Effect Of Single Intravenous Administration Research Articles

Clozapine-Induced Acute Hyperglycemia Is Accompanied with Elevated Serum Concentrations of Adrenaline and Glucagon in Rats.

Clozapine, an atypical antipsychotic agent, has been reported to cause acute hyperglycemia. However, the mechanism of clozapine-induced rapidly developing hyperglycemia is not well elucidated. To clarify the mechanism underlying clozapine-induced acute hyperglycemia, we investigated the effects of single intravenous administration of clozapine on the serum concentrations of glucose and several endogenous substances in rats. Male Wistar rats received an intravenous injection of saline (control) or clozapine 2.5, 5, 10 mg/kg. Blood samples were obtained periodically after clozapine administration to determine the serum concentrations of glucose, adrenaline, glucagon, insulin, corticosterone, and clozapine. The serum concentrations of glucose, adrenaline, and glucagon increased dose-dependently after the administration of clozapine at 2.5-10 mg/kg, and reached maxima at 5 mg/kg of clozapine. The serum concentration of corticosterone increased after the administration of clozapine, but no significant variation was observed with the dosage of clozapine. The concentration of serum insulin increased in a dose-dependent manner after clozapine administration. In conclusion, a single administration of clozapine increased the serum concentration of glucose in rats, and adrenaline and/or glucagon would be associated with clozapine-induced acute hyperglycemia.

Effect of single intravenous administration of batroxobin on erythrocyte aggregability in patients with acute-stage cerebral infarction

(Received 27.09.1994; accepted 24.11.1994) We examined the effect of defibrinogenation with batroxobin on the erythrocyte aggregability (RBC-A) in 16 patients with cerebral infarction during the acute phase (less than 72 hours after onset). Eight patients received a single intravenous administration of 10 units of batroxobin (BU), while the other 8 patients received 5 BU. The RBC-A was examined using the whole-blood erythrocyte aggregometer developed by us (Am. J. Physiol. 251, H1205H1210, 1986) with concomitant measurement of the hematocrit, albumin:globulin ratio and concentration of fibrinogen. The RBC-A values before, and at 1,2, and 7 days after 10 BU administration were 0.154±0.017/s, 0.117 ±0.029/s (76% of the value before the administration, P<O.Ol), 0.105±0.029/s (68%, P<O.Ol), and 0.124±0.015/s (81 %, P<O.Ol), respectively. The fibrinogen concentrations before, and at 1,2, and 7 days after the batroxobin were 364±81 mg/dl, 150±35 mg/dl (41 %, P<O.Ol), 129±35 mg/dl (35%, P<O.01), and 211±42 mg/dl (58%, P<O.Ol), respectively; On the other hand, the RBC-A values before, and at 1, 2, and 7 days after 5 BU administration were 0.143±0.021/s, 0.131±0.036/s, 0.130±0.028/s, and 0.141±0.029/s, respectively. The fibrinogen concentrations before, and at 1,2, and 7 days after the batroxobin were 318±57 mg/dl, 255±60 mg/dl (80%, P<O.Ol), 259±68 mg/dl (81 %, P<O.Ol), and 319±87 mg/dl, respectively. We conClude that a single intravenous administration of batroxobin at 10 BU reduced the RBC-A in patients with cerebral infarction during the acute phase in accordance with a decrease in the fibrinogen level. The effect appeared to last for more than 7 days.