Inhibitory effects of cadmium on peripheral blood mononuclear cell proliferation and cytokine release are reversed by zinc and selenium salts.

Zinc (Zn) and selenium (Se) exert regulatory activities on immune functions, while cadmium (Cd) is an immunotoxic agent. The object of this study was to detect effects of 10(-4), 10(-5), and 10(-6) M Cd sulphate, Zn sulphate, and sodium selenite, and their combinations on human peripheral blood mononuclear cell (PBMC) proliferation and IFN-gamma and TNF-alpha production. Only 10(-5) M Zn sulphate significantly enhanced spontaneous PBMC proliferation, which was unaffected by the other salts. At 10(-4) and 10(-5) M, Cd sulphate exerted a dose-response inhibitory action on phytohemagglutinin- (PHA-) stimulated PBMC proliferation and cytokine release, while 10(-4) M and 10(-5) M Zn sulphate and 10(-5) M sodium selenite induced a stimulatory effect on both proliferation and cytokine release; 10(-4) M sodium selenite enhanced only the PBMC proliferation; at 10(-6) M, none of the salts changed the PHA-stimulated immune activity. Moreover, 10(-4) and 10(-5) M Zn and 10(-5) M Se strongly upregulated IFN-gamma (a Th1 cytokine) release, even in presence of 10(-5) M Cd, and reduced the inhibitory effects of Cd on PBMC proliferation and TNF-alpha release. This study confirms that Zn and Se both strongly enhance cytokine release induced by mitogenic stimulation, showing also that Zn acts with a broader range of concentrations than Se. This suggests that dietary excess of Se may not have beneficial effects.

Spinal 2-chloroprocaine: a comparison with lidocaine in volunteers.

UNLABELLED: Subarachnoid lidocaine has been the anesthetic of choice for outpatient spinal anesthesia. However, its use is associated with transient neurologic symptoms (TNS). Preservative-free formulations of 2-chloroprocaine are now available and may compare favorably with lidocaine for spinal anesthesia. In this double-blinded, randomized, crossover study, we compared spinal chloroprocaine and lidocaine in 8 volunteers, each receiving 2 spinal anesthetics: 1 with 40 mg 2% lidocaine and the other with 40 mg 2% preservative-free 2-chloroprocaine. Pinprick anesthesia, tolerance to transcutaneous electrical stimulation and thigh tourniquet, motor strength, and a simulated discharge pathway were assessed. Chloroprocaine produced anesthetic efficacy similar to lidocaine, including peak block height (T8 [T5-11] versus T8 [T6-12], P = 0.8183) and tourniquet tolerance (46 +/- 6 min versus 38 +/- 24 min, P = 0.4897). Chloroprocaine anesthesia resulted in faster resolution of sensory (103 +/- 13 min versus 126 +/- 16 min, P = 0.0045) and more rapid attainment of simulated discharge criteria (104 +/- 12 min versus 134 +/- 14 min, P = 0.0007). Lidocaine was associated with mild to moderate TNS in 7 of 8 subjects; no subject complained of TNS with chloroprocaine (P = 0.0004). We conclude that the anesthetic profile of chloroprocaine compares favorably with lidocaine. Reliable sensory and motor blockade with predictable duration and minimal side effects make chloroprocaine an attractive choice for outpatient spinal anesthesia. IMPLICATIONS: The spinal anesthetic profile of chloroprocaine (40 mg) compares favorably with the same dose of spinal lidocaine. Reliable sensory and motor blockade with predictable duration and minimal side effects and without signs of transient neurological symptoms make chloroprocaine an attractive choice for outpatient spinal anesthesia.