Suppressive effect of human blood coagulation factor XIII on the vascular permeability induced by anti-guinea pig endothelial cell antiserum in guinea pigs.

We investigated the effect of blood coagulation factor XIII (FXIII) on enhanced permeability induced by anti-endothelial cell antiserum, that was produced by the immunization of guinea pig endothelial cells with adjuvant into rabbits repeatedly. We have found that this antiserum reacts to human and guinea pig endothelial cells but not guinea pig fibroblast cells. The permeability was enhanced by intradermal injection of 400-fold dilution of this antiserum into dorsal skin of guinea pigs. The mixture of equal volume of antiserum and FXIII was intradermally injected into dorsal skin of guinea pig after Evans blue injection, and 15 minutes later the quantity of Evans blue at the each injection site was determined. We recognized the suppressive effect of FXIII on the dye leakage. We also studied the suppressive effect on swelling induced by the antiserum. After the subcutaneous injection of the mixture of antiserum and FXIII into the back of guinea pigs, we measured the thickness of skins at the injection site after day 1, 2 and 3. As a result, FXIII significantly suppressed the swelling. We found that FXIII suppresses the acute and subacute permeability enhancement. These results suggest that FXIII plays an important role on an inflammatory site and that it may exert as an anti-inflammatory protein.

[Diagnosis of anterior perineal anus (APA)--significance of electromyographic evaluation of the external anal sphincter location].

APA is a common cause of constipation, and is the mild case of the imperforated anus. On diagnosing APA, anterior displacement of the anus and normal distribution of the external anal sphincter to the anus are essential. To determine the location of the anus in the perineum simple clinical technique was developed. In 61 normal cases, the result of measurement was almost same in each sex, but in 3 APA cases the location were anteriorly dislocated than normal cases. Distribution of the external anal sphincter was evaluated with electromyographic technique, and location map of the sphincter was made. In 3 APA cases, the anus was totally surrounded by the external anal sphincter, but in 17 ano-cutaneous fistula cases, the opening was anteriorly dislocated to the sphincter distribution map. As a conclusion, newly proposed simple clinical technique to determine anal location and electromyographic examination of the external and sphincter distribution are very useful in objective diagnosis of APA.

Role of serotonin in the regulation of beta-adrenoceptors by antidepressants.

The role of serotonin (5-HT) in the regulation of the beta-receptor density induced by long-term treatment with typical and atypical antidepressants was examined. Treatment with either mianserin (15 mg/kg, twice daily) or maprotiline (10 mg/kg, twice daily) for 7 days caused a significant decrease in the beta-receptor density, measured 6 h after the last dose, without a change in affinity. The reduction in beta-receptors disappeared rapidly (within 24 h). However, treatment with mianserin or maprotiline combined with fluoxetine, a selective 5-HT uptake inhibitor, significantly decreased the beta-receptor density even 24 h after the last dose. The combined administration of mianserin and 5-hydroxytryptophan (5-HTP) mimicked the effect of the combination with fluoxetine. Following pretreatment with p-chlorophenylalanine (PCPA) for 6 days, desipramine treatment for 3 days significantly decreased the beta-receptors 6 h after the last dose but this desipramine-induced decrease in beta-receptors was rapidly reversible (within 24 h). These results demonstrate that while intrasynaptic 5-HT levels are not a factor in the decrease in beta-receptors, they do play an important role in the preservation of the down-regulated state of the beta-receptor caused by antidepressants from rapid reversibility.

Slow-type C-protein in dystrophic chicken fast pectoralis muscle.

C-protein isoform expression in hereditary dystrophic chicken skeletal muscle was compared with that in normal chicken muscle during postnatal development by immunocytochemical and immunoblot methods. In the pectoralis muscle (PM) of both normal and dystrophic chicken, slow- and fast-type C-proteins were coexpressed in the vast majority of myofibers at neonatal age, but the slow C-protein disappeared, leaving continued expression of only the fast-type C-protein as muscle development progressed up to 2 weeks posthatch. In the dystrophic chicken PM, however, myofibers containing slow-type C-protein reappeared about 1 month posthatch and increased in number with the progression of muscular dystrophy. We conclude that C-protein isoform expression in dystrophic myofibers resembles that in neonatal myofibers and that the expression of slow-type C-protein can be seen as a marker for chicken muscular dystrophy.