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Biomedical subjects

J Baumann

Publications and source records attributed to J Baumann.

At least 55 records · Page 3Linked to original sources
PubMed1984

Studies on the possible involvement of singlet oxygen and superoxide anion radicals in the cyclo-oxygenase reaction.

The influence of several naphthalene and furan derivatives which are potent singlet oxygen (1O2) acceptors on two prostaglandin synthetase preparations derived from bovine seminal vesicles or rat kidney medulla was studied. Also the effects on the formation of superoxide anion radicals (O2-.) were measured to give further evidence for or against the possible involvement of 1O2 or O2-. in the cyclo-oxygenase reaction. The data we have attained make an essential role of these activated oxygen species as initiators of the cyclo-oxygenase reaction unlikely and thereby support the hypothesis that cyclo-oxygenation during prostaglandin biosynthesis is a lipoxygenase type of reaction.

Animals↗
PubMed1984

Interactions of inhibitors of the lipoxygenase and cyclooxygenase pathways with a supplementary binding site on soybean lipoxygenase.

The oxygenation of [1-14C]-arachidonic acid by a soluble soybean lipoxygenase (E.C.1.13.11.12) preparation was determined in the presence of various cyclo-oxygenase and lipoxygenase inhibitors. The results showed that several non-inhibitory compounds drastically blunted the inhibitory potency of potent lipoxygenase inhibitors. Studies on the combined effects of a variety of structurally unrelated inhibitors of lipoxygenase, cyclo-oxygenase or both oxygenation pathways provided strong evidence for the existence of a supplementary binding site on soybean lipoxygenase which reduces the effective interactions of inhibitors with the catalytic site. Thus several cyclo-oxygenase inhibitors (which do not inhibit at the lipoxygenase catalytic site), as well as low concentrations of lipoxygenase inhibitors, interact with this putative supplementary site and blunt the inhibitory efficacy of potent lipoxygenase inhibitors. Although the degree of interaction with the catalytic site determines the absolute potency of inhibitors, the additional interaction at the putative supplementary binding site is also obligatory for inhibitory potency. In this new multiple-site model the potent lipoxygenase inhibitors (e.g. acetone phenylhydrazone, phenidone) possess high affinities for both sites, whereas weak inhibitors and certain cyclo-oxygenase inhibitors (e.g. benoxaprofen, phenylbutazone, indomethacin) interact predominantly with the supplementary site on the lipoxygenase but lack affinity for the catalytic site.

Binding Sites↗
PubMed1984

[Lipophilic naphthols and 1,4-naphthoquinones as inhibitors of prostaglandin synthesis. 6. Study of 1,4-naphthoquinones].

A number of plumgagin homologues (2-alkyl-1,4-naphthoquinones) and their 3-methyl derivatives are synthesized to enhance the inhibition of the prostaglandin synthetase (PGS)-activity by the natural compound plumbagin and to minimize its toxicity. The inhibition of the enzyme activity by the new naphthoquinones is only weak but their naphthol precursors are strong PGS-inhibitors. The mechanism of this enzyme interaction by the lipophilic naphthol derivatives is discussed in context with their singlet oxygen (1O2) reactive properties.

Animals↗
PubMed1984

[Vitamin B12 levels in the serum in gastrectomized patients].

In 17 totally gastrectomised patients the vitamin B12-serum level was analyzed by 57Co-marked vitamin B12 according to the principle of competitive protein-bounding. Pathological low B12-serum levels in 10 patients refer to the lack of this vitamin. This, however, was only clinically manifested in one case by a megalocytic anaemia. The control of B12-serum levels by running substitution is only useful at the end of the interval between two injections. It is only at this time that it is a help in evaluating the effect of substitution. The monthly or 2-monthly vitamin B12-substitution should be preferred. No optimal substitutional effect can be achieved by injecting 1000 micrograms of vitamin B12 every three months.

Gastrectomy↗
PubMed1984

[Nutritional status and quality of life following gastrectomy].

The nutritional status of 18 patients after total gastrectomy was recorded by anthropometric measures, serum protein and immunological investigations. 15 patients underwent gastrectomy due to carcinoma, the others due to benign diseases. Those patients with carcinoma had been free of signs of malignancy for at least 6 months. According to the elected criteria no patient had a normal nutritional status, there were slight to moderate disturbances of the protein metabolism. By mass reduction the body of the gastrectomised patients had adapted to the decreased intake of protein and calories. In this way the body reaches a new balance and remains efficient. The quality of life of most gastroectomised patients is satisfactory. It depends on the incidence of alimentary complaints and the ability of intake of sufficient food. On the basis of these results there are no serious arguments against Graham's oesophagojejunostomy.

Adult↗
PubMed1984

In vitro deacetylation studies of acetamidophenolic compounds in rat brain, liver and kidney.

The in vitro deacetylation of ortho-, meta- and para-substituted acetophenetidines and acetamidophenols including acetanilide by arylacylamidases in rat brain, liver and kidney was investigated. In general, deacetylation rates were highest in liver and kidney preparations, whereas brain exhibited lower enzyme activities. Acetophenetidines were more suitable N-deacetylation substrates in comparison to acetamidophenols, whereby o-substituted compounds were split more easily than their corresponding m- or p-analogues. Among the arylacylamides tested, o-acetophenetidine was the predominant substrate in all tissues. It was deacetylated by far more rapidly than phenacetin. The enzymic deacetylation of acetophenetidines in kidney and brain was inhibited by p-nitrophenylacetate revealing that N-acetylamides as well as O-acetyl esters undergo similar degradation by carboxylesterase-amidases. The organophosphorous diester bis(p-nitrophenyl)-phosphate which is known to be a rather selective inhibitor of acetanilide-cleaving hydrolases in rat liver suppressed the deacetylation of acetanilide in all tissues investigated. In contrast to acetanilide, the deacetylation of acetophenetidines was inhibited by bis(p-nitrophenyl)-phosphate in liver and kidney, but bis(p-nitrophenyl)-phosphate was by far less active against acetophenetidine hydrolases in brain.

Acetamides↗
PubMed1983

Propranolol enhances the effect of ACTH on plasma cortisol, but not on aldosterone in man.

An accidental observation led to the suspicion that propranolol (P) enhances the effect of exogenous ACTH on plasma cortisol. To examine this matter further, large-dose ACTH tests (25 IU im) were performed in 10 normal young males: i) without treatment (n =10); ii) after 11/2 days of P treatment (n = 10); iii) after 11/2 days of metoprolol treatment (n = 6). Six other subjects received infusions of 0.2 IU of ACTH/hour for 12 h: i) without pretreatment; ii) after 11/2 days of P treatment. P pretreatment (80 mg t.i.d.) led to a small but significant decrease in plasma cortisol (9.4 +/- 0.8 micrograms/100 mg; mean +/- SE, vs. 11.3 +/- 0.7 micrograms/100 ml in controls). The maximum percentage increase of plasma cortisol after ACTH injection was 383% +/- 35% (mean +/- SE) after P and 253% +/- 22% in controls (p less than 0.05). The enhancement of the absolute and relative increase of plasma cortisol after ACTH injection seems to be mainly due to lowering of basal cortisol levels, since the effect of ACTH on plasma cortisol in normal subjects in inversely related to basal cortisol. The effect of metoprolol on basal cortisol and the cortisol response to ACTH was less pronounced than that of P. In the long-term-infusion study the effect of P was less apparent than in the acute study. P had no significant effect on basal plasma aldosterone or on the aldosterone response to ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1983

Inhibition of prostaglandin synthetases derived from neuronal and glial cells and rat renal medulla by ortho-, meta- and para-substituted aminophenolic compounds.

Acetophenetidines, acetamidophenols, phenetidines and aminophenols substituted in o-, m- or p-position inhibit prostaglandin-synthetases originating from C 1300 mouse neuroblastoma cells (clone N2A), rat astrocytoma cells (clone C 6) and rat renal medulla. Desacetylated compounds were more potent inhibitors than their corresponding acetyl derivatives and many o- and m-analogues were more active than p-substituted structures like paracetamol (p-acetamidophenol) or phenacetin (p-acetophenetidine). When twelve o-, m- or p-aminophenolic test compounds were compared to acetylsalicyclic acid and indomethacin, o-, and p-phenetidine and o-aminophenol were as effective as acetylsalicyclic acid. All aminophenol derivatives which inhibited prostaglandin synthesis suppressed cultured nervous cell and kidney cyclo-oxygenases to similar extents. Our results suggest that aminophenolic drugs are not more effective against prostaglandin-synthetases in the CNS than against those in the periphery.

Acetaminophen↗
PubMed1983

Decreasing inhibitory potency of prostaglandin synthetase inhibitors during their cooxidative metabolism. Studies on aminophenols, pyrazolon derivatives and 1,3-diphenylisobenzofuran.

A variety of prostaglandin synthetase inhibitors are cooxygenated during arachidonic acid peroxidation catalyzed by rat renal medulla prostaglandin synthetase or soybean lipoxygenase. Phenylbutazone, aminopyrine, 1,3-diphenylisobenzofuran, paracetamol, p-aminophenol, p-phenetidine and other o- and m-substituted aminophenol derivatives were cooxygenated, whereby prostaglandin synthetase inhibition was significantly weakened due to the formation of less inhibitory metabolites. In contrast, the inhibitory potency of diclofenac, indomethacin and phenacetin and its analogues remained unchanged during prostaglandin synthesis inhibition, because these compounds were no suitable cooxygenation substrates. Evidence is given that quinone imines may not be involved in the cooxidative metabolism of paracetamol and other aminophenols. As to the mechanisms of cooxygenation of suitable substrates dependent on their chemical structures either the arachidonic acid oxygenase or the subsequent hydroperoxidase reaction may trigger the oxygenation. 1,3-Diphenylisobenzofuran is metabolized during the formation of arachidonic acid hydroperoxides in contrast to paracetamol, which requires an additional peroxidase reaction to yield reactive metabolites.

Acetaminophen↗
PubMed1982

Inhibitory actions of desacetylation products of phenacetin and paracetamol on prostaglandin synthetases in neuronal and glial cell lines and rat renal medulla.

The inhibitory actions of phenacetin and paracetamol and of their desacetylation products on prostaglandin synthesis were studied on enzyme preparations originating from a neuronal cell line (mouse neuroblastoma, clone N2A), a glial cell line (rat astrocytoma, clone C6) and rat renal medulla. All compounds tested inhibited cultured cell and kidney prostaglandin synthetases to similar extents. p-Phenetidine and p-aminophenol, the desacetylated metabolites of phenacetin and paracetamol, were either 7-10 times or 4 times more potent than paracetamol. Thus, p-Phenetidine inhibited prostaglandin synthesis as efficaciously as did acetylsalicylic acid. The possible roles of p-phenetidine as the active metabolite of phenacetin for cyclo-oxygenase inhibition in brain and of phenacetin as an organ pro-drug are discussed.

Acetaminophen↗
PubMed1982

Soybean lipoxygenase-1 inhibition by ketone hydrazones.

Acetone phenylhydrazone has recently been discovered as a predominant inhibitor of arachidonic acid lipoxygenase in platelets [1]. We found that besides this compound a variety of hydrazones derived from other ketones and hydrazines exhibited similar or more interesting inhibition patterns both against soybean lipoxygenase and rat renal prostaglandin synthetase. Depending on their molecular structure, relatively selective inhibitors of the two arachidonate peroxidation pathways are introduced which may be useful tools for further investigation of the fatty acid oxygenation cascade.

Animals↗
PubMed1982

The effect of captopril on renin, angiotensin II, cortisol and aldosterone during ACTH-infusion in man.

Prolonged low-dose ACTH infusion (5 or 10 iU/24h) leads to a transient increase in plasma renin activity and angiotensin II concentration in normal man. In order to find out whether the increase in angiotensin II stimulates aldosterone secretion, 12 normal men received ACTH (10 IU/24h) for 34 hours altogether, 6 with and 6 without simultaneous administration of captopril, 50 mg every 6 hours. Captopril prevented the increase in plasma angiotensin II during ACTH infusion and lowered its levels below those on the control day two hours after a new dose of the converting enzyme inhibitor was given. The increase in plasma cortisol was similar in both groups. The increase in plasma aldosterone was significantly blunted by captopril. The early blood pressure rise and the kaliuresis during ACTH infusion were also significantly decreased in the captopril group. These results suggest that angiotensin II mediates in part the effect of ACTH on aldosterone and blood pressure during the first 2 days of infusion. Since captopril reduced plasma angiotensin II for some time below normal, it is alternatively possible that ACTH requires normal plasma angiotensin II levels for a full effect on aldosterone secretion.

Adrenocorticotropic Hormone↗
PubMed1982

[Penetrating thoracic and abdominothoracic wounds. Results of treatment in 221 cases (author's transl)].

Overall mortality after treatment of 221 thoracic or abdominothoracic wounds was 5 p. cent in a recent series, mortality from bullet wounds being the double of that from other weapons. Isolated thoracic wounds without cardiac lesions have a good prognosis, whereas mortality after heart or abdominothoracic wounds remains high (12.5 p. and 14 p. cent respectively). Apart from those with severe hepatic injuries or wounds of the suprahepatic veins, most of the injured patients that died were in cardiac arrest on arrival. Different therapeutic attitudes are necessary for pure thoracic wounds and those involving the abdominothoracic region. It is essential to gain as much time as possible at all stages, particularly during transport of the injured and when deciding the course of treatment, to avoid losing patients with curable lesions.

Abdominal Injuries↗