Since the norepinephrine (NE) was introduced to the psychiatric field as one of the possible major causes of depression, many researchers and clinicians have devoted their attention to investigation of the possible link between brain noradrenergic activity and depression. Much data about NE turnover and its receptor function have been provided by many investigators. However, the results of studies are much controversial.
Thus the authors inve. -igated 28 endogenous depressed patients and measured their plasma levels of NE major metabolite 3-methoxy-4-hydroxyphenyleneglycol (MHPG) as a valid indirect index of NE turnover and also measured their plasma levels of cortisol as an indirect evidence of receptor function, and simultaneously applied dexamethason suppression test (DST) to the subjects, and repeated these measures after first, second & third weeks of treatment with tricyclic antidepressants. So the authors compared noradrenergic function in dexamethason-resistant and dexamethason-sensitive depressed patients and correlated NE function with plasma levels of cortisol, prior to and of ter treatment. The results as follows:
1. In the plasma levels of MHPG at the pretreatment state, depressed patients are distributed in clearly defined 2 groups, high and low, out of relation to clinical subgroups, bipolar or unipolar. Mean plasma MHPG level of each group is 20. 40 (1.75) ng/ml and 12.59 (0.99) ng/ml respectively (p <. 001).
2. All patients except two of the 28 endogenous depressives do not show diurnal rhythm in plasma MHPG levels, prior to and after 3 weeks of treatment.
3. At the pretreatment llpm plasma cortisol levels, all subjects except two of 28 depressive patients are cortisol hyper-secretors. Plasma levels of cortisol at 11 pm in the high plasma MHPG group (mean 11.808 (2.790),ag/dl) are signifi cantly higher than those in the low plasma MHPG group (mean 8.722(2. 701) ug/dl) (p <. 01) .
4. In the pretreatment DST, depressed patients with high plasma MHPG levels are all nonsuppressors, and those with low plasma MHPG levels all suppressors, suggesting that baseline plasma MHPG values may predict the adequacy of a patient´s postdexamethason cortisol response.
5. After 3 weeks of treatment, plasma levels of MHPG decreassed significantly in the improved patients, especially in the high pretreatment plasma MHPG group (p <. 005).
6. After 3 weeks of treatment, plasma levels of cortisol decreased significantly in the improved patients, especially in the high pretreatment plasma MHPG group (p <. 002).
7. Ten depressed patients among 13 dexamethason nonsuppressors in the pretreatnent state became to suppressors after 3 weeks of treatment.
From the above results, the authors could suggest that there might be two different subgroups in the plasma levels of MHPG in the endogenous depressive patients. The depressive patients with the pretreatmenthigh plasma levels of MHPG could be attributed to the functional impairment in the brain noradrenergic activity, but those with the pretreatment low plasma levels of MHPG probably to the impairment of other neurotransmitters.
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