Biomedical subjects
Publications and source records attributed to G Hauser.
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The mechanism underlying the alteration of phospholipid metabolism in rat pineal gland in vitro produced by propranolol and tertiary amine local anesthetics was investigated. 0.1 mM propranolol did not affect either the levels or specific activity of [32P]ATP in glands. In the presence of the drug, the incorporation of cytidine, but not of inorganic phosphate, into phosphatidyl-CMP (CDP-diacylglycerol) was dependent on the cytidine concentration. The incorporation of glycerol into phosphatidyl-CMP, phosphatidylinositol and phosphatidylglycerol was enhanced by propranolol, whereas labeling of phosphatidylcholine was decreased. When both 1 mM propranolol and 1 mM inositol were present, labeling of phosphatidylinositol was further increased, stimulation of phosphatidyl-CMP and phosphatidylglycerol labeling was reduced and incorporation into phosphatidylcholine and triacylglycerol was depressed. The incorporation of [3H]inositol into pineal lipids was also enhanced by propranolol. 10 microM propranolol inhibited rat liver phosphatidic acid phosphohydrolase by 50%, while local anesthetics were less potent in the decreasing order: dibucaine greater than tetracaine greater than lidocaine greater than procaine. The propranolol-induced accumulation of phosphatidyl-CMP was prevented by supplying adequate freely diffusible inositol in the medium. The phosphatidyl-CMP which accumulated was not utilized for the enhanced formation of phosphatidylinositol brought about by norepinephrine. The results indicate that propranolol and local anesthetics redirect pineal phospholipid metabolism in part by inhibition of phosphatidic acid phosphohydrolase.
Familial prevalence of some congenital cardiopathies leads to the conclusion that genetic factors might be involved. The case histories are presented of three families with atrial septal defect, Type II (ASD II) in which autosomal dominant inheritance was assumed on account of the pedigree analysis. Each family member was examined serologically, morphologically and morphometrically. One family was also tested for cytogenetic abnormalities. It is highly probable that the gene responsible for the defect is linked to the HLA system (Lod score = + 3.612) and is, therefore, located on the short arm of chromosome 6. The morphological examinations demonstrated uniformity of individual ear traits in related patients; moreover, the palmar dermatoglyphics showed a tendency to shortening of main line C, to ulnar and distal shifting of the carpal triradius and to an increase in hypothenar patterns. In addition a study was carried out of patients with apparently sporadic cardiopathy. A similar trend as to palmar configuration was observed. An attempt was made to connect known factors causing malformations with the results of this investigations.
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A procedrue is described for the preparation of [32P]phosphatidyl-CMP(CDP-diacylglycerol) from rat pineal glands incubated with [32P]orthophosphate and DL-propranolol. The product is 95% radiopure and a high specific acitivity. The yield of liponucleotide is 0.4--0.9 micron Ci/mCi of [32P]orthophosphate in the medium. The same method can also be used for the biosynthesis and purification of [3H]phosphatidyl-CMP when [3H]cytidine is the precursor.
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CDP-diglyceride, an important metabolic intermediate in the biosynthesis of phospholipids, has been isolated for the first time from a mammalian tissue. The isolated material, labeled in incubations of intact rat pineal glands with 32P, [3H]cytidine, or [3H]CTP in the presence of DL-propranolol, was chromatographically identical with authentic CDP-diglyceride and was able to serve as phosphatidyl donor in the enzymatic synthesis of phosphatidylinositol and phosphatidyglycerol. It yielded the expected products upon enzymatic and chemical degradation. No dCDP-diglyceride was detected No radioactive CDP-diglyceride was detected following incubations in the absence of propranolol. Stimulation of CDP-diglyceride labeling from 32P1 occurred at propranolol concentrations between 0.03 and 1.0 mM. Net synthesis of the liponucleotide was shown. At 0.1 mM, propranolol incrased the incorporation of radioactivity into phosphatidylglycerol, phosphatidylinositol, and phosphatidic acid. When inositol (10 mM) and propranolol (0.1 mM) were both present, phosphatidylinositol labeling was further increased, wheas stimulation of phosphatidylglycerol and CPD-diglyceride labeling was abolished. Since CDP-diglyceride did not accumulate in the absence of the drug, its availability may normally be the limiting factor in phosphatidylinositol and phosphatidylglycerol biosynthesis. When propranol is present, inositol may become limiting and thus may lead to the observed labeling pattern.
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