Kanji Koyama

A case of transient diabetes insipidus associated with poisoning by a herbicide containing glufosinate.

Background: The herbicide BASTA® (AgrEvo, Germany), containing glufosinate ammonium (20%) and an anionic surfactant, polyoxyethylene alkylether sulfate (33%), is widely used. In acute oral BASTA poisoning, patients develop a variety of clinical signs, including disturbed consciousness, convulsions, and apnea. These effects are suspected to be due to the effects of glufosinate on the central nervous system. Case Report: A 60-year-old man ingested 500 mL of BASTA herbicide in a suicide attempt. He developed not only unconsciousness, respiratory distress, and convulsions but also an increase in urine output (7885 mL/d), elevated serum sodium (167 mEq/L), elevated plasma osmolality (332 mOsm/kg), and a decrease in both urine osmolality (200 mOsm/kg) and urine specific gravity (1.003), which suggested the development of diabetes insipidus. The plasma level of antidiuretic hormone remained within the normal range (1.3 pg/mL), despite high plasma osmolality. The administration of desmopressin was successful in normalizing urine volume, specific gravity, and osmolality. Serum sodium corrected gradually within 48 hours. The possible mechanisms causing the diabetes insipidus are discussed.

Mechanisms of hypotension in iminoctadine poisoning: pharmacological analysis in rats

Iminoctadine, a fungicide used widely in fruit culture, causes hypotension in human acute oral poisoning. In an attempt to elucidate this mechanism, we investigated the effects of iminoctadine on the cardiovascular system of rats. In anesthetized rats, intravenously administered iminoctadine produced hypotension and tachycardia. In isolated right atria beating spontaneously in Krebs-Ringers solution, iminoctadine produced an increase in heart rate. It also produced a positive inotropic response in electrically driven left atria. These responses were partially diminished by atenolol, a beta 1-adrenoceptor antagonist, and also partially diminished to a similar degree in atria of reserpinized rats. Therefore, the positive inotropic and chronotropic effects of iminoctadine were partially mediated via the release of norepinephrine from sympathetic nerve terminals. In aortic ring segments, iminoctadine caused a rightward shift of the concentration-contractile response curve for phenylephrine but did not affect those for prostaglandin F2 alpha or KCl. Iminoctadine produced a potent vasodilation in aortic segments precontracted with phenylephrine. Removal of the aortic endothelium produced a rightward shift of the concentration-response curve for iminoctadine. When the aortic ring preparations were precontracted with prostaglandin F2 alpha or KCl, iminoctadine produced only slight vasodilation. Therefore, the vasodilation caused by iminoctadine is due mostly to its alpha 1-adrenoceptor antagonizing action, and partly to endothelium-dependent mechanisms our data suggest that the hypotension induced by iminoctadine is due to its vasodilator effects.

Dependence of the dose-response curve on incision site for intrathecal morphine

This study consisted of 204 patients of ASA class I or II. The patients were divided into 3 groups according to the sites of surgical incisions: Group I : the upper end of the incision was between Th6 and Th9 derrnatomes; Group II : between Th I0 and Th 12 dermatomes; and Group III : S dermatome. The types of surgery in each group were: Group I : gastrectomy and cholecystectomy (n = 106); Group II : hysterectomy (n =53); and Group III : TUR-P and TUR-Bt (n = 45).