Intravenous injection of vasopressin LVP) in unanesthetized rats at an ambient temperature of 18°C caused a decrease in heat production (M) followed by a fall in colonic temperature (T01). These changes were preceded by an elevation of aortic blood pressure (BP) and bradycardia, and were related to the dosage of LVP administered. Temperature of the interscapular brown adipose tissue (BAT) significantly fell after LVP injections. Therefore, it can be said that the decrease in metabolism by the peripheral LVP is at least partly due to suppression of BAT thermogenesis. After bilateral sinoaortic deafferentation, however, the changes in these variables were greatly but not completely reduced except for the elevation of BP. LVP of 0.25 ,ug, more than sufficient to cause a significant elevation of BP when administered peripherally, had no effect on M and Tco1 when injected into the anterior hypothalamus. From these results, we conclude that the hypothermic effect of vasopressin administered peripherally is largely attributed to the baroreflexive suppression of nonshivering thermogenesis, and is not due to the action on the temperature regulatory centers. The slight but insignificant suppression of metabolism in the sinoaortic denervated rats following injection of LVP may be caused by a decreased blood flow to the thermogenic tissues.

Summary:Purpose: To examine a patient with valproic acid (VPA)-induced hyperammonemic encephalopathy accompanied by triphasic waves.Methods: A 61-year-old male patient with epilepsy experienced disturbance of consciousness after VPA dose was increased because of poor seizure control. The electroencephalogram (EEG) taken on admission revealed triphasic waves and high-amplitude &activity with frontal predominance. Although serum hepatic enzymes, such as AST and ALT, were normal, serum ammonium level was high at 96 pg/dl (normal range, 3-47 pg/dl). Serum amino acid analysis showed multiple minor abnormalities. Administration of VPA was discontinued immediately after admission, while other anticonvulsants were continued.Results: The patient's condition was improved on the fourth day of admission. An EEG, serum ammonium level, and amino acid profile were normal on the eighth day. Based on VPA administration, serum ammonium levels, and results of amino acid analysis, this patient had VPA-induced hyperammonemic encephalopathy .Conclusions: Our case indicates that caution is required if triphasic waves appear in VPA-induced hyperammonemic encephalopathy.

No abstract

No abstract

The mechanisms of the hypothermic effect of angiotensin II (All) injected into the lateral ventricle were investigated in unanesthetized rats at an ambient temperature of 18°C. Mean blood pressure (BP), heart rate (HR), metabolic rate (M), colonic temperature (T01), and temperatures of the interscapular brown adipose tissue (TBAT), and the tail skin (TSk) were continuously monitored. All at a dose of 5 ug produced a sharp and marked elevation in BP accompanied by bradycardia, and a decrease of M and Tco1 in the sinoaortic baroreceptor intact rats. The difference between TBAT and Tool decreased significantly, which suggests a suppression of nonshivering thermogenesis of the BAT. TSk was not changed by the All injection. After sinoaortic deneravation, however, the decrease in Tco1 and M with All injection was significantly reduced despite a marked elevation in BP. In addition, intravenous arginine-vasopressin antagonist pretreatment suppressed the elevation in BP and the decrease in HR, Tool, and M after All injection. From these results, it is concluded that the hypothermia which occurred after All injection into the lateral ventricle can be largely attributed to the baroreflexive suppression of M, and to some extent to the direct effect on the thermoregulatory center in rats.