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Biomedical subjects

J Svensson

Publications and source records attributed to J Svensson.

At least 127 records · Page 7Linked to original sources
PubMed1979

Structure and quantitative determination of the major urinary metabolite of thromboxane B2 in the guinea pig.

2,3-Dinor-thromboxane B2 was the major urinary metabolite of thromboxane B2 in the guinea pig. The structure was assessed mainly by mass spectrometric analysis of a number of derivatives of the metabolite and by chemical degradation by oxidative ozonolysis. A method for quantitative determination of 2,3-dinor-thromboxane B2 in guinea pig urine based on multiple ion analysis and octadeuterated 2,3-dinor-thromboxane B2 as internal standard was developed. The basal excretion of the metabolite was 65 +/- 36 (S.D.) ng/kg x 24 h (n = 19; range 19--140 ng). This level corresponded to an endogenous synthesis of 543 +/- 300 ng of TXB2. No increase in the excretion was seen after anaphylaxis, in contrast to what has earlier been reported for PGF2 alpha.

Anaphylaxis↗
PubMed1979

Male hypospadias, 625 cases, associated malformations and possible etiological factors.

Records from 625 patients with hypospadias have been reviewed, with reference to associated malformations. Cryptorchidism was found to be the most common associated malformation and was present in 6% of cases with hypospadias. The highest incidence of cryptorchidism was found in the more severe forms of hypospadias. Other concomitant genital malformations, such as bifid scrotum, hypoplasia of penis and remnants of the Müllerian system showed the same pattern. The recorded incidence of bifid scrotum and hypoplasia of the penis was 4% and 8% respectively. A high incidence of abnormalities in the lower urinary tract was found; 50% of 84 patients investigated. The hypothesis of hypospadias being a result of testicular hormone insufficiency is discussed.

Abnormalities, Multiple↗
PubMed1979

Formation and action of prostacyclin in the isolated human umbilical artery.

The transformation of [1-14C]arachidonic acid by homogenates of human umbilical arteries was studied. The major compound formed was the stable end product of PGI2, i.e. 6-keto-PGF1 alpha (lactol form) as analyzed by gas-liquid chromatography-mass spectrometry. PGI2 was generated by incubating PGH2 with a lyophilized pig aorta microsome preparation. PGI2 concentrations around 10 ng/ml relaxed the human umbilical artery preparation significantly. Formation of PGI2 by umbilical arteries during pregnancy might be a mechanism for regulation of blood flow to the fetus.

Animals↗
PubMed1979

Reduction of androstenedione by skin in vitro and serum levels of gonadotrophins and androgens in men with hypospadias.

The reduction of 4-[1,2-3H]androstene-3,17-dione (androstenedione) in vitro by scrotal skin was measured in samples from nine men (16--34 years old) with hypospadias and from ten male control subjects. The reduction of androstenedione was also studied in axillary and upper arm skin of seven control subjects. Androstenedione was reduced to material with chromatographic characteristics of 5 alpha-androstane-3,17-dione and to 3 alpha- and 3 beta-hydroxy-5 alpha-androstan-17-one. No difference in 5 alpha-reductase activity (defined as the sum of these three metabolites formed) was found in scrotal skin from hypospadic and control men. The mean concentration of 5 alpha-dihydrotestosterone in serum from men with hypospadias was lower than that in serum from control subjects (P less than 0.01). The mean ratio of the serum concentrations of testosterone and 5 alpha-dihydrotestosterone was higher in hypospadic men than in control subjects (P less than 0.05). No differences between the two groups were found in the mean serum concentrations of LH, FSH, prolactin, dehydroepiandrosterone, androstenedione, testosterone or testosterone-binding globulin.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

A method for measurement of platelet regeneration in man.

Platelet suspensions obtained at different time intervals following a single dose of oral aspirin were incubated with [1-(14)C]-arachidonic acid and the amount of [1-(14)C]thromboxane B2 formed was determined by a double isotope technique. Since aspirin is an irreversible inhibitor of platelet cyclooxygenase and since circulating platelets do not synthesize cyclooxygenase the rate of reappearance of active cyclooxygenase determined in this way was a measure of the rate of regeneration of functioning platelets. In two subjects the regeneration half-times were 4.2 and 4.8 days.

Aspirin↗
PubMed1978

Metabolism of androstenedione in skin and serum levels of gonadotrophins and androgens in prepubertal boys with hypospadias.

The metabolism of 4-[1,2-3H]androstene-3,17-dione in the prepuce, axillary skin and skin from the arm was investigated in 27 boys operated for phimosis (controls) and 13 unselected boys with hypospadias (a congenital defect of the male urethra). In all types of skin investigated, androstenedione was metabolized to 5alpha-androstane-3,17-dione, 3alpha-hydroxy-5alpha-androstan-17-one, 3beta-hydroxy-5alpha-androstan-17-one and testosterone. Conversion to testosterone was found in the prepuce of two out of 11 boys with hypospadias. Mild forms of hypospadias in the age group 1--4 years had a higher level of 5alpha-reductase activity in the prepuce than controls in the same age group (P less than 0.05); no such differences were found in the few severe cases of hypospadias in this group. No other differences in 5alpha-reductase activity were found between hypospadic boys and controls. The ratio of 5alpha-reductase activity in the prepuce: 5alpha-reductase activity in skin from the arm was significantly higher (P less than 0.05) in hypospadic boys than in controls in the age group 1--4 years. Serum levels of LH and FSH were the same in normal and hypospadic boys but the concentration of prolactin in the serum was lower in boys with hypospadias compared with control subjects in the age group 1--4 years (P less than 0.005). No differences were found in serum concentrations of androstenedione, testosterone, oestradiol and testosterone-binding globulin.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

Inhibition of platelet aggregation by alpha-tocopherol and its nicotinate and acetate esters.

Two esters of vitamin E, dl-a-tocopheryl nicotinate and dl-a-tocopheryl acetate were found to be more inhibitors than tocopherol itself on platelet aggregation induced by arachidonic acid and collagen. The nicotinate was 1--5 times more potent than the acetate and 2--18 times more potent than the unesterified tocopherol in inhibiting collagen induced aggregation in human citratet platelet-rich plasma.

Arachidonic Acids↗
PubMed1978

Biosynthesis and biological properties of prostaglandin endoperoxides and thromboxane A2.

Two prostaglandin endoperoxides, i. e. PGG2 and PGH2 were detected and isolated. They were unstable in aqueous medium (t1/2 at 37 degrees C about 5 min) and were converted to PGF2alpha by mild reducing agents. Human platelets as well as guinea pig lung and spleen converted the endoperoxides into thromboxane A2, an unstable (t1/2 at 37 degrees C about 30 s) oxetane/oxane derivative. Thromboxane A2 was converted into a stable hemiacetal derivative, thromboxane B2, by addition of 1 H2O. The two prostaglandin endoperoxides as well as thromboxane A2 caused platelet aggregation and the platelet release reaction. In addition they were potent stimulators of vascular and airway smooth muscle in vitro and in vivo.

Animals↗
PubMed1976

Thromboxane A2 and prostaglandin H2: potent stimulators of the swine coronary artery.

Thromboxane A2 was generated by incubation of arachidonic acid with a suspension of human platelets. The filtrate contained 266 +/- 46 ng/ml (n=10) of thromboxane A2 and 25 ng/ml or less of prostaglandin endoperoxides (prostaglandins G2+H2). Thromboxane A2 was 2-10 times more potent than prostaglandin H2 and 9-102 times and 26-308 times more potent than prostaglandins E2 and F2alpha, respectively, in causing contractions of the superfused swine coronary artery.

Animals↗
PubMed1976

On the formation and effects of thromboxane A2 in human platelets.

Incubation of arachidonic acid and prostaglandin G2 with a suspension of human platelets led to formation of an unstable (t1/2, 41+/-7 s) compound, thromboxane A2. Thromboxane A2 induced irreversible aggregation of washed platelets and of platelets in platelet-rich plasma and caused release of serotonin and ADP from platelets in platelet-rich plasma.

Adenosine Diphosphate↗
PubMed1976

Involvement of endoperoxides and thromboxanes in anaphylactic reactions.

Our recent work on prostaglandin endoperoxides in the lung has shown that: 1. The endoperoxides were 5 to 10 times more potent than PGF2alpha in an in vitro preparation of respiratory smooth muscle, i.e., the guinea pig trachea. 2. The endoperoxides were 5 to 10 times more potent than PGF2alpha in causing an increase in tracheal insufflation pressure in the anaesthetized, artificially ventilated guinea pig. 3. Endoperoxides formed from exogenous arachidonic acid in homogenates of guinea pig lung and in intact guinea pig lung were converted to a large extent into metabolites different from the classical prostaglandins, i.e., thromboxane B2 (8-(1-hydroxy-3-oxopropyl)-9-12L-dihydroxy-5,10-heptadecadienoic acid) and HHT (12L-hydroxy-5,8,10-heptadecatrienoic acid). 4. Injection of antigen into sensitized guinea pig lungs caused a significant release of the endoperoxide metabolite, thromboxane B2. PGF2alpha has previously been implicated to be involved in anaphylaxis (14). The findings described above show that the prostaglandin endoperoxides are important not only as precursors of PGF2alpha but also through their own effects on airway smooth muscle. Furthermore, the release of thromboxane B2 indicates that its immediate precursor, the biologically active thromboxane A2 is also formed in this system (15). This compound, which has a half-life of 30 to 40 sec causes platelet aggregation and contraction of the isolated rabbit aorta (15). Work is in progress to study the respiratory effects of thromboxane A2 and its possible role in anaphylactic reactions.

Anaphylaxis↗
PubMed1975

Prostaglandin d2 as a potential antithrombotic agent.

Prostaglandin D2 was found to be a potent inhibitor of platelet aggregation. Aggregation of human platelets by ADP, collagen and prostaglandin G2 was inhibited more strongly by PGD2 than by PGE1. Although ADP-induced aggregation of rabbit platelets was inhibited more strongly by PGE1 than by PGD2 the latter prostaglandin gave a more long-lasting inhibitory effect on platelet aggregation following intravenous or oral administration. These results coupled with the finding that PGD2 has less hypotensive effects on the cardiovascular system than PGE1 suggest the possible use of PGD2 as an antithrombotic agent.

Adenosine Diphosphate↗
PubMed1975

Physiological role of an endoperoxide in human platelets: hemostatic defect due to platelet cyclo-oxygenase deficiency.

The endoperoxide prostaglandin G2 (PGG2) induced platelet aggregation as well as the platelet release reaction (release of ADP and serotonin) when added to human platelet-rich plasma. Formation of a metabolite of PGG2 [8-(l-hydroxy-3-oxopropyl)-9,12L-dihydroxy-5,10-heptadecadienoic acid] and a lipoxygenase product [12L-hydroxy-5,8,10,14-eicosatetraenoic acid] accompanied the release reaction caused by aggregating agents such as collagen, ADP, epinephrine, and thrombin. Indomethacin inhibited the release reaction and PGG2 formation induced by these agents but had no effect on PGG2-induced release reaction. The aggregating effect of PGG2 was abolished by furosemide, which is a competitive inhibitor of ADP-induced primary aggregation. These data indicate that the aggregating effect of PGG2 is due to release of ADP and that PGG2 synthesis is required for induction of the release reaction by various aggregating agents. A subject with a hemostatic defect due to abnormal release mechanism [decreased aggregation with epinephrine (second wave) and collagen and normal platelet ADP] had a deficiency of the cyclo-oxygenase that catalyzes formation of PGG2. Normal aggregation and release reaction were obtained with added PGG2. Ii is concluded that the endoperoxide (PGG2) is essential in normal hemostasis because of its role in initiating the release reaction required for aggregation by collagen and the second wave of aggregation caused by, e.g., ADP.

Adenosine Diphosphate↗