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Biomedical subjects

A Gecse

Publications and source records attributed to A Gecse.

At least 37 records · Page 2Linked to original sources
PubMed1982

Histamine-stimulated prostaglandin synthesis in rat brain microvessels.

The histamine-sensitivity of prostacyclin and prostaglandin synthesis was investigated in isolated brain microvessels prepared from normal and hypoxic exercised rats. 10(-4) M histamine stimulated the in vitro synthesis of all components of arachidonate cascade. The chronic hypoxic exercise also resulted in an enhanced production of each fraction. Hypoxia and histamine showed an additive effect in the synthesis of PGE2 only. The possible molecular mechanism induced by hypoxia and histamine is discussed.

Animals↗
PubMed1982

Prostacyclin and prostaglandin synthesis in isolated brain capillaries.

The synthesis of prostacyclin and prostaglandins was examined in isolated blood-free brain capillaries of guinea-pigs and rats using 1-14C-arachidonic acid as a precursor. The main prostaglandins synthesized by guinea-pig microvessels were prostaglandin D2 and prostaglandin E2. Substantially less prostaglandin F2 alpha or the prostacyclin stable metabolite, 6-oxo-prostaglandin F1 alpha was synthesized. Rat capillary prostaglandin distribution differed substantially from that of the guinea-pigs although the principle prostaglandin was also PGD2. Total prostaglandin conversion was greater in guinea-pig capillaries than in the rat. Norepinephrine stimulated the prostaglandin forming capacity of blood free cerebral microvasculature of guinea-pigs. Prostacyclin and prostaglandins could be involved in the activity dependent regulation of regional cerebral blood flow and permeability.

Animals↗
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↗
PubMed1981

Regulation of brain prostaglandins by sexual steroids.

Hypothalamic PGF2 alpha content was determined by radioimmunoassay in rats. The male animals had significantly higher PGF/2 alpha level than the females. The hypothalamic PGF2alpha content increased following orchidectomy (GDX), while ovariectomy alone or combined with oestrone (100 microgram/kg or 1mg/kg i.m.) resulted in a significant i.m.) alone was ineffective. Testosterone (1 or 5 mg/kg i.m.) in GDX animals restored the hypothalamic PGF2 alpha content to the control level. The synthesis and breakdown of prostaglandins were also studied in the microsomal and cytosol fraction of brain homogenate. The PGD2 was the main product of the arachidonate cascade in rat brain microsomes. OVX increased the formation of PGD2 and diminished the biosynthesis of PGF2 alpha. Oestrone administration to OVX rats enhanced the formation of PGF2 alpha. Progesterone injection decreased the biosynthesis of PGF2 alpha and PGD2 alpha and PGD2 in OVX animals. Combined administration of progesterone and oestrone to OVX rats failed to restore the PGF2 alpha synthesis. In orchidectomized animals the arachidonate cascade was found to be depressed, further the synthesis of prostaglandins was normalized after testosterone substitution. The inactivation of 3H-PGF2 alpha by rat brain cytosol fraction was negligible.

Animals↗
PubMed1980

Effects of ACTH on the synthesis and metabolism of prostaglandin in rat kidney.

Prostaglandin (PG) synthetase activity of rat kidney medulla microsomal fraction was determined in vitro using I-14C-arachidonic acid as substrate. Natural ACTH resulted in a dose dependent suppression of PGE2 formation in vitro. The biosynthesis of PGE2 alpha was enhanced in the presence of ACTH (cortrophin). ACTH4--10 (1-Phe7 or d-Phe7) resulted in decreased PGE2 synthesis. The ratio of PGF2 alpha/PGE2 increased in proportion to the concentration of natural ACTH. The increase in the ratio of PG-s was more pronounced when ACTH4--10 fragments were applied. Natural ACTH in a dose dependent manner inhibited the prostaglandin dehydrogenase activity of kidney cytosol fraction in vitro. Prostaglandin inactivation was suppressed only by high doses of ACTH4--10 (d-Phe7). The data indicate that the natural ACTH and ACTH4--10 fragments might have a physiological role in the regulation of the prostaglandin system of a non-steroidogenic tissue.

Adrenocorticotropic Hormone↗
PubMed1980

Effect of ACTH on prostaglandin induced vascular permeability.

Increased vascular permeability was induced by prostaglandin E2 (PGE1), arachidonic acid and compound 48/80 in male rats. Natural ACTH in a dose-dependent manner inhibited Evans blue exudation elicited by arachidonic acid or compound 48/80, however, it was ineffective against PGE1. ACTH4--10 (d-Phe7 and 1-Phe7) injected together with the prophlogistic agents depressed the arachidonic acid and compound 48/80 induced vascular reaction. Indomethacin pretreatment inhibited the effect of arachidonic acid on vascular permeability suggesting that arachidonic acid evoked its vascular activity by means of affecting the endogenous synthesis of prostaglandins and, on the other hand, the prostaglandin system played a role in the vascular permeability inducing effect of compound 48/80. ACTH4--10 peptide fragments free of steroidogenic action and natural ACTH inhibited locally the in vivo formation of PGS from arachidonic acid in the rat skin, resulting in a nonspecific decrease of local inflammation.

Adrenocorticotropic Hormone↗
PubMed1979

Bradykininase and protease inhibitors in seminal plasma of fertile and infertile men.

The level of protease acrosin in the seminal plasma of oligozoospermic men was significantly higher than that of normozoospermic men. The amount of bradykininase in the seminal plasma was very high in both normozoospermic and oligozoospermic patients. When the acrosin and kininase content was referred to one million spermatozoa, seminal plasma kininase was significantly enhanced in oligozoospermic men, while the acrosin activity was similar in normozoospermic fertile men and infertile men. Human seminal plasma inhibitor I (HUSI I) increased along with sperm count. Human seminal plasma inhibitor II (HUSI II) showed no change. The motility of spermatozoa was depressed in oligozoospermic patients.

Acrosin↗
PubMed1979

The effect of adrenal and gonadal hormones on vascular permeability in rat skin.

The effect of adrenal and gonadal hormones on vascular permeability induced by intradermal injection of prostaglandins (PGs) E1, F2alfa, arachidonic acid and compound 48/80 have been examined in the rate. PGE1, arachidonic acid and compound 48/80 produced an increase in local vascular permeability. PGF2alfa decreased the action of these vasoactive agents, when it was injected in a mixture intradermally with PGE1, arachidonic acid and compound 48/80. Vasoactive response induced by PGE1, arachidonic acid and compound 48/80 was inhibited by the removal of adrenals and testes, and it was restored to normal by injection either of cortisol, deoxycorticosterone (DOC) or testosterone. In adrenalectomized rats, no change was observed in the inhibition of vascular permeability elicited by PGF2alfa response to compound 48/80. The blocking effect of PGF2alfa on vascular permeability evoked by PGE1 and arachidonic acid showed a considerable decrease. After orchidectomy the inhibitory effect of PGF2alfa on the vascular permeability induced by arachidonic acid and compound 48/80 was completely blocked, while in the case of PGE1 the inhibition was partial. Testosterone treatment restored the anti-inflammatory effect of PGF2alfa against compound 48/80. Ovariectomy was without any effect on vascular response.

Animals↗
PubMed1977

Further studies on the anti-inflammatory effect of insulin.

Experiments performed on rats showed that insulin, when applied i.v. or s.c., inhibited the foot edema induced by carrageenin, thermic effect of 45.7 degrees C, compound 48/80 and 5-HT, but moderately increased the paw swelling evoked by kallikrein, a kinin-forming enzyme. The increased vascular permeability elicited by intradermal injection of histamine, 5-HT, bradykinin, PGE1, carrageenin and compound 48/80 was also suppressed. The anti-inflammatory effect was not significantly altered by propranolol and adrenalectomy on the thermal and carrageenin edema, it was variably inhibited on the skin test, and was completely abolished on the paw swelling induced by 5-HT and compound 48/80. Since insulin had little or no effect on the vascular response when given topically together with the vasoactive agents, its complex effect on the acute inflammation appears to be brought about via indirect mechanisms.

Administration, Topical↗
PubMed1977

Involvement of the kinin system in the insulin-induced inhibition of carrageenin oedema in rats.

The carrageenin-induced foot oedema in rats is considerably decreased by insulin pretreatment, but increased in alloxan diabetes. Maximum inhibition by insulin occurs in the early phase of the oedema reaction and the insulin action is even further increased when it is administered 30 min after carrageenin. Doses of insulin as low as 1 U/kg intravenously produce significant inhibition. Determinations of the components of the kinin system indicate that the kininogenase activity is increased, and both the kininogen and kininase content are in turn decreased in the plasma of insulin-treated animals. When the carrageenin-induced oedema fluid of the paw after insulin is analysed for kininogen and kininase, their levels are significantly decreased when compared with those of oedema fluid without insulin. Histamine content in the oedema fluid is significantly enhanced by insulin. The anti-inflammatory effect of insulin under these conditions therefore appears to involve changes in the kinin system.

Animals↗