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Biomedical subjects

E Erdmann

Publications and source records attributed to E Erdmann.

At least 307 records · Page 17Linked to original sources
PubMed1988

[Percutaneous transfemoral foreign body removal from the heart or great vessels].

Removal of foreign bodies in the heart or great vessels was attempted via percutaneous transfemoral catheter retrieval system in 32 patients, antibiotic treatment--sometimes continued over many months--having failed to eradicate any septicaemia. In 28 patients it was possible to remove the foreign body with a special basket, forceps or sling catheter retrieval system. Most of the foreign bodies were broken-off pacing electrode fragments (n = 18). The most common site was the right ventricle (n = 15). 28 patients had had recurrent high fever; in 21 of them it was possible to identify the causative microorganism. Any fever ceased abruptly after removal of the foreign body. There were no complications ascribable to the procedure. The results indicate that, after foreign-body embolization, immediate removal is both necessary and possible.

Adolescent↗
PubMed1988

Enhancement of the effectiveness of milrinone to increase force of contraction by stimulation of cardiac beta-adrenoceptors in the failing human heart.

The positive inotropic effect of milrinone was investigated in isolated, electrically driven (1 Hz) human papillary muscle strips from nonfailing myocardium (control) and from patients with moderate (NYHA II-III) and severe (NYHA IV) heart failure. In the control hearts, milrinone increased force of contraction to about the same degree as Ca2+ at 15 mmol/l. In NYHA II-III, the positive inotropic effect was significantly reduced compared with the control hearts. In NYHA IV, the effectiveness (maximal increase in force of contraction) and potency (as judged from the EC50 values) were significantly less than in NYHA II-III and controls. Preexposure of the preparations to isoprenaline in NYHA II-III and NYHA IV shifted the concentration-response curve for milrinone to the left and, moreover, restored the effectiveness of the compound (i.e., similar positive inotropic effect as Ca2+). No difference in the cAMP-phosphodiesterase inhibition by milrinone could be detected between controls, NYHA II-III, and NYHA IV. It is concluded that diminished basal cAMP production is responsible for reducing the effectiveness of milrinone in the failing human heart. A diminished inhibition of cAMP-phosphodiesterase does not play a role. The fact that stimulation of cardiac beta-adrenoceptors increased the effectiveness of milrinone provides evidence that combined application of catecholamines and phosphodiesterase inhibitors may be useful in the treatment of patients with terminal heart failure.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Human colonic (Na+ + K+)-ATPase and specific ouabain binding are not influenced by lipoxygenase products or superoxide radicals.

The effects of lipoxygenase products (5-, 12-, 15-HETE, LTB4) and superoxide radicals on human colonic (Na+ + K+)-ATPase and specific ouabain binding were measured. No significant inhibition in concentrations up to 3 x 10(-5) M was observed. The results are discussed with regard to a possible role of lipoxygenase products and radicals in the pathogenesis of water and electrolyte disturbances in various diarrheal states including inflammatory bowel disease.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

The effectiveness of inotropic agents in isolated cardiac preparations from the human heart.

This review analyses the present knowledge on differences in human and animal heart preparations in respect to positive inotropic stimulation. The pharmacological effects of new positive inotropic drugs usually are evaluated in cardiac preparations from healthy and young animals. Human myocardium, especially from patients with heart failure has, however, distinctly different properties in respect to the positive inotropic effectiveness of several agents. This fact prohibits the extrapolation of results of experiments in laboratory animals to the diseased human heart. The partial ineffectiveness of several established positive inotropic substances in papillary muscles from failing human hearts indicates a membrane defect not present in healthy animal myocardium.

Calcium↗
PubMed1988

Positive inotropic effects of the calcium channel activator Bay K 8644 on guinea-pig and human isolated myocardium.

1. The positive inotropic effects of the dihydropyridine calcium activator Bay K 8644 were studied in guinea-pig isolated contracting myocardium and human papillary muscle strips obtained from patients undergoing mitral valve replacement or cardiac transplantation. 2. Bay K 8644 produced a slowly developing, concentration-dependent positive inotropic response in all cardiac tissues studied. In guinea-pig papillary muscle, the increase in force of contraction was half-maximal at 3.9 x 10(-8) mol/l and the maximal inotropic effect was comparable to that obtained with ouabain, dobutamine or calcium. The guinea-pig left atrium (EC50, 2.1 x 10(-7) mol/l) was fivefold less sensitive than the papillary muscle. 3. The maximal inotropic response to dihydroouabain was significantly increased after preincubation with Bay K 8644 (1 x 10(-6) mol/l) in papillary muscles from both guinea-pig and human. In guinea-pig papillary muscles, the maximal inotropic response to dobutamine was not changed by preincubation with Bay K 8644 whereas in human papillary muscle strips, Bay K 8644 increased the inotropic response to dobutamine. 4. Bay K 8644 increased force of contraction (EC50, 4 x 10(-8) mol/l) in human papillary muscle strips from patients undergoing mitral valve replacement. However, the maximal inotropic response to Bay K 8644 was reduced to 32 +/- 4.4% that of calcium (15 mmol/l) measured in the same muscle strips. 5. A further reduction in maximal inotropic response to Bay K 8644 to 13 +/- 1.2% that of calcium (15 mmol/l) with no change in potency was measured in human papillary muscle strips taken from terminally failing hearts of cardiac transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Properties of cardiac alpha- and beta-adrenoceptors in spontaneously hypertensive rats.

The effects of isoprenaline, Ca2+ and phenylephrine (in the presence of propranolol) on force of contraction were studied in isolated electrically driven papillary muscles of spontaneously hypertensive rats (SHR) and age-matched (14-18 weeks) Wistar Kyoto control rats (WK). Cardiac alpha- and beta-adrenoceptors were characterized by radioligand binding studies. The positive inotropic effect of isoprenaline in SHR was less effective than in control rats. The EC50 values did not differ in both groups. In SHR, isoprenaline was less effective than Ca2+ to increase force of contraction whereas in WK it had the same effectiveness as Ca2+. The positive inotropic effect of phenylephrine in the presence of propranolol was similar in SHR and WK. In SHR, both the densities of cardiac alpha- and beta-adrenoceptors were reduced. In beta-adrenoceptor binding experiments, the nonhydrolysable GTP analog Gpp(NH)p caused a rightward shift of agonist competition curves of isoprenaline. Biphasic competition curves revealed a similar percentage of low and high affinity sites in SHR and WK, respectively. In alpha-adrenoceptor binding experiments, Gpp(NH)p caused no detectable shift of agonist competition curves with norepinephrine. It is suggested that cardiac beta-adrenoceptor down-regulation is involved in the reduced positive inotropic effect of isoprenaline in SHR. Functional uncoupling of beta-adrenoceptors does not appear to be involved in the reduced beta-adrenoceptor-mediated positive inotropism in SHR. Binding studies do not show evidence for a large number of alpha-adrenoceptors coupling to a guanine-nucleotide binding protein in the rat heart. Finally, in ventricular myocardium of SHR, cardiac alpha-adrenoceptors do not serve as a reserve mechanism during impaired beta-adrenergic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Inverse relationship between colonic (Na+ + K+)-ATPase activity and degree of mucosal inflammation in inflammatory bowel disease.

In inflammatory bowel disease (IBD), mucosal damage and loss of colonic function are regarded as major consequences of inflammation. Decreased colonic (Na+ + K+)-ATPase activities with diminished reabsorption of sodium and water have been found in active stages of ulcerative colitis. In this study, we report an inverse relationship between colonic (Na+ + K+)-ATPase activity and the degree of mucosal inflammation in 19 patients with IBD of mild to moderate disease activity. Various macroscopic and histologic types of mucosal lesions were differently associated with the (Na+ + K+)-ATPase activities. 5'-nucleotidase activity was not associated with the degree of mucosal inflammation or the kind of macroscopic or histologic lesions. Our findings support the view that, in contrast to 5H-nucleotidase, (Na+ + K+)-ATPase activity may better reflect the severity of mucosal damage and the degree of inflammation in IBD.

5'-Nucleotidase↗
PubMed1988

h-ANF does not play a role in the regulation of myocardial force of contraction.

In the present study, h-ANF failed to reduce myocardial force of contraction alone and in the presence of isoprenaline. This lack of effect was observed in electrically driven, isolated human papillary muscle strips and rat papillary muscles. In contrast, adenosine and carbachol exerted antiadrenergic actions in rat and human myocardium. It is concluded that h-ANF obviously does not play a role in the regulation of human and rat myocardial force of contraction, whereas adenosine and carbachol are capable to produce antiadrenergic effects in the human and rat myocardium.

Adenosine↗
PubMed1988

Reduction of beta-adrenoceptor density and evaluation of positive inotropic responses in isolated, diseased human myocardium.

Cardiac beta-adrenoceptors and the positive inotropic effects of adenylate cyclase-dependent (dobutamine, histamine, forskolin) and adenylate cyclase-independent agents (isobutylmethylxanthine (IBMX), dibutyryl-cAMP (db-cAMP), digoxin, digitoxin and calcium were measured in papillary muscle strips from severely failing (NYHA IV), moderately failing (NYHA II-III) and non-failing (NYHA I) human hearts. The density of beta-adrenoceptors in three NYHA I patients were 40.0, 42.0 and 42.9 fmol mg-1 protein. The density of cardiac beta-adrenoceptors was significantly reduced in NYHA II-III to 18.0 +/- 1.1 fmol mg-1 protein (n = 16) and further reduced in NYHA IV to 9.5 +/- 1.6 fmol mg-1 protein (n = 7). The KD values did not differ between the groups. Correspondingly, the positive inotropic effect of dobutamine was significantly reduced in NYHA II-III and almost lost in NYHA IV. The positive inotropic effect of histamine was similar in non-failing and moderately failing myocardium but reduced in preparations from severely failing hearts (NYHA IV). The positive inotropic effect of IBMX was diminished in moderately and severely failing myocardium depending on the functional class of heart failure. In contrast, the effects of forskolin, db-cAMP, digoxin and digitoxin were not impaired in NYHA IV when compared with the maximal positive inotropic effect of calcium. It is concluded that in the failing human heart (a) the number of cardiac beta-adrenoceptors is reduced proportional to the severity of heart failure; (b) the receptor coupling of H2-receptors to adenylate cyclase may be impaired, but only in severe heart failure; (c) the basal cAMP formation may be diminished; and that (d) the catalytic subunit of the adenylate cyclase and the cAMP-dependent protein kinases may be promising targets for drugs to restore force of contraction in human heart failure.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Positive inotropic effect of DPI 201-106 in spontaneously hypertensive rats: lack of inhibition by adenosine and cholinergic agents.

The positive inotropic effect of DPI 201-106 has been studied in isolated, electrically driven papillary muscles of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WK). The positive inotropic effect of isoprenaline (Iso) and Ca2+ was studied for comparison. The maximal positive inotropic effect of Iso was less in SHR than in WK. In SHR, DPI 201-106 more effectively increased force of contraction than Iso. The positive inotropic effects of DPI 201-106 and Ca2+ were not different in SHR and WK. The EC50 values of DPI 201-106, Iso, and Ca2+ did not differ in either group. Furthermore, adenosine and carbachol reduced the positive inotropic effect of Iso but failed to exert a negative inotropic action when force of contraction has been increased with DPI 201-106. The isoprenaline-antagonistic effect of adenosine and carbachol was not different in SHR and WK. We conclude that DPI 201-106 might be an effective positive inotropic agent in states in which adrenergic function is compromised. The lack of inhibition by adenosine or m-cholinoceptor agonists could contribute to the effectiveness of the compound to increase myocardial force of contraction.

Adenosine↗
PubMed1988

Alpha-adrenoceptors and alpha-adrenoceptor-mediated positive inotropic effects in failing human myocardium.

Experiments were designed to characterize cardiac alpha-adrenoceptors and the alpha-adrenoceptor-mediated positive inotropic effects in human myocardial tissue from patients with moderate New York Heart Association (NYHA) class II-III and severe (NYHA class IV) heart failure. The number of cardiac alpha-adrenoceptors was low but similar in moderate and severe heart failure (NYHA class II-III: 6.7 +/- 0.8 fmol/mg protein 3H-prazosin bound, n = 12; NYHA class IV: 7.4 +/- 0.9 fmol/mg protein 3H-prazosin bound, n = 9; NS). Correspondingly, the alpha-adrenoceptor-mediated positive inotropic effect (phenylephrine in the presence of propranolol) did not significantly differ in both groups. In the same hearts, the number of beta-adrenoceptors was measured. The number of beta-adrenoceptors was significantly reduced in severe heart failure (NYHA class II-III: 22.0 +/- 1.5 fmol/mg protein 3H-CGP 12177 bound, n = 12; NYHA class IV: 11.9 +/- 0.8 fmol/mg protein 3H-CGP 12177 bound, n = 9; p less than 0.05). The positive inotropic effect of isoprenaline was significantly reduced in NYHA class IV. The positive inotropic effect of Ca2+ was similar in both groups. In conclusion, cardiac beta-adrenoceptors and the beta-adrenoceptor-mediated positive inotropic effects were reduced in severely failing myocardium. Cardiac alpha-adrenoceptors and the positive inotropic effect resulting from their stimulation is unchanged. Therefore, down regulation in response to increased sympathetic stimulation or a compensatory increase of alpha-adrenoceptors does obviously not occur in the human heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Subsensitivity of the failing human heart to isoprenaline and milrinone is related to beta-adrenoceptor downregulation.

The number of cardiac beta-adrenoceptors and the positive inotropic effect of isoprenaline and milrinone were measured in cardiac membranes and isolated, electrically driven muscle strips from nonfailing donor hearts and from patients with mitral valve disease (NYHA II-III), ischemic heart disease, and dilated cardiomyopathy (NYHA IV). In nonfailing hearts, the number of beta-adrenoceptors were 41.5 fmol/mg protein (mean, n = 3). In ischemic heart disease and NYHA II-III, there was a loss of cardiac beta-adrenoceptors (22.1 fmol/mg protein, mean, n = 3; 23.2 +/- 2.7 fmol/mg protein, n = 30), respectively. In NYHA IV, there was a pronounced reduction of the number of cardiac beta-adrenoceptors to 12.1 +/- 1.5 fmol/mg protein (n = 15). The Kd value did not differ in either group. Correspondingly, the positive inotropic effect of isoprenaline was more pronounced in nonfailing myocardium, reduced in NYHA II-III and ischemic heart disease and almost blunted in NYHA IV. Similar results were observed with the phosphodiesterase inhibitor milrinone. A good correlation of the beta-adrenoceptor density to the maximal positive inotropic effect of isoprenaline and milrinone was observed. Neither the number of cardiac beta-adrenoceptors nor the positive inotropic effect of isoprenaline correlated with the age of the patients. We conclude that the number of cardiac beta-adrenoceptors and the positive inotropic effect of beta-adrenoceptor agonists are reduced in the failing human heart depending on the severity of heart failure. Furthermore, the positive inotropic effect of milrinone is also reduced and related to the reduction of beta-adrenoceptors. The lack of correlation with the age of the patients provides evidence for a predominant role of heart disease rather than aging in the reduction of beta-adrenoceptors and subsensitivity to cyclic AMP-increasing positive inotropic agents in the failing human heart.

Aging↗
PubMed1988

Positive inotropic effects in isolated ventricular myocardium from non-failing and terminally failing human hearts.

The positive inotropic responses to isoprenaline, dobutamine, histamine, forskolin, isobutyl-methylxanthine (IBMX), dibutyryl-cyclic adenosine monophosphate (db-cAMP), ouabain and calcium were studied in isolated, electrically driven papillary muscle strips from either terminally failing human hearts or non-failing donor myocardium. The positive inotropic effect of calcium has been taken to evaluate the maximal force of contraction of each individual muscle strip ('contractile reserve'). In the non-failing heart, the maximal positive inotropic effect of isoprenaline, dobutamine, IBMX, ouabain and calcium were not significantly different, but were significantly greater than histamine. In terminally failing hearts, the positive inotropic effects of agents stimulating the adenylate cyclase by a receptor-dependent mechanism (isoprenaline, dobutamine and histamine) and the phosphodiesterase inhibitor IBMX are less than in the normal heart. Furthermore, these compounds gave a markedly reduced inotropic effect compared with forskolin, db-cAMP and ouabain, which gave maximal responses similar to calcium in the failing hearts. The data did not differ when the increase of force of contraction was related to the diameter of each preparation. These results indicate that a defect in adenylate cyclase occurs in the failing human heart, presumably located at the regulatory stimulatory subunit (Gs) of the adenylate cyclase since effects through stimulatory receptors were reduced. Responses from activation of the catalytic subunit or through cAMP-dependent protein kinases were less affected. Since the positive inotropic effect of IBMX is also impaired, it is suggested that the basal rate of cAMP production is also reduced in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1988

[Aortic isthmus stenoses--dilatation in adulthood. A German cooperative study].

An analysis of percutaneous transluminal angioplasty of the coarctation of the aorta in adults was evaluated in a cooperative study of the German Working Group of Angioplasty of the German Society of Cardiology. Dilation was performed in 18 patients with a mean age of 26 years (14-49 years). The success rate (gradient less than or equal to 20 mm Hg) was 78% regarding peak to peak gradient, 89% regarding mean gradient. The peak-to-peak gradient decreased from 82 +/- 16 mm Hg to 18 +/- 11 mm Hg. The diameter of the aortic isthmus increased from 0.7 +/- 0.3 cm to 1.3 +/- 0.4 cm (p less than 0.01). After six months only one restenosis occurred. The peak-to-peak gradient measured 10 +/- 12 mm Hg, the diameter 1.4 +/- 0.5 cm. In two patients a balloon rupture occurred without rupture-related complications. No patients died, no cross paralysis or aortic rupture occurred. In three of seven patients with trans-esophageal echocardiographic monitoring a small intimal flap was found; in one patient a media dissection occurred leading to a 15-min period of chest pain and spontaneous healing. In another patient successful dilation was controlled by acute control aortography and computer tomography. After discharge severe chest pain developed. A subtraction angiography of the aorta was negative. Six months later a biplane aortography of the distal thoracic aorta confirmed the diagnosis of aortic dissection type III DeBakey, previously diagnosed by transesophageal echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗