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Biomedical subjects

B Noll

Publications and source records attributed to B Noll.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Effects of lipid lowering measures on coronary perfusion].

Secondary intervention trials in coronary heart disease have unequivocally proven the effectiveness of lipid-lowering medication in addition to dietary means. Orderly application of available drugs leads to reductions in LDL cholesterol and triglycerides accompanied by increases in HDL cholesterol. Specifically, LDL cholesterol lowering is associated with clinical benefits in coronary heart disease, it reduces the necessity of hospitalization and interventions, and leads to significant reductions in coronary as well as in overall mortality. Besides morphological changes of coronary vessels like regression or retarded progression of plaques, lipid-lowering was shown to normalize endothelial dysfunction associated with hyperlipidemia. Restoring endothelial function and improving coronary perfusion may be one of the factors responsible for the huge clinical benefits in secondary intervention trials as compared to the modest morphological changes. As the fact of lipid-lowering rather than the means by which it is achieved is of specific importance, dietary means have to precede and then accompany an eventual additional drug treatment.

Combined Modality Therapy↗
PubMed1996

Heat shock protein-peptide complexes for use in vaccines.

The heat shock proteins gp96, HSP70, and HSP90 are complexed to a diverse array of cellular proteins and peptides as a consequence of their chaperone functions. There is good experimental evidence that vaccination with these heat shock protein-peptide complexes elicit immune responses against chaperoned peptide antigens. As shown with gp96, this requires internalization of the heat shock protein-peptide complexes by macrophages and processing of the chaperoned peptides for class I restricted presentation. Via this process, primarily CD8+ antigen-specific T cells are primed by gp96 vaccination. This might represent a general mechanism for priming of MHC-class I restricted T cells by professional antigen-presenting cells. At least gp96 has been shown to be associated with peptides that are not selected by the MHC haplotype of the harboring cell. This allows for immunization with gp96-peptide complexes across MHC barriers, for example against shared tumor antigens or viral antigens.

Animals↗
PubMed1995

An angiotensin-converting enzyme gene variant is associated with acute myocardial infarction in women but not in men.

We believe our data may speak to the issue of sexual dimorphism with respect to MI. Most studies have concentrated on men with this disease. In a recent study, Lindpaintner et al10 could find no relationship between the D/D genotype and AMI in subjects of the Physicians Health Study. However, this study consisted entirely of men. The D allele may provide an avenue to discern differences in the pathogenesis of MI in men and women.

Adult↗
PubMed1995

Sources of radiochemical impurities in the 99mTc/S-unprotected MAG3 system.

With the aim of obtaining a general insight into the technetium/S-unprotected MAG3 system, the reactions of technetium with the unprotected MAG3 ligand, both at c.a.- and n.c.a.-level, were investigated. Based on a profound knowledge of the reaction route and the TcMAG3 complexes, sources of by-products were identified and eliminated as far as possible. Only a small percentage (< 5%) of intermediate Tc-MAG3 complexes occurs, but this may increase by improper handling of the kit, such as insufficient reaction time. In conclusion, two kinds of impurity may occur in the Tc/MAG3 kit: One is derived from impurities in the ligand (MAG3 disulphide), which can be excluded by careful preparation and storage. The other is caused by insufficient reaction time according to the scheme (Fig. 3) during the labelling procedure. Its content can be minimized by optimization of the reaction time. A reaction time of at least 10 minutes gives about 98% of the renal agent.

Drug Contamination↗
PubMed1995

[Retrospective studies and prospects of therapy for hypertension].

Future trends in hypertensive treatment have to rely on our past and present experience with antihypertensive drugs as well as on emerging concepts of blood pressure regulation, on which some new drugs in the "pipeline" are based. Early detection of hypertension, before organ manifestations particularly in the heart, the kidney and the vessels occur, remain mandatory since in most of the patients with mild and moderate hypertension the high blood pressure is not diagnosed at all or treated inadequately. Prevention of cardiac, vascular, renal or metabolic complications has always been better for the patient and less costly than their repair or reparation. Our present treatment goals have often not reached far enough. Normalisation of blood pressure demonstrates only surrogate efficacy of our treatment. Our ultimate goal has to be improvement of total or cerebrovascular or cardiovascular and cardiac mortality. Important steps on that road are the prevention or reparation of cardiac hypertrophy, of the increased extracellular matrix and collagen deposition, the conservation of vascular integrity including both coronary and systemic microangiopathy and macroangiopathy. For the patient this means integrated care of his associated disorders that is of coronary artery disease, diabetes mellitus, lipid disorders, overweight and the metabolic syndrome. True health efficacy (= reduction of total or cerebro- and cardiovascular mortality) has been demonstrated so far only by blood pressure reduction with diuretics (thiazides) and beta-blockers in long term studies, whereas sufficient surrogate efficacy, the lowering of blood pressure, has been demonstrated with almost all the others drugs either in mono- or in combinationtherapy. Together with ACE-inhibitors, which have demonstrated their prognostic value in patients with heart failure of different causes, thiazides (as the most representative diuretic) and betablockade can be considered first line drugs in the treatment of hypertension. Long-term mortality trials for ACE-inhibitors in hypertension are needed, however, to prove that the anticipated benefit from the heart failure megatrials can also be taken for granted for hypertensive patients without coronary artery disease as well. All other drugs should not or not yet be considered first line medication, although treatment behavior in the US and in Europe shows wide-spread use of calcium antagonists in short- and long-acting dihydropyridine type hypertensive patients. No peer reviewed journal has so far published a randomized double-blind trial with the endpoint of total or cardiovascular mortality in hypertension using calcium antagonists. A recent case control study, as well as the preliminary data from MIDAS and GLANT, for which event rates are available in abstract form, suggest that short acting calcium-antagonists of the dihydropyridine type, though controlling blood pressure well, are not reducing mortality but show a trend to increase cardiovascular events particularly when given in higher doses. In contrast the unpublished data from a Chinese megatrial with dihydropyridines (STONE) demonstrate effective blood pressure reduction and benefit in mortality in a population that differs from patients in Europe and in the USA because of the low prevalence of coronary artery disease. No randomized, double blindly acquired data on mortality as the primary end of antihypertensive treatment are yet available for verapamil, diltiazem and the new class of longer acting calciumantagonists. Only when speculating from trials with calcium antagonists in coronary artery disease e.g. the DAVIT II study, one could imagine so far that prognostic benefit may be expected from drugs that do not or very little activate the adrenergic and the renin-angiotensin-aldosterone system and the baroreceptors and reduce or at least maintain heart rate. The need for double blind, randomized trials with the different Ca-antagonists is obvious, before a further w

Antihypertensive Agents↗
PubMed1992

Cardiac natriuretic peptide hormones during artificial cardiac pacemaker stimulation and left heart catheterization.

Brain natriuretic peptide (BNP) is synthesized and released predominantly in the ventricular myocardium whereas atrial natriuretic peptide (ANP) is produced mainly in the atria. This study evaluated whether artificial pacemaker stimulation or left heart catheterization results in specific changes in BNP and ANP plasma levels. Both BNP and ANP responded sensitively to changes in pacemaker stimulation (single-chamber pacemakers; pacing rates of 72 and 92/min) and during the left heart catheterization procedure. However, whereas higher pacing resulted in a more pronounced increase in plasma BNP levels, a stronger ANP release followed catheterization. This incongruous rise in ANP and BNP plasma concentrations points to at least partly independent mechanisms governing the release of BNP and ANP.

Atrial Natriuretic Factor↗
PubMed1992

Preparation of the renal function and imaging agent 99mTc-MAG3 starting from S-unprotected mercaptoacetyltriglycine.

A new approach that obviates inconvenient heating of the labelling solution when preparing the renal function and imaging agent 99mTc-MAG3 is described. The labelling procedure involves reduction of 99mTc-generator eluate with stannous chloride in alkaline solution in the presence of S-unprotected mercaptoacetyltriglycine (MAG3) and the co-ligand sodium tartrate, followed by neutralization with a phosphate buffer solution. After optimization of the kit preparation the radiochemical purity of the radiopharmaceutical amounts to greater than 98%. During the labelling process intermediate Tc-species occur.

Oligopeptides↗
PubMed1990

[Cardiac findings in alcoholic liver disease].

In a prospective study 53 patients with alcohol-induced liver disease (fatty liver in 27, cirrhosis in 26) were studied clinically and with non-invasive techniques (electrocardiogram, systolic time intervals, M-mode echocardiography, upright bicycle stress test) to detect a possible cardiac involvement. Mean daily alcohol consumption was comparable in both groups (136 g/day over 16 years vs 124 g/day over 14 years). 15 to 41% of patients (more patients with fatty liver) complaint of angina pectoris and dyspnea at exercise or had palpitations. Echocardiography and systolic time intervals demonstrated in both groups (in patients with cirrhosis despite of a more intensive therapy with digitalis and diuretics) a marked enlargement of left ventricular dimensions with a significant (p less than 0.05) degree of dysfunction (PEP/LVET). Electrocardiography showed abnormalities in 26 to 44% of patients: signs of right ventricular enlargement in 26% of patients with fatty liver, and a prolongation of myocardial repolarisation (QTc) in 44% of patients with cirrhosis. Patients with alcohol-induced liver disease deserve more attention of their cardiac complaints, clinical and functional findings.

Adult↗
PubMed1990

Atrial natriuretic factor has a weak insulinotropic action in the isolated perfused rat pancreas.

The effect of atrial natriuretic factor (ANF; 1, 10, 100, 1000 pmol/l) on insulin release from the isolated perfused rat pancreas was studied. ANF weakly augmented the glucose (10 mmol/l)-stimulated insulin release during the second (controls: 100%; 1 pmol/l: 99%; 10 pmol/l: 149%, P less than 0.05; 100 pmol/l: 111%; 1000 pmol/l 135%), but not the first phase of the secretory response. In contrast, the first, but not the second phase of arginine (10 mmol/l)-stimulated insulin release was significantly enhanced by ANF (1000 pmol/l; controls: 100%; 1000 pmol/l: 235%, P less than 0.05). The hormone did not influence basal insulin secretion. Our data indicate an insulinotropic effect of ANF on the rat pancreas, which is dependent on the utilized background secretagogues.

Animals↗
PubMed1990

Atrial natriuretic peptide levels reflect hemodynamic changes under pacemaker stimulation.

Pacemaker stimulation influences plasma levels of atrial natriuretic peptide (ANP). This study evaluated in individuals without impaired myocardial function whether a consecutive increase of pacing rates results in reduced alteration of plasma ANP levels mirroring a putative decrease of atrial contribution to cardiac output. In nine resting patients with DDD pacemakers, absolute and relative ANP plasma levels were determined under DDD (175 msec AV delay) and VVI pacing at a pacing rate of 72, 82, 92, and 113 beats/min. When pacing rates were consecutively increased, higher plasma ANP concentrations were measured. However, the differences in relative ANP levels were nearly identical. Therefore, it seems likely that the atrial contribution to cardiac output at high pacing rates is less important than at lower frequencies, at least when the overall myocardial function is not impaired.

Aged↗
PubMed1990

[Changes in atrial natriuretic peptide in patients with lung embolism and obstructive respiratory tract disease].

Plasma levels of atrial natriuretic peptide (ANP) correlate closely with the pressure and mural tension of the right atrium and with pulmonary arterial pressure. We determined ANP levels in eight patients with scintigraphically confirmed pulmonary embolism, before and after reperfusion. Furthermore, ANP was measured in ten patients with acute obstruction of the airways, and during the course of clinical recovery. Peripheral venous blood was saved for determination of ANP plasma levels. The hormone concentrations were measured by radioimmunoassay. In ten patients with scintigraphically confirmed pulmonary embolism clearly higher ANP plasma levels were determined than after complete reperfusion (p less than 0.05). In patients with acutely exacerbated airways obstruction, hormone levels were measured which were significantly higher than those observed after clinical improvement (p less than 0.01). Since it is known, that ANP reduces pulmonary arterial smooth muscle tone and resistance, the hormone appears to be of physiological significance in pulmonary embolism and acute airways obstruction by lowering right ventricular afterload.

Adult↗
PubMed1989

Influence of pacing mode and rate on peripheral levels of atrial natriuretic peptide (ANP).

The effect of acute modifications of pacing mode and rate on plasma ANP levels was evaluated. ANP was determined in ten resting patients with DDD pacemakers due to binodal disease or intermittent second-and third-degree AV block. At 82/minute pacing rate the ANP plasma levels (normal range 2 to 30 fmol/mL) corresponded to those under AAI (4.05 +/- 2.10 fmol/mL) and DDD (4.18 +/- 2.02 fmol/mL) pacing, but increased significantly (P 0.05) during VVI pacing (6.96 +/- 3.70 fmol/mL). Acceleration of DDD stimulation frequency from 82 to 113/minutes led to significant increase of ANP levels by the factor of three in all chosen AV delays. The lowest ANP plasma levels were measured at 175 msec AV delay under 82/minute pacing rate in DDD mode. Under 113/minutes the differences of ANP concentration after variations of AV delays were less pronounced. The influences of altered atrial pressure and tension on ANP release are discussed to account for changes in ANP plasma levels following different modes and rates of pacemaker stimulation.

Aged↗
PubMed1988

[Modification of atrial natriuretic factor by the AV transmission time in pacemaker patients].

The possible relationship of variations in the programmed a-v interval on the peripheral-venous plasma level of the atrial natriuretic factor (ANF) was investigated in nine patients with dual-chamber pacemakers (DDD). During atrial and ventricular stimulation at 82 beats/min the pacemakers of the resting patients were programmed to give successive a-v intervals of 200, 175, 150, 125, 100, 50 and 15 ms. Blood samples were obtained from a peripheral arm vein ten minutes after each change of programme. ANF was extracted from each sample and determined by radioimmunoassay. Both the absolutely and relatively lowest plasma ANF level was obtained at an a-v interval of 175 ms. Lengthening the interval to 200 ms or shortening it to 150 ms or less increased the level. It is possible that both "too long" and "too short" a-v intervals produce an increase in atrial pressure and stretch, to which ANF reacts highly sensitively with an increase in peripheral-venous plasma levels of ANF.

Adult↗
PubMed1988

Influence of experimental hyperthyroidism on blood and myocardial serotonin in rats.

Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.

Administration, Oral↗
PubMed1988

Influence of experimental hyperthyroidism on the adult rat pancreas, small intestine, and blood gastrin levels.

Thyroxine modulates the ontogenic changes of animal tissues. In this study, the effects of experimental hyperthyroidism on the adult rat pancreas, small intestine, and serum gastrin were evaluated. Hyperthyroidism was induced by oral feeding of thyroxine (T4) in increasing dosages (150-450 micrograms/kg body weight; 3 weeks) and controlled by measurements of the circulating hormones. The increase of thyroid hormones in blood (T4 ng/dl: thyroxine-treated rats 10.8 vs. controls 3.3; p less than 0.01; given are means) was accompanied by hypergastrinemia (IR-gastrin pg/ml: T4-treated rats 169 vs. controls 25; p less than 0.05). The T4-treated animals consumed more food but lost about 20 g of their initial body weight. Pancreatic wet weight (g: T4-treatment 1.72 vs. controls 1.42; p less than 0.05), DNA (micrograms/g body weight: T4-treatment 2.42 vs. controls 1.5; p less than 0.05), and protein (micrograms/g body weight: T4-treatment 131.7 vs. controls 63.5; p less than 0.05) were increased, whereas no pronounced influence on pancreatic amylase, trypsin, and chymotrypsin was found. The gut wet weight after thyroxine administration (18.1 g vs. 15.4 g of controls; p less than 0.05) was elevated, but length, DNA, protein, and brush border enzyme activities remained unaltered. Our data demonstrate in adult rats a small but significant trophic response of pancreas and gut to repeated oral thyroxine administration.

Animals↗