The incidence of inguinal hernia is clearly increased in men who have undergone radical retropubic prostatectomy plus pelvic lymph node dissection compared with those who undergo no surgery for prostate cancer. Inguinal hernia appears to develop more often in men with prostate cancer who undergo radical retropubic prostatectomy and pelvic lymph node dissection than in those who undergo pelvic lymph node dissection only. While surgical factors trigger hernial development, previous hernial surgery and post-prostatectomy anastomotic stricture may be important risk factors. In fact, the latter may largely explain the difference in the incidence of inguinal hernia in our lymph node dissection and prostatectomy groups. Prophylactic surgical procedures must be evaluated to address this problem.

Catechols are known to react readily with molecular oxygen to form the corresponding quinones together with reduced oxygen species. These products have been shown to be toxic in in vivo and in vitro systems. 5-S-Cysteinyl adducts of catechols are believed to be formed through the spontaneous reaction between quinones and thiol-containing compounds, like cysteine and glutathione (GSH). Thus, the brain levels of these adducts probably indicate the autoxidation rate of catechols in vivo. In the present study, the striatal concentrations of 5-S-cysteinyldopamine (5-S-cysteinyl-DA), 5-S-cysteinyl-3,4-dihydroxyphenylalanine (5-S-cysteinyl-DOPA), and 5-S-cysteinyl-3,4-dihydroxyphenylacetic acid (5-S-cysteinyl-DOPAC) were determined in 2-week-, 2-month- and 3-year-old guinea pigs. In addition, brain levels of DA, the DA metabolite DOPAC, and GSH were assessed. The concentration of 5-S-cysteinyl-DA increased markedly with age. The 3-year-old guinea pigs had the highest level, i.e., 248% of the concentration in the 2-week-old animals and 219% of the concentration in the 2-month-old animals. Furthermore, the striatal 5-S-cysteinyl-DOPA level in the 3-year-old group was 68% higher than in the 2-week-old group and 46% higher than in the 2-month-old group. No age difference in the striatal concentration of DA was found. In contrast, the concentration of DOPAC increased with age: The DOPAC level in the 3-year-old animals was 153% of the level in the 2-week-old animals and 116% of the level in the 2-month-old animals.(ABSTRACT TRUNCATED AT 250 WORDS)

The pivotal role for voltage‐sensitive calcium channels in initiating synaptic transmitter release is undisputed, but it is only partly known to what extent the different subtypes contribute in vivo. Their importance for the dendritic release of dopamine has not been investigated in vivo previously. To evaluate comprehensively the relative importance of different voltage‐sensitive calcium channel subtypes for striatal dopamine release, and to further investigate the mechanism of dendritic dopamine release in the reticulate part of substantia nigra, dopamine was measured by in vivo microdialysis in the striatum or substantia nigra of awake rats. The calcium channel blockers nimodipine, ω‐conotoxin‐GVIA, ω‐agatoxin‐IVA, and neomycin were administered locally through the dialysis probes and compared with calcium‐free perfusion. Results indicate that dopamine release in the striatum is mainly dependent on N‐ and P/Q‐type channels, but the dendritic dopamine release in the substantia nigra is mediated mainly by some other calcium‐dependent mechanism, for example, calcium mobilization through T‐, O‐, or R‐type calcium channels. A portion of the dendritic release is calcium independent but can be inhibited partially by neomycin, which might suggest a role for inositol 4,5‐bisphosphate breakdown products.

Sprague-Dawley rats were anesthetized with chloral hydrate, and plastic cannulae were permanently implanted into the lateral ventricles. The animals then were allowed to recover for 1-2 days. L-Buthionine sulfoximine (L-BSO), a selective inhibitor of glutathione (GSH) synthesis, and 6-hydroxydopamine (6-OH-DA), a selective catecholaminergic neurotoxin, were administered intracerebroventricularly. The striatal concentrations of GSH and monoamines were determined by HPLC with electrochemical detection. Two injections of L-BSO (3.2 mg, at a 48-h interval) resulted in a 70% reduction of striatal GSH. 6-OH-DA (150 or 300 micrograms) reduced the concentrations of striatal dopamine and noradrenaline 7 days after the administration, but left the concentrations of 5-hydroxytryptamine unaltered. L-BSO treatment did not produce any changes in the levels of monoamines per se but it potentiated the catecholamine-depleting effect of 6-OH-DA in the striatum. Thus, GSH appears to suppress the toxicity of 6-OH-DA, probably by scavenging the toxic species formed during 6-OH-DA oxidation. In view of these results one may suggest an important role for GSH in catecholaminergic neurons: protecting against the oxidation of endogenous catechols.

Following intraperitoneal administration of the non-competitive N-methyl-D-aspartate (NMDA) antagonist dizocilpine (MK-801), levels of the dopamine (DA) metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) increased in mouse striatum and limbic forebrain. When dizocilpine was given to animals treated with NSD 1015, an inhibitor of 3,4-dihydroxyphenylalanine (DOPA) decarboxylase and monoamine oxidase, there was an increase in levels of DOPA and 3-methoxytyramine (3-MT). These findings suggest that dizocilpine stimulates DA synthesis and release in mouse brain. Following dizocilpine treatment a clear-cut increase in spontaneous locomotor activity was observed, probably partly due to enhanced dopaminergic tone. The competitive NMDA antagonist D-CPPene produced locomotor stimulation as well, but in contrast to following dizocilpine treatment levels of 3-MT decreased. Thus the stimulation of locomotor activity following D-CPPene treatment does not seem to be mediated through activation of central dopaminergic systems. However, haloperidol pretreatment antagonized this locomotor response, indicating that the dopaminergic system plays a permissive role in this context.