituted complexes [XSb(Cr(CO)(5))(3)](2-) (X = Br, 5; X = Cl, 6). Moreover, the dihaloantimony complexes [XX'Sb(Cr(CO)(5))(2)](-) can be obtained from the reaction of 2b with the appropriate organic halides. In this study, a series of organoarsenic and antimony chromium carbonyl complexes have been synthesized and structurally characterized and the role of the main group on the formation of the resultant complexes is also discussed.

Terminal cardiac electrical activity in adults who die without apparent cardiac disease.

Prolonged electrocardiographic (Holter) recording was performed to analyze terminal electrical events in 23 hospitalized adults who died without apparent cardiac disease. Most patients showed a gradual slowing of heart rate with shifting of cardiac pacemaker downward from the sinus node or atria to the atrioventricular junction and ventricles, resulting in cardiac asystole. Dominant bradyarrhythmia was more common than ventricular tachyarrhythmia (83 vs 17%). Agonal ST-segment elevation was not uncommon (26%). These terminal electrical events became manifest from 1 to 450 minutes (mean 62) before cessation of cardiac electrical activity. Forty-eight percent of the patients continued to show deteriorating sinus or atrial activity up to the last moment. The mechanism of bradycardiac asystole in patients with no apparent cardiac disease may be attributed to generalized anoxic and toxic depression of the sinus node and subsidiary pacemakers, together with neurogenic suppression of these structures.