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Biomedical subjects

W Heller

Publications and source records attributed to W Heller.

At least 91 records · Page 5Linked to original sources
PubMed1988

[Changes in the kallikrein-kinin and complement system in angiography using non-ionic contrast media].

To examine alterations of the kallikrein-kinin system and of the complement due to the bolus injection of newer non-ionic contrast agents, venous blood samples were taken before and 3 min after angiography. There were no adverse contrast reactions clinically evident. Prekallikrein, kallikrein inhibition, beta-factor XIIa inhibition, C1-esterase inhibitor, C1q, C3, ATIII, HMW-kininogen, fibrinogen and factor XII were determined. Bolus injection of the contrast medium caused an activation of the kallikrein-kinin system (p less than 0.05) with reduction of prekallikrein, kallikrein-inhibition, beta-factor XIIa inhibition and C1-esterase inhibitor. The levels of C1q and C3 were also decreased (p less than 0.05) indicating an activation of the complement. Our results demonstrate, that angiography causes a significant activation of the kallikrein-kinin as well as of the complement system in spite of the use of newer non-ionic contrast agents.

Angiography↗
PubMed1988

[Activation of the kallikrein-kinin system by intravenous administration of ionic and non-ionic radiographic contrast media].

Conventional ionic contrast media (sodium meglumine and amidotrizoate) were injected intravenously in 22 patients (group A); the nonionic, low-osmolar contrast medium iohexol was similarly administered to 24 patients (group B). This resulted in a significant (group A: P less than 0.05; group B: P less than 0.01) reduction in prekallikrein (93 and 94%, respectively), inhibition of kallikrein (90 and 88%), beta-factor XIIa inhibition (86 and 85%), and C1 inhibition (90 and 91%). Factor XII levels remained unchanged in both groups. These results indicate that the kallikrein-kinin system is activated even during routine, complication-free radiographic procedures involving contrast-media injection. There was no difference between ionic and nonionic contrast media.

Complement C1 Inactivator Proteins↗
PubMed1988

A modification of Reiber's laser-nephelometric protein determination method interferences of selected substances.

A modification of Reiber's laser-nephelometric protein quantitation method is described. Salts, (zwitterionic) buffers, sugars, chelating and reducing agents do not interfere with this method. Protein quantitation in the presence of Percoll or nonionic detergents yields erroneous results. The method is compared with two modifications of Lowry's protein determination.

Indicators and Reagents↗
PubMed1987

Red blood cell T-activation and hemolysis in surgical intensive care patients with severe infections.

The exposure of Thomsen-Friedenreich (T) antigens on RBCs, serum neuraminidase, and serum hemoglobin levels were investigated in 53 adult surgical intensive care unit (ICU) patients with septicemia. Unmasked T-antigens were assayed by a hemagglutination test using peanut agglutinin (PNA) (direct anti-T test), and by an indirect anti-T test employing rabbit anti-PNA globulin. RBC T-activation was demonstrated in 17/53 patients (32%); in 2/53 patients (4%) the direct anti-T test was positive, indicating strong T-exposure. No polyagglutination phenomena were observed. Serum neuraminidase was elevated in 12/17 (71%) patients with T-activation and in 7/36 (19%) patients without T-activation. Free serum hemoglobin was elevated in 12/17 (71%) patients with T-activation and in 5/36 (14%) patients without T-activation. Correlations between T-activation and serum neuraminidase and between T-activation and serum hemoglobin were significant (p less than 0.001). Potentially neuraminidase-releasing bacteria were demonstrated in 13/17 (76%) patients with RBC T-exposure. We conclude that neuraminidase-induced RBC T-activation and subsequent hemolysis may be involved in the pathomechanism of hemolytic anemia in patients with severe infections.

Adult↗
PubMed1987

Chlorogenic acid biosynthesis: characterization of a light-induced microsomal 5-O-(4-coumaroyl)-D-quinate/shikimate 3'-hydroxylase from carrot (Daucus carota L.) cell suspension cultures.

Microsomal preparations from carrot (Daucus carota L.) cell suspension cultures catalyze the formation of trans-5-O-caffeoyl-D-quinate (chlorogenate) from trans-5-O-(4-coumaroyl)-D-quinate. trans-5-O-(4-Coumaroyl)shikimate is converted to about the same extent to trans-5-O-caffeoylshikimate. trans-4-O-(4-Coumaroyl)-D-quinate, trans-3-O-(4-coumaroyl)-D-quinate, trans-4-coumarate, and cis-5-O-(4-coumaroyl)-D-quinate do not act as substrates. The reaction is strictly dependent on molecular oxygen and on NADPH as reducing cofactor. NADH and ascorbic acid cannot substitute for NADPH. Cytochrome c, Tetcyclacis, and carbon monoxide inhibit the reaction suggesting a cytochrome P-450-dependent mixed-function monooxygenase. Competition experiments as well as induction and inhibition phenomena indicate that there is only one enzyme species which is responsibl for the hydroxylation of the 5-O-(4-coumaric) esters of both D-quinate and shikimate. The activity of this enzyme is greatly increased by in vivo irradiation of the cells with blue/uv light. We conclude that the biosynthesis of the predominant caffeic acid conjugates in carrot cells occurs via the corresponding 4-coumaric acid esters. Thus, in this system, 5-O-(4-coumaroyl)-D-quinate can be seen as the final intermediate in the chlorogenic acid pathway.

Carbon Monoxide↗
PubMed1987

[Complement activation after the intravascular administration of contrast media: a comparison between ionic and nonionic x-ray contrast media].

The effects of intravascular radiographic contrast media on the complement system were investigated in 46 patients. An ionic (sodium-/meglumine amidotrizoate, n = 22) or a non-ionic (iohexol, n = 24) contrast agent was applied for an i.v. urography. The levels of the complement-compounds C1q, C3, C5 and of the C1 inhibitor were determined at the end of the infusion and 20 minutes later. In both groups we obtained a significant (p less than 0.01) decrease of C3 during infusion for 10 to 15%. 20 minutes later these values were almost normalized again. Infusion of iohexol additionally caused a marked consumption of C5 and C1q (reduction to 85%), while the ionic contrast agent had no significant effect on these components. Both contrast media caused a decrease of the C1-inhibitor levels. Our results demonstrate an activation of the complement system by i.v. application of radiographic contrast media. The decrease of the C1q-level due to infusion of iohexol indicates an additional involvement of the classical activation pathway of the complement cascade.

Complement Activating Enzymes↗
PubMed1987

Studies on the interference of selected substances with two modifications of the Lowry protein determination.

Two modifications of Lowry's procedure (Markwell's and Kresze's) were investigated for interference by zwitterionic buffers) (HEPES, HEPPS, PIPES, MES, MOPS, CHES, CAPS, Tris, glycylglycine, bicine), detergents (Triton-X-100, digitonin), sugars (sucrose, mannitol, sorbitol), salts (NaCl, KCl, ammonium acetate), chelators (EDTA), and reducing agents (dithiothreitol, GSH, ascorbic acid). The degree and type of interference are presented, and possible means of elimination of interference are discussed.

Buffers↗
PubMed1986

Function and energy-rich phosphate content of the hypertrophied ventricle after global ischemia and reperfusion.

Using an isolated rat heart preparation (Langendorff perfusion, perfusion pressure 100 cm H2O) the response of the hypertrophied heart (spontaneous hypertensive rats lv/bw ratio 3.6 +/- 0.5) to global normothermic (30 min) and hypothermic (25 degrees C, 120 min) ischemic and cardioplegic arrest and reperfusion (30 min) was examined and compared with normal hearts (Wistar rats lv/bw ratio 2.0 +/- 0.3). St. Thomas solution and verapamil (2 mg/l Ringer solution) were used as cardioplegic agents. Before ischemia hypertrophied hearts had a significantly higher pressure-rate product, a lower myocardial perfusion/g myocardium and a lower myocardial ATP and adenine nucleotide content. Unmodified ischemia reduced myocardial function in the hypertrophied hearts to a greater degree than in normal hearts in both normo- and hypothermia. St. Thomas solution and verapamil protected significantly the myocardial function in the normal and hypertrophied heart after normothermic ischemia in a similar manner (60-70% of the initial value). In the hypertrophied ventricle ATP decay and adenine nucleotide loss was greater in verapamil than in St. Thomas solution treated hearts. In hypothermic ischemia only St. Thomas solution protected left ventricular function and adenine nucleotide loss in both normal and hypertrophied hearts. Verapamil was ineffective in the normal ventricle and protected left ventricular function but not the ATP and adenine nucleotide decay in the hypertrophied heart.

Animals↗
PubMed1986

[Hemostaseologic study in the use of midazolam-ketamine].

The combination of derivatives of benzodiazepine and analgetics is used now routinely in clinical situations. In former investigations we studied the effect of these drugs on substrates and enzymes of glycolysis and metabolism of lipids, whereby we focused our interest on changes of phosphofructokinase activity. The aim of this study was to monitor the influence of anaesthesia on parameters of haemostasis (Kallikrein-kinin-system, coagulation, fibrinolysis and several proteinase inhibitors). Therefore plasma samples of patients undergoing diagnostic endoscopy were analysed. For anaesthesia a combination of midazolam and ketamine was used.

Adolescent↗