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Biomedical subjects

G Baumann

Publications and source records attributed to G Baumann.

At least 343 records · Page 19Linked to original sources
PubMed1982

Insulin resistance and insulin receptors in hepatic cirrhosis.

To explore the influence of extrahepatic factors in the pathogenesis of insulin resistance in hepatic cirrhosis, we studied 125I-insulin binding to erythrocytes and monocytes of 14 clinically stable cirrhotic individuals and compared the results with a normal control group. All patients had fasting normoglycemia at the time of the study but abnormal glucose tolerance was detected in 7 of 9 cirrhotic patients after an oral glucose load. Seven patients (group N) had normal fasting serum insulin levels, and 7 patients (group H) manifested fasting hyperinsulinemia. However, all patients had elevated insulin levels after oral glucose. Insulin binding to erythrocytes was significantly decreased in both cirrhotic subgroups; monocyte studies in 5 hyperinsulinemic patients revealed a similar decrease in binding. Scatchard analysis in monocytes suggests that this decreased binding is secondary to a decrease in the receptor number per cell. No correlation between insulin binding and fasting plasma insulin, glucagon, or growth hormone levels was seen. Sera from 4 patients were examined for the presence of a non-specific inhibitor of insulin binding, but no evidence for such a factor was found. We conclude that the decrease in insulin binding is mediated in the monocyte by a reduction of receptor concentration; in the erythrocyte the mechanism for decreased binding could not be clearly delineated. The insulin resistance seen in cirrhosis may result in part from decreased binding of insulin to target tissues; an additional postreceptor defect cannot be excluded in hyperinsulinemic individuals.

Adult↗
PubMed1981

Cardiac contractile and metabolic effects mediated via the myocardial H2-receptor adenylate cyclase system. Characterization of two new specific H2-receptor agonists, impromidine and dimaprit, in the guinea pig and human myocardium.

The present study chartacterizes myocardial effects of two new histaminergic H2-receptor specific compounds, impromidine, and dimaprit, on cardiac contractile and metabolic parameters of the guinea pig heart and human papillary muscle in comparison to the well-known effects of catecholamines. Impromidine and dimaprit produced a dose-dependent stimulation of the right and left ventricular contractile force in the isolated perfused biventricular catheterized guinea pig heart with maximal stimulation rates equal to those of isoproterenol. Hemodynamic equieffective doses of isoproterenol (2.8X10(-9) mol/l), histamine (1.1X10(-5) mol/l), impromidine (4.6X10(-7) mol/l, and dimaprit (8.5X10(-6) mol/l) induced nearly identical increases in tissue concentrations of c-AMP. All compounds dose-dependently enhanced the activity of the myocardial adenylate cyclase with very similar KA-values in a particulate sarcolemmal membrane preparation of both guinea pig ventricles and human papillary muscles. No effect of either compound was seen on cardiac phosphodiesterase activity. Selective administration of the beta1-blocking agent metoprolol and the H2-receptor antagonist cimetidine clearly discriminates two independent receptors linked to the sarcolemmal adenylate cyclase system in the guinea pig and human myocardium. This is further supported by results obtained from beta-receptor-binding studies in which an interference of impromidine and dimaprit with the stereospecific binding of (-)[3H]-dihydroalprenolol to cardiac beta-receptors could be definitely excluded. The possible therapeutic role of both H2-agonists on the non-ischemic, surviving myocardium, which is transiently refractory to beta-adrenergic stimulation by catecholamines after myocardial infarction, will be discussed.

Adenylyl Cyclases↗
PubMed1981

Impaired beta-adrenergic stimulation in the uninvolved ventricle post-acute myocardial infarction: reversible defect due to excessive circulating catecholamine-induced decline in number and affinity of beta-receptors.

Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to isoproterenol was tested in the isolated perfused heart preparation. Adenylate cyclase activity, phosphodiesterase activity, and beta-receptor binding characteristics were determined in a sarcolemmal preparation of the right ventricle of the same hearts. Three days post-AMI the dose-response curve for isoproterenol of right ventricular dP/dtmax was significantly depressed, while the inotropic effect of histamine was not impaired. Stimulation of adenylate cyclase activity by isoproterenol was reduced by 70% in the membrane preparation, whereas histamine and NaF stimulation rates were unaltered; phosphodiesterase activity was unchanged. In contrast, beta-receptor binding studies with [3H]-DHA1 indicated 74% loss and 10 times lowered affinity (KD) of the remaining beta-receptors, while specific [3H]-QNB1 binding was unchanged. All of the above alterations were prevented by pretreatment with reserpine or metoprolol. It is concluded that these abnormalities in the nonischemic surviving myocardium post-AMI are the result of specific reversible damage of sarcolemmal beta-receptors due to excessive levels of circulating catecholamines.

Adenylyl Cyclases↗
PubMed1981

Experimental evidence consistent with aggregation kinetics in the sodium current of Myxicola giant axons.

Aggregation kinetics, in contrast to the Hodgkin-Huxley equations, predict that if an axon is subjected to a brief perturbing depolarization of large amplitude, the resulting perturbed current will cross over the response to a conventional maintained depolarization, and then remain smaller for the remainder of the depolarizing step. This has been experimentally tested using voltage-clamped Myxicola giant axons, compensated for series resistance and bathed in 10% Na+ sea water to minimize possible artifacts. Under such conditions perturbed and unperturbed currents are observed to cross over in a manner qualitatively consistent with the behavior predicted by an aggregation model. We suggest, therefore, that the aggregation concept may warrant further experimental and theoretical investigation.

Animals↗
PubMed1981

Isolation of human growth hormone isohormones D and E in milligram amounts (I), using isotachophoresis on polyacrylamide gel.

Human growth hormone (hGH) isohormones D and E were isolated from a plasmin digest of 150 mg hGH. Isotachophoresis on a cylindrical polyacrylamide gel of 18 mm diameter served to separate the various isohormone species. The "extended stack" was sliced, and slices containing hGH-D and -E were extracted by Steady-State Stacking on 1% agarose gel and collected in a 1 ml volume. The extract was purified on gel chromatography and lyophilized. The overall yield was approximately 19 mg of hGH (D + E) and 16 mg of hGH-(D, minor E). This represents a 62% recovery of the amount of hGH-D and -E in the digest estimated densitometrically. The purity of the product, based on Lowry analysis, specific RIA or UV-absorbance, was 91%. The isolated hGH-(D+E) exhibited an enhanced bioactivity in the rat tibia line assay.

Animals↗
PubMed1981

Inhibitory action of adenosine on histamine- and dopamine-stimulated cardiac contractility and adenylate cyclase in guinea pigs.

Infusion of adenosine into the coronary arteries of isolated guinea pig hearts produced a dose-dependent inhibition of cardiac contractile force development elicited by bolus injections of histamine (7.5 X 10(-9) mol) or dopamine (1.5 X 10(-8) mol). Threshold concentration of adenosine was 10(-7) M and maximal inhibition (90%) was obtained at 3 X 10(-5) M. Adenosine in the effective concentration range did not alter Ca2+-induced increases in contractile force. The rise in tissue levels of cAMP induced by equieffective doses of histamine (7.5 X 10(-9) mol) and dopamine (1.5 X 10(-8) mol) was inhibited by adenosine (3.5 X 10(-5) M) by about 60%. In a particular membrane preparation of guinea pig ventricles the adenylate cyclase activity stimulated by the histamine (10(-5) M) and dopamine (10(-4) M) was inhibited in a dose-dependent manner by adenosine. This effect could be reversed by theophylline (5 X 10(-5) M) in a competitive manner. The hormone-insensitive adenylate cyclase of a Lubrol-PX solubilized membrane preparation stimulated by NaF or 5'-guanylylimido-diphosphate (GppNHp) was also inhibited by adenosine (40% and 90% inhibition at 10(-5) M and 10(-4) M, respectively). Adenosine did not influence the Km value of the adenylate cyclase for ATP, but markedly lowered Vmax of the enzyme. From additional studies with purine-substituted (N6-methyl-adenosine, N6-phenylisopropyl-adenosine) and ribose-substituted (2'-deoxy-adenosine and arabino-furanosyl-adenine) adenosine analogues, we conclude that adenosine may inhibit the inotropic responses to hormones as well as the adenylate cyclase activity by specifically interacting with at least two different sites associated with the adenylate cyclase.

Adenosine↗
PubMed1981

Hepatic insulin and glucagon receptors in pregnancy: their role in the enhanced catabolism during fasting.

The response to dietary deprivation in late pregnancy, as compared to the non-pregnant condition, is more rapid and profound in terms of mobilization of fuels frm peripheral tissues as well as hepatic ketogenesis and gluconeogenesis ("accelerated starvation"). We examined the potential role of hepatic insulin and glucagon receptors in mediating these changes by comparing 48-h fasted 18-day pregnant and age-matched nongravid rats. Molar ratios for insulin:glucagon in peripheral and portal blood were significantly higher in the pregnant rats. Insulin binding to purified liver plasma membrane receptors, when appropriately corrected for differences in insulin degradation by the membrane system, was marginally diminished in the pregnant animals. Glucagon binding and adenylate cyclase activation by glucagon was indistinguishable in the two groups of animals. On the basis of portal vein hormone concentrations and the values for receptor binding, liver insulinization relative to glucagonization appears to be unchanged or slightly increased in the fasted pregnant rat compared to the fasted nongravid rat. Thus, it seems unlikely that much of the "accelerated starvation" response in late pregnancy can be ascribed to diminished insulin and/or increased glucagon availability at the hepatocellular level. Instead, it is hypothesized that postreceptor events play the major role in sustaining the intrahepatic realignments of established fasting in late pregnancy.

Adenylyl Cyclases↗
PubMed1980

[Technic of venous access for infusion therapy and parenteral nutrition].

The creation of a secure venous access is the basis of the infusion therapy and the parenteral nutrition. As ways of access are suited above all the subclavian vein, the internal jugular vein and the basilic vein. Taking into consideration the contraindications and the exact performance of the various methods early complications such as punctures of the arteries, pneumothorax, rupture of the catheter and extended haematomata may be reduced to a minimum. Abnormal positions are avoided by control of the position by means of endo-ECG via steel mandrin. As late complications are observed infections at the place of puncture, unclear, partly septic temperatures and clinically manifest thromboses. Own experiences with 3,282 central venous catheters (2,057 subclavian catheters, 63 catheter into the internal jugular vein and 1,162 central catheters with access via arm veins) are taken into consideration.

Catheterization↗
PubMed1979

Metabolic clearance rates of isohormones of human growth hormone in man.

The charge isomers of human GH (/GH), isohormones C, D, and E, which result from limited proteolytic cleavage exhibit enhanced biological activity in the rat and in man compared to the intact polypeptide and most abundant form, isohormone B. The mechanism leading to enhanced activity is unknown. To examine the possibility that different in vivo metabolism may represent one such mechanism, the MCRs of radioiodinated hGH-B, -C, and -D were measured in seven normal adults. Significant differences in metabolic clearance were found between isohormones (hGH-B, 108.4; hGH-C, 67.9; hGH-D, 55.7 liters/m2-day). It is concluded that in man, the enzymatically cleaved hGH isohormones are cleared more slowly than hGH-B. Slower metabolism may be a factor responsible for the enhanced biological activity of proteolytically cleaved hGH isohormones.

Adult↗
PubMed1979

[Studies of necrotizing enteritis of suckling piglets (Cl. perfringens typc C enterotoxemia) in industrialized sow breeding units. 3. Experimental reproduction of the disease].

Experimental reproduction of necrotising enteritis of sucking pigs was successfully achieved by using both Clostridium perfringens Type C strains, which had been isolated from sucking pigs with necrotising enteritis, and Type C strain 3628 of A.T.C.C. (sub-type C1). The lethal dose for sucking pigs was between 20 X 10(6) and 12 X 10(7) pathogens per animal. The disease could not even be induced by repeated application of no-bacterial toxin of Cl. perfringens Type C nor by administration of Cl. perfringens Type A strains which had been cultured from broilers with necrotising enteritis. Necrotising enteritis was found to develop in two phases in sucking pigs. First, the pathogen will deposit to the villous epithelium and then penetrate the superficial strata of the mocous membrane. In the second phase, the villous structure will be destroyed by the lethal, haemolysing, and necrotising toxins of Cl. perfringens. The role played by individual toxin fractions is discussed together with the importance of humoral and localised infection defence. Sucking pigs may be sufficiently protected against infection based on single or ten-fold lethal infectious dosage by two vaccinations of the mother animal, five and three weeks prior to parturition, using "Enterotoxaemia Vaccine Dessau bivalent". Infection then would not occur unless a hundredfold lethal dose was applied. Characteristics include diarrhoea, apathy, exhaustion, and death.

Animals↗