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Z Mezei

Publications and source records attributed to Z Mezei.

23 records · Page 2Linked to original sources
PubMed1981

Histamine in brain capillaries.

A high amount of histamine was found in capillaries isolated by subcellular fractionation from the brain. In view of the important effects of histamine on vascular permeability in peripheral vessels, it was thought that histamine had a similar function in the cerebral vasculature. Intracarotic histamine infusion resulted in an enhanced pinocytosis of endothelial cells and te oedematous swelling of the astrocytic end-feet system. [3H]-Histamine, injected in the cerebral ventricles, accumulated in the capillary wall. Histamine and cimetidine activated hydroxyfatty acid and prostaglandin D2 synthesis in isolated brain capillaries. The possible function of the capillary histamine in the regulation of permeability of microvessels is discussed.

Animals↗
PubMed1981

Prostacyclin and prostaglandin synthesis in rat brain microvessels: characteristic changes in hypoxaemia.

The effects of hypoxaemia on the synthesis of prostacyclin and prostaglandins in the cerebral microvessels and on the ultrastructure of brain cortex capillaries were investigated in three groups of rats. Series I: rat embryos were kept in hypoxic-hypobaric condition for 42 hours. It resulted in the enhancement of synthesis of PG2alfa and PGE2 even two months after birth. The fine structure of the capillary endothelium remained without any pathological change. Series II: adult male rats were on hypoxic-hypobaric environment for 42 hours. There was a slight increase in the synthesis of PGE2 and PGD2 while the ultrastructure of brain capillaries was found to be normal. Series III: the hypoxic-hypobaric condition lasted for 240 hours in adult male rats. This long term hypoxaemia affected greatly the prostaglandin synthesis of brain cortex capillaries and resulted in changes in the fine structure of brain microvessels as well. The possible molecular mechanism activated by hypoxaemia in brain capillaries is discussed.

Animals↗
PubMedDate not supplied

Effects of inflammatory neuropeptides on the arachidonate cascade of platelets.

BACKGROUND: During neurogenic inflammation, neuro-peptides (substance P, SP, calcitonin gene-related peptide, CGRP, and neurokinin A) are released from nerve endings, and these peptides initiate inflammatory reactions in the microcirculation. Platelets are one of the most important elements of the microcirculation. METHODS: Our in vitro experiments were carried out to determine the effects of inflammatory neuropeptides (SP, and CGRP) on the arachidonate cascade of isolated rat platelets. Cells were labeled with 1-14C-arachidonic acid, then the eicosanoids were separated with overpressure thin-layer chromatography or high-performance liquid chromatography and were quantitatively determined with a liquid scintillation analyzer. RESULTS: SP (10(-9) and 10(-8) mol/l) significantly increased the activity of the arachidonate cascade. The lipoxygenase pathway was significantly stimulated by SP (10(-11), 10(-9) and 10(-8) mol/l), while the cyclooxygenase system was inhibited by 10(-12) mol/l, and stimulated by 10(-9) mol/l SP. The dose-response curve of TxA2 to SP exhibited a similar pattern to that detected for the cyclooxygenase pathway. Among the vasodilator cyclooxygenase metabolites, only the synthesis of PGE2 was significantly elevated by SP (10(-9) mol/l ). CGRP either in low (10(-12)-10(-11) mol/l) or in high concentrations (10(-6) mol/l) activated the cyclooxygenase pathway, while it had no effect on the lipoxygenase pathway. CGRP (8-37), a specific CGRP1 receptor antagonist, inhibited the effects of CGRP. CONCLUSIONS: Our data suggest that the arachidonate metabolites of platelets may play a role in the process of neurogenic inflammation.

Animals↗
PubMedDate not supplied

The effect of substance P on the arachidonate cascade of rat platelets.

The role of substance P (SP) in neurogenic inflammation is well known. Through neurokinin receptors, SP activates cells, including the arachidonate cascade of platelets. Our in vitro experiments were carried out to determine the effect of SP on the arachidonate cascade of rat platelets. The platelets were labelled with 14C-arachidonic acid, and the 14C-eicosanoids were then separated by means of overpressure thin-layer chromatography or high-performance liquid chromatography and were quantitatively determined. SP (10(-9) and 10(-8)) mol/L significantly increased the rate of the arachidonate cascade. The lipoxygenase pathway of platelets was stimulated by SP, which can result in the activation of protein kinase C mediated intracellular events. The cyclooxygenase system was inhibited by 10(-12) mol/L, and stimulated by 10(-9) mol/L SP. In our experiments SP in the physiological range of plasma concentration (10(-12) mol/L) decreased the synthesis of vasoconstrictor arachidonate metabolites (TxA2 and PGF2 alpha). These data suggest that in physiologic conditions the arachidonate cascade of platelets may play role in the vasodilator effect of SP. The formation of thromboxane in rat platelets was stimulated by higher concentration of SP (10(-9) mol/L), and therefore the SP-induced cytotoxicity against parasites might be mediated by the stimulation of thromboxane A2 synthesis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗