Diagnostic biomarkers of essential arterial hypertension: the value of prostacyclin, nitric oxide, oxidized-LDL, and peroxide measurements.

Endothelial function is impaired in hypertensive patients. Decreased nitric oxide and prostacyclin production as well as increased oxidative stress are involved in this abnormality. The aim of the present study was to evaluate whether biomarkers of endothelial dysfunction and oxidative stress have diagnostic value in patients with essential hypertension. We measured nitric oxide, prostacyclin, and oxidized-LDL levels and assessed oxidative status in 62 patients with diagnosed essential arterial hypertension and 45 healthy controls. In the hypertensive group, among measured parameters, the median prostacyclin level was significantly lower, when compared to healthy controls (125.57 pg/mL, 25%; 75% quartile range: 84.99; 275.93 and 462.9 pg/mL, 25%; 75% quartile range: 107.69; 849.3, respectively, P = 0.009). The largest area under the ROC curve was found for prostacyclin; 0.647 (95% C.I. 0.549 to 0.737). In the analysis of logistic regression, the prostacyclin and oxidized-LDL cut-off values were associated with a 4.9 higher significant risk of hypertension (O.R. 4.91 and 4.99, respectively; P = 0.0008 and P = 0.00065, respectively). Oxidized-LDL, a biomarker of endothelial damage, was the only one that had a significant negative correlation with protective prostacyclin in hypertensive patients (r = -0.29, P = 0.02). Of all the biomarkers prostacyclin and oxidized-LDL had the best diagnostic value for patients with hypertension.

The morphological and histochemical neurosecretory magnocellular system in the rat after administration of chlorpromazine.

The effect of chlorpromazine (CPZ) on the neurosecretory action of the hypothalamo- hypophyseal system was investigated in 72 male rats. The experimental animals received CPZ in a dose of 0.4 mg, 4.0 mg and 20.0 mg/kg b.w. for 30 days. The rats were sacrificed by decapitation at 24 h and 7 days after the last dose of the drug. The neurosecretory material was stained with paraldehyde fuchsin in the supraoptic nucleus, paraventricular nucleus, eminentia mediana and neurohypophysis, the tigroid was stained with toluidine blue and the acid phosphatase activity was evaluated histoenzymatically. It was found that CPZ reduced the content of the neurosecretory material after 24 h, while an increase was observed 7 days after the last drug administration.

Dactinomycin-induced veno-occlusive disease in rats. The hepatoprotective action of amifostine. Evaluation in a light and electron microscope.

The purpose of the study was to draw upan experimental model of hepatic veno-occlusive disease (VOD) induced by dactinomycin (ACT) and to investigate the possible hepatoprotective effects of Ethyol (amifostine). Pathological changes corresponding to a VOD picture of varying intensification were found in the liver samples obtained from all the rats receiving ACT. Amifostine appears to act protectively to liver changes caused by dactinomycin.

A preliminary evaluation of thyroid and respiratory tract neuroendocrine cells in the rat after experimental hypercalcaemia.

The goal of this study was to investigate the influence of experimentally induced hypercalcaemia (after 100000 UI Vigantol and CaCl2) on neuroendocrine cells (NECs) in the thyroid and airways in the rat. After 24 h, 7 days and 14 days the thyroid and lungs were collected. Paraffin sections were immunocytochemically stained with specific antibodies against CGRP, calcitonin (CT) and synaptophysin (SY) in the airway NECs and thyroid C cells. The largest hypercalcaemia were observed in experimental rats after 7 days. More significant changes in the number and size of neuroendocrine cells were observed in the thyroid gland as well as in the airways. In the airways only a slight increase in the number of neuroepithelial bodies (NEBs) was observed, some of which gave evidence of hypertrophy symptoms.