Catecholamine changes in patients with depression under the action of high-intensity light. / Zminy katekholaminiv u khvorykh z depresiieiu pid diieiu svitla pidvyshchenoï intensyvnosti.

Preponderance in depression of the melancholy affect was characterized by a drop in the level of norepinephrine (NE) and rise in epinephrine (E). Exposure to light was associated with fall in E, with no change recordable in NE. In anxious depression, following light therapy, high levels of excretion of both catecholamines tended to return to normal. Ligh was found to cause opposite changes in the quantitative measures depending upon the initial value for the E:NE ratio (above or below control).

[Melatonin excretion in patients with depression under the action of light of increased intensity]. / Ekskretsiia melatonina u bol'nykh depressiei pri deistvii sveta povyshennoi intensivnosti.

The effects of 1 and 10 bright light exposures (2600-8000 lux) on melatonin excretion in patients with melancholic and anxious depressions were examined. Before treatment the increased basic levels of melatonin excretion were observed in patients with anxious depression. Melatonin excretion had been gradually normalized after 1 and 10 sessions of light therapy. The basic melatonin excretion in melancholic depressed patients was low and hadn't been changed after light therapy. Long term effects of light therapy depend upon the initial levels of melatonin excretion: low pretreatment levels increased and high pretreatment levels decreased after the therapy. The authors proposed that bright light exposures stimulated the restoration of adaptive function of pineal gland in depressed patients.

Changes in norepinephrine output following light therapy for fall/winter seasonal depression.

Recurrent fall/winter depressions that remit during spring and summer have been called Seasonal Affective Disorders (SAD) (Wehr and Rosenthal 1989). The pathophysiology of SAD, its relationship to nonseasonal affective disorders, and the mechanism of action of light therapy, which is effective in treating SAD, remain to be elucidated (Depue et al 1989; Jacobsen et al 1987; James et al 1986; Joseph-Vanderpool et al 1991; Skwerer et al 1988, Terman et al 1989). Norepinephrine (NE) may play a role in the mechanisms of action of many antidepressant treatments (Schildkraut 1965) that alter NE metabolism (Schildkraut et al 1964 and 1965) and decrease the urinary output of NE and its metabolites, i.e., "whole-body NE turnover" (WBNET) (Golden et al 1988; Potter et al 1988). The present study explored whether light therapy also reduces the urinary output of NE and its metabolites.

Incomplete syndrome of renal tubular acidosis induced by lithium carbonate.

Renal acidification was studied in 10 control subjects and 15 lithium carbonate-treated psychiatric patients of similar age. Seven lithium-treated patients were unable to lower urine pH normally after short duration acid-loading (Li-1:5.35 to 6.25), while 8 (Li-ll:4.52 to 5.17) did not differ from control subjects (4.49 to 5.07). Li-l patients excreted significantly less titratable and net acid than the other groups. Baseline urine pH was higher in both lithium-treated groups than in control subjects, and although this was due in part to the carbonate moiety of the medication, the abnormal minimal urine pH of Li-l patients was not carbonate-dependent. Li-l patients had normal arterial pH and bicarbonate concentrations, trival bicarbonaturia, and no evidence of generalized proximal tubular dysfunction. These data demonstrate that lithium therapy can induce the syndrome of incomplete distal renal tubular acidosis at serum lithium concentrations within the accepted therapeutic range.