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Biomedical subjects

A Ottlecz

Publications and source records attributed to A Ottlecz.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1979

Dextran anaphylactoid reaction in Sprague-Dawley CFY rats.

From a closed colony of randomly-bred Sprague-Dawley CFY rats about 23% failed to respond to intravenous dextran with the characteristic generalized anaphylactoid reaction, but still exhibited an inflammatory response when dextran was given into the foot pad. Brother-sister mating of rats showing the most expressed generalized reaction (reactor rats) yielded good responder offsprings, while the non-reactors had descendants completely unresponsive to systemic dextran. Brother-sister mating of selected non-reactor rats led to a gradual decrease in dextran paw oedema in the subsequent generations, and after the third mating, a complete local non-reactivity developed. In these rats the intradermal injection of dextran failed to increase vascular permeability, while the inflammatory response evoked by histamine, 5-HT, bradykinin, and compound 48/80 remained unchanged as compared to that of the reactor animals. These result show that the anaphylactoid reaction in Sprague-Dawley CFY rats is under genetic control.

Anaphylaxis↗
PubMed1979

Some characteristics of the insulin-induced potentiation to anaphylactoid reaction in Sprague-Dawley rats.

The insulin-induced sensitization to generalized and local anaphylactoid reaction evoked by dextran was studied in Sprague-Dawley CFY rats. The generalized reaction was shown to be potentiated by insulin given subcutaneously in a dose-related manner. The minimum effective dose was as low as 0.04 U/kg. When this dose was injected intravenously, a marked but short-lived potentiation was observed. The insulin response could be elicited throughout the whole year. The local oedema induced by subplantar injection of dextran was found to be much less sensitive to insulin. Potentiation was observed during the period from March to October, while in the intermediate months, no such effect could be seen. The seasonal refractory state to insulin was abolished by bilateral adrenalectomy, and daily pretreatment of the rats with insulin for several days. Actinomycin D prevented the restorative effect of insulin pretreatment. Sensitization by a single insulin dose to both systemic and local dextran was suppressed in rats older than 6 months, and the refractoriness was in part reversed by adrenalectomy.

Adrenalectomy↗
PubMed1978

Contribution to the regulatory role of insulin in inflammation and anaphylaxis.

Insulin, in doses which did not influence the blood sugar level, potentiated the anaphylactic shock in ovalbumin-sensitized CFLP mice and moderately inhibited the carrageenan-induced paw edema. Higher doses were found to produce a dose-dependent inhibition of the inflammatory process at the 2nd hour, and caused less suppression at the 4th hour of the swelling. These results suggest that insulin may play a complex regulatory role in hypersensitivity and inflammatory reactions, and its effect is not necessarily related to hypoglycemia.

Anaphylaxis↗
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↗
PubMed1976

Effect of insulin and alloxan diabetes on carrageenin inflammation in rats.

Some hypersensitivity reactions and allergic responses are known to be increased by insulin treatment and decreased in diabetes. In contrast, the present experiments showed that paw swelling induced by carrageenin in rats was inhibited by insulin. The anti-inflammatory activity, to some extent, paralleled the dose applied and did not appear to be due to hypoglycaemia. Alloxan diabetes in turn increased the vascular response to carrageenin and abolished the anti-inflammatory effect of insulin. The experiments call attention to the possible significance of insulin in the regulation of the acute non-immune inflammatory process.

Animals↗
PubMed1975

Anaphylactoid-inflammation-promoting factor. An insulin-induced factor derived from non-sensitized lymphocytes increases anaphylactoid inflammation in rats.

The experiments reported here indicate that, when exposed to insulin, viable lymphocytes rapidly released into the incubation medium a factor capable of increasing the dextran-induced anaphylactoid reaction, but having no effect on the inflammatory response evoked by 5-HT. This pro-inflammatory factor was shown to be elaborated by cell suspensions derived from lymph nodes of rats, rabbits, pigs or calves as well as from human tonsils. Thymus cells showed no such activity. The pro-inflammatory factor was termed as anaphylactoid-inflammation-promoting factor (AIPF). Its production depended upon the dose of insulin, and the time of exposure. AIPF was found to have an elution pattern in Sephadex G-100 gels similar to that of BSA (67,000 daltons). The activity was abolished by heat or incubation with DNase or a-chymotrypsin, but was not influenced by RNase. AIPF by itself did not induce increased vascular permeability, and proved to be distinct from the permeability factors present in the lysate of lymph node cells.

Adrenalectomy↗