Arylsulphatase A activity and sulphatide concentration in placenta, membranes and cord after delivery.

AIM: We evaluated variations in behavior of arylsulphatase A activity (an enzyme that catabolizes sulphatides) and of sulphatide concentration in the placenta, cord and membranes of healthy gravidas at term pregnancy, following spontaneous birth. METHODS: We extracted and biochemically determined arylsulphatase A and sulphatide concentration in placenta, cord and membranes (far from and close to internal uterine os) in 14 patients. RESULTS: Activity of arylsulphatase A decreased in the cord, in membranes far from the internal uterine os, in membranes close to the internal uterine os and in the placenta. Sulphatide concentration was minimal in the cord and maximal in placenta, with intermediate values in the membranes. No correlation was found between arylsulphatase A activity and sulphatide concentration, nor among arylsulphatase A activities, nor among sulphatide concentrations among the different tissues. It seems that multiparity may increase and the duration of active labor may decrease arylsulphatase A activity in membranes far from the internal uterine os, while active labor duration does not appear to have any implication on sulphatide concentration in membranes close to the internal uterine os. CONCLUSIONS: Arylsulphatase A activities and sulphatide concentrations in fetal adnexa show significant differences.

Biochemical determinations of arylsulphatase A activity and sulphatide concentrations in decidua of women at 41 and 42 weeks of gestation.

OBJECTIVE: To evaluate arylsulphatase A activity and sulphatide concentrations in decidua of women at 41 and 42 weeks of gestation. STUDY DESIGN: Enzyme activity and sulphatide concentrations were determined by biochemical procedures on samples of women at 41 and 42 weeks of gestation; thin-layer chromatography was also prepared to separate and visualize sulphatides and other lipid fractions. RESULTS: The spectrophotometric values of arylsulphatase A showed very low values at 41 weeks, which reduced to a half at 42 weeks of gestation, while values of sulphatide concentrations increased in 42 weeks. CONCLUSIONS: The behavior of two parameters examined could be due to the amount of placental estriol reduction, because of sudden placental aging.

The cerebral cortex of spontaneously hypertensive rats: a quantitative microanatomical study.

The morphology of cerebral cortex was investigated in male spontaneously hypertensive rats (SHR) aged 2, 4 and 6 months (pre-hypertensive, developing hypertension and established hypertension respectively) and in age-matched normotensive Wistar-Kyoto (WKY) rats using quantitative microanatomical techniques. Analysis included frontal and occipital cortex as a paradigm of motor and sensory cerebrocortical areas respectively. Values of systolic pressure were slightly higher in 2-month-old SHR compared to age-matched WKY rats and augmented progressively with increasing age in SHR. In frontal cortex of SHR a decrease of nerve cell number and of cortical volume was observed in layers V and VI of 4- and 6- month-old SHR, and in layers I-IV of 6- month-old SHR. In occipital cortex a decrease of the number of nerve cells and of cortical volume was observed in layers V and VI of 2-, 4-, 6- month-old SHR, and in layers I-IV of 6-month-old SHR. Numerical decrease of neurons in SHR affected to a greater extent occipital cortex than frontal cortex. An increase in the number of glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes (hyperplasia) as well as in the mean immune reaction area (hypertrophy) was found in the two cerebrocortical areas investigated of 6-month-old SHR. The occurrence of apoptosis and/or necrosis identified using the terminal deoxyribo-nucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labeling (TUNEL) technique was also observed in frontal and occipital cortex of 6-month-old SHR, but not of younger cohorts. These findings indicate the development of microanatomical changes in the cerebral cortex of SHR, the extent of which increases parallel with the progression of hypertension. The occurrence of cerebrocortical apoptosis and/or necrosis as well as the obvious astrogliosis occurring in established hypertension may account for the increased risk of vascular dementia that represents a specific trait of complicated hypertension.

Increased expression of glial fibrillary acidic protein in the brain of spontaneously hypertensive rats.

Astrogliosis, consisting in astroglial proliferation and increased expression of the specific cytoskeletal protein glial fibrillary acid protein (GFAP) is common in several situations of brain damage. Arterial hypertension, which induces cerebrovascular changes, can cause also brain damage, neurodegeneration and dementia (vascular dementia). This study was designed to assess astroglial reaction in different brain areas (frontal cortex, occipital cortex, hippocampus and striatum) of spontaneously hypertensive rats (SHR) in the pre-hypertensive phase (2 months of age), in the developing phase of hypertension (4 months of age) and in established hypertension (6 months of age). SHR were compared to age-matched normotensive Wistar-Kyoto (WKY) rats. Analysis included reverse transcription-polymerase chain reaction (RT-PCR) of GFAP mRNA, GFAP immunochemistry (Western blot analysis) and immunohistochemistry. A significant increase of GFAP mRNA and an increase of GFAP immunoreactivity were noticeable in different brain areas of SHR compared to normotensive WKY rats at 6, but not at 2 or 4 months of age. Immunohistochemistry revealed a numerical augmentation (hyperplasia) and an increase in size (hypertrophy) of GFAP-immunoreactive astrocytes in frontal cortex, occipital cortex and striatum of SHR. In the hippocampus of SHR only a numerical increase of GFAP-immunoreactive astrocytes was found. These finding demonstrating the occurrence of astrogliosis in the brain of SHR with established hypertension suggest that hypertension induces a condition of brain suffering enough to increase biosynthesis and expression of GFAP similarly as reported in several neurodegenerative disorders and in brain ischemia.

Morphological and conduction changes in the sciatic nerve of spontaneously hypertensive rats.

The morphology and function of sciatic nerve were investigated in spontaneously hypertensive rats (SHR), either control or hydralazine-treated, and in normotensive Wistar Kyoto rats of 6 months of age. In control SHR decreased percentages of class I fibers (20-15 microm in diameter), of axonal NFP-H 200 kDa neurofilament protein immunoreactivity and of nerve conduction velocity were found. The percentages of class III (10-5 microm in diameter) and IV (<5 microm in diameter) and of S100beta-immunoreactive Schwann cell profiles were increased. Treatment with the hypotensive drug hydralazine countered sciatic nerve changes. The shift of nerve composition vs. smaller fibers is probably the cause of reduced nerve conduction velocity found in SHR and is consistent with the occurrence of a sympathetic hyper innervation in this animal model of hypertension. Our findings support the hypothesis that arterial hypertension may represent a risk factor of neuropathy.

Lysosomal glycosidases and their natural substrates in major salivary glands of hamsters treated with 7,12-dimethylbenzanthracene (DMBA).

Oro-maxillofacial diseases may influence structure and function of salivary glands. In this study, 32 hamsters were treated with topical application of 7,12-dimethylbenzanthracene (DMBA) on the buccal pouch. After 16 weeks, the animals were killed and the major salivary glands extracted. The activities of some lysosomal glycosidases and their natural substrates were measured to understand how the carcinogenetic stress and the inflammatory reaction could influence the physiology of the salivary glands. Large differences were observed in lysosomal activities among treated and untreated animals. Similarly, large differences were shown in the concentration of natural substrates, including sialic acids. These results suggest that inflammation and/or tumors induce profound changes in the biology of the salivary glands.

Effects of dihydropyridine-type Ca2+ antagonists on the renal arterial tree in spontaneously hypertensive rats.

The effects of hypertension and of treatment with dihydropyridine-type Ca2+ antagonists and the vasodilator hydralazine on renal arterial tree were investigated in spontaneously hypertensive rats (SHR) with quantitative microanatomical techniques. Pharmacological treatment decreased to a similar extent systolic blood pressure values in SHR. Increased thickness of the tunica media of intrarenal arteries accompanied and luminal narrowing were observed in control SHR. Lercanidipine, manidipine, and nicardipine significantly countered wall thickening and luminal narrowing. Hydralazine countered luminal narrowing only. Dihydropyridines exerted renal vasocilatory activity primarily on resistance arteries, being lercanidipine the only compound active on small sized arteries.