Microdetermination of the prostaglandin B1 in human plasma by gas chromatography/selected ion monitoring using [18O]prostaglandin B1 as an internal standard.

We devised a simple and effective purification for the microdetermination of prostaglandin B1 (PGB1), a metabolite of PGE1. [18O]PGB1 was synthesized by the repeated base-catalyzed hydrolysis of methyl ester derivatives in H(2)18O, to obtain an internal standard for the gas chromatography/selected ion monitoring (GC/SIM) of PGB1. The methyl ester-methoxime-dimethylisopropylsilyl ether derivative was prepared, then GC/SIM was carried out by monitoring the ion at m/z 448.3 for PGB1 and that at m/z 452.3 for internal standard. A good linear response over the range of 10 pg to 100 ng was demonstrated. We detected PGB1 to a level of about 40 pg/mL in human plasma. This method can be used to determine PGB1 in biological samples.

Relationships of prostaglandin levels and natural killer (NK) cell cytotoxicity of mononuclear cells in cord blood.

Natural killer cell cytotoxicity of mononuclear cells and the corresponding plasma prostaglandins were examined in cord blood. Low NK cell cytotoxicity was demonstrated against three target cells: NK(K562), NK(HSV-1) and NK(Fs). Prostaglandins of the B, E and F series were examined and found to be higher than adult values. A significant correlation (p less than 0.05) between NK cell cytotoxicity and the prostaglandin F series was demonstrated.

[Behavior of several prostaglandins (PGA, PGB, PGE 1, PGE 2, PGF 1, PGF 2) in normal and leukemic leukocytes. Radioimmunological method on intact cells]. / Comportamento di alcune prostaglandine (PGA, PGB, PGE 1, PGE 2, PGF 1, PGF 2) nei leucociti normali e leucemici. Metodo radioimmunologico su cellule integre.

The behaviour of prostaglandins A, B, E 1, E 2, F 1 and F 2 has been examined in the granulocytes and lymphocytes of the peripheral blood of normal subjects and in circulating leucocytes of patients with CML, AML, CLL and ALL. At the same time, modifications of PGE 2 in the granulocytes of normal subjects and in patients with CML or AML before and after phagocytosis of latex particles were monitored. The general observation was a lowering in PGE and PGF in acute myeloid and lymphatic leukaemia, while the variations in CML and CLL were rather complex. Also observed was a reduction in PGE 2 in AML but not in CML, including a reduced response to phagocytosis in granulocytes. The data are compared with previous reports of AMPc and GMPc in the same cells and commented on, taking into consideration their possible reflexion on the proliferative and functional activity of the cells examined.

Distribution of prostaglandins B, E and F series in plasma of cancer patients.

Plasma prostaglandins (PGs) of normal individuals and cancer patients have been examined. With the exception of a breast carcinoma patient, all patients demonstrated significant elevations in PGE levels. Lung cancer patients showed a significant decrease in PGF, while stomach cancer patients showed a marked decrease in PGB. It is suggested that the changes in PGs may play a significant role in host-tumor metabolism.

Corticosteroid-induced avascular necrosis: an experimental study in rabbits.

New Zealand white rabbits were divided into 4 groups for the study of the etiology of corticosteroid-induced osteonecrosis (avascular necrosis). Group A and B received intramuscular injections of methylprednisolone acetate and methylprednisolone succinate respectively. Group C, on semirestricted diets, and Group D, on ad libitum diets, were controls. Osteocyte death, necrotic debris and intravascular fat emboli were evident in sections of proximal and distal femur by the 2nd week in experimental animals. Blood analysis revealed elevated lipid and prostaglandin levels. Osteoporosis was first observed at 6 weeks. Evidence of advanced osteonecrosis was present histologically at 18 weeks. It is concluded that osteonecrosis probably develops as the result of the interaction of several corticosteroid-induced alterations, including circulating fat emboli and inflammatory unbound free fatty acids or prostaglandins. Osteoporosis may also be a factor in explaining the sporadic nature of the disorder.

Prostaglandins in renovascular and renal hypertension.

PG A1, B1, E2, F1,2alpha and PRA have been measured in 8 hypertensive patients with unilateral renal arterial stenosis, 7 hypertensive patients with unilateral renal atrophy and 20 control normotensive subjects. PRA and PGA1 were significantly increased in patients with renovascular hypertension but not in patients with atrophy. PGE2 and PGF1,2alpha were increased in both groups of patients, especially on the stenotic or atrophic side. The increase of PGA1 and PGE2, represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF1,2alpha a direct hypertensive mechanism.