Syndrome of endemic arsenism and fluorosis. A clinical study.

Sixty-five patients in Xinjiang with syndrome of endemic arsenism and fluorosis (SEAF) were investigated clinically from March 1982 to August 1989. SEAF is a kind of chronic syndrome resulting from the combined, harmful effects of two trace elements, arsenic and fluorine. Peripheral neuritis and cardiovascular changes were observed in this syndrome more often than in simple arsenism or simple fluorosis. The excessive quantities of these two trace elements in blood might have a synergic, harmful effect on the nervous and circulatory systems. No definite conclusion could be reached with regard to the morbidity of skin and visceral tumors in this series. The incidence of associated skin cancer was found to be 7.7% and an associated Grade II squamous cell carcinoma of the esophagus was encountered in one patient.

Electrophysiological effects of cimetidine on rabbit myocardium.

Effects of cimetidine (Cim) were studied electrophysiologically on fast action potential (AP) in rabbit papillary muscle and slow AP in pacemaker cell of rabbit sinoatrial node (SAN) as well as on atrioventricular (A-V) conduction in anesthetized rabbit. Cim (0.01, 0.1, 1, and 2 mmol.L-1) induced prolongations of AP duration (APD) and effective refractory period (ERP), slowing down of the maximal rate of rise of phase 0 (Vmax) and of the slope of phase 4 depolarization (SP4), and a decrease of AP amplitude (APA) in concentration-dependent manners. Cim (100 mg.kg-1 iv) prolonged the A-V conduction. The results suggest that Cim, like quinidine, shows a membrane stabilizing effect, which may be the electrophysiological basis of the anti-arrhythmic effect of Cim.

Tetrandrine, a Ca++ antagonist: effects and mechanisms of action in vascular smooth muscle cells.

Tetrandrine, an alkaloid extracted from the Chinese medicinal herb Radix stephania tetrandrae, has traditionally been used to treat hypertension. In the present study, the effect of tetrandrine on vascular smooth muscle was investigated by using the rat tail artery as a model of a resistance vessel. Tetrandrine relaxes the tension in tail artery helical strips produced by depolarization with 60 mM KCl. Further studies show that tetrandrine inhibits the KCl-induced intracellular Ca++ increase and L-type voltage-dependent Ca++ channel currents, suggesting that tetrandrine relaxes the vessel via inhibition of Ca++ influx through Ca++ channels. Tetrandrine also inhibits norepinephrine (NE)-induced vasocontraction in the presence of extracellular Ca++. It does not, however, inhibit NE-induced vasocontraction in the absence of extracellular Ca++. Tetrandrine also inhibits the NE-induced intracellular Ca++ increase in the presence of extracellular Ca++ and has no effect on the NE-induced intracellular Ca++ increase in the absence of extracellular Ca++. This suggests that tetrandrine also blocks NE-induced Ca++ influx but not NE-induced Ca++ release from the intracellular Ca++ stores. Furthermore, tetrandrine inhibits thapsigargin-induced intracellular Ca++ concentration increase, suggesting that, in addition to blocking Ca++ influx, tetrandrine also may interfere with the interaction between thapsigargin and Ca++ adenosine triphosphatase.