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Biomedical subjects

J Zähringer

Publications and source records attributed to J Zähringer.

At least 19 recordsLinked to original sources
PubMed1989

[Modification of blood coagulation by antihypertensive therapy? Effect of enalapril and hydrochlorothiazide on blood coagulation parameters in patients with essential hypertension].

An increased tendency of the blood to clot in patients with arterial hypertension is not desirable, since cardiovascular and cerebrovascular sequelae may be aggravated. Recently, activation of coagulation under ACE inhibition with captopril has been described. In an open, randomized study, we compared the influence of enalapril on various coagulation parameters with that of hydrochlorothiazide. In contrast to the latter, we detected no unfavorable influence of enalapril on the coagulation factors investigated. A transient increase in fibrin monomeres was observed in one patient each on enalapril and hydrochlorothiazide.

Adult↗
PubMed1987

Baseline and stimulated ANF plasma levels: is an impaired stimulus-response coupling diagnostically meaningful?

Plasma levels of ANF were determined and chromatographically analysed in normotensive controls, cirrhotic patients with and without ascites, hypertensive patients, patients with congestive heart failure and heart transplant recipients. A comparison of baseline plasma levels allowed for the conclusion that cirrhotic patients do not differ in this regard from control subjects (9.0 +/- 1.3, n = 41 vs. 9.6 +/- 1,0 fmol/ml, n = 51). Cirrhotic patients with ascites do not have lower plasma levels than cirrhotic patients without ascites (8.8 +/- 1.4, n = 8 vs 8.6 +/- 1.5 fmol/ml, n = 10). Stimulation of the ANF-system by head-out water immersion, however, revealed an impaired increase in ANF release in cirrhotic patients with ascites (146 +/- 18% vs 204 +/- 16%). Patients with cardiovascular disease display tonically-elevated ANF plasma levels. Heart failure patients displayed the highest plasma concentration (81.5 +/- 32.7 fmol/ml, n = 17), whereas plasma levels in hypertensive patients ranged from normal to greatly elevated (61.7 +/- 13.2 fmol/ml, n = 36). Heart transplant recipients also had significantly elevated plasma levels as compared to control subjects (31.2 +/- 7.9 fmol/ml, n = 14) but levels were lower than in hypertensive patients in spite of a comparable arterial pressure. Short term ventricular pacing (f = 150/min for 5 min) revealed an impaired phasic activity of the ANF system in heart failure patients and heart transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1986

Basis and clinical significance of regression of hypertensive hypertrophy.

The basis of every therapy in hypertensive heart disease is blood pressure normalization. However, blood pressure should be lowered through antihypertensive drugs, which can regress LV hypertrophy, increase myocardial perfusion and improve LV function depending on the stage of hypertensive heart disease. Such a step-care of hypertensive heart disease must not be understood as a therapeutic scheme, but should be considered as an attempt to cover the clinical therapy of common hypertensive cardiac complications.

Animals↗
PubMed1986

Atrial natriuretic factor in plasma of patients with arterial hypertension, heart failure or cirrhosis of the liver.

Since the discovery of the atrial natriuretic factor (ANF) an endocrine function has been attributed to the mammalian heart. This function may include definition of optimal conditions for efficient performance of the heart, e.g. by reduction of afterload in hypertension or of preload and afterload in heart failure. Plasma ANF levels were measured in various cardiovascular disease states and compared with those of controls and of patients with liver cirrhosis. Plasma ANF levels in hypertensive patients were sevenfold higher than in controls, and in patients with heart failure 40-fold higher than normal values. Small differences were detected between controls and patients with cirrhosis of the liver, in spite of the impaired renal sodium handling seen in cirrhotics. Plasma ANF levels were significantly correlated with haemodynamic parameters and were inversely related to the cardiac index. Treatment with an angiotensin converting enzyme inhibitor led to a significant decrease in plasma ANF levels in parallel with the haemodynamic improvement. Preliminary chromatographic analysis suggested differences in the structure of plasma ANF between normotensive and hypertensive subjects.

Atrial Natriuretic Factor↗
PubMed1985

Demonstration and characterization of alpha-human atrial natriuretic factor in human plasma.

This paper describes a highly specific and sensitive radioimmunoassay for alpha-human atrial natriuretic factor (alpha-hANF), the C-terminal 28-amino-acid residue portion of human prepro-ANF in human plasma. A novel extraction and prepurification procedure allowed for detection of levels of immunoreactive-alpha-hANF as low as 0.5 fmol/ml. In normotensive subjects, levels in the range 1-23 fmol/ml (mean = 8.9 fmol/ml) were found. Combined gel permeation and HPLC analysis demonstrated that this ir-alpha-hANF was comprised virtually exclusively of authentic 28-residue alpha-hANF. No evidence for occurrence of larger precursor forms in human plasma was acquired. A heterogenous group of hypertensive patients displayed considerably higher levels (mean = 62.2 fmol/ml), of interest in view of the hypotensive properties of ANF.

Adsorption↗
PubMed1985

Virus myocarditis: molecular hybridization allows the detection of virus-RNA in heart muscle after virus infection.

In most patients with virus myocarditis, the diagnosis is still based on clinical data alone. Endomyocardial biopsies subjected to electron microscopy, immunofluorescence techniques and virus isolation procedures provide additional, but only occasionally conclusive information. In this communication we describe a new method which could possibly be used to improve the diagnostic possibilities in patients with suspected virus myocarditis. The method is based on the hybridization of radioactive complementary nucleotide sequences to virus-RNA. It is shown that in an experimental model (reovirus infected baby mice) this method can be used to demonstrate the virus infection of cardiac muscle. It is suggested that the method could be adapted to other viruses (e.g. coxsackie virus) and to endomyocardial biopsies derived from patients with suspected virus myocarditis.

Animals↗
PubMed1985

Regression of heart muscle hypertrophy after nifedipine therapy: changes in cardiac gene expression.

Changes in cardiac gene expression were studied during development and regression of cardiac hypertrophy in spontaneously hypertensive rats (SHR) in an attempt to determine some of the biochemical factors responsible for alterations in cardiac mass. Chronic nifedipine treatment of SHR (30 mg/kg per day for 20 weeks) led to a marked reduction in arterial blood pressure and to a subsequent regression of cardiac hypertrophy. Cardiac mRNA concentration decreased, whereas cardiac protein concentration remained unchanged. Changes in cardiac gene expression, as reflected by the decrease in cardiac mRNA concentration, were thus identified as a major factor responsible for the regression of cardiac hypertrophy after nifedipine therapy of SHR.

Animals↗
PubMed1985

[Regression of biochemical changes in heart muscle hypertrophy].

Reduction in arterial blood pressure caused by ACE inhibitors, calcium antagonists and beta-blockers leads to regression of heart muscle hypertrophy. However, this regression may also occur in the absence of a significant reduction in blood pressure (alpha-Methyldopa), whereas no decrease in heart muscle mass may be observed in the presence of pronounced decreases in blood pressure (hydralazine, minoxidil, diuretics). In the present review, biochemical factors are analyzed that might be important in the regression of heart muscle hypertrophy. It will be seen that angiotensin II and cardiac catecholamines play important roles in modifying the influence of various drugs on regression of heart muscle hypertrophy. Reductions in angiotensin II and cardiac catecholamines lead to decreases in cardiac mRNA contents and thus to a decrease in the myocardial protein synthesis. Changes in myocardial protein degradation do not contribute to the regression of heart muscle hypertrophy.

Adrenergic beta-Antagonists↗
PubMed1985

Quantitation of cardiac messenger RNA in heart-muscle biopsies.

A method has been developed that allows the direct quantitation of cardiac messenger RNA in heart-muscle biopsies. This provides a new tool to directly assess changes in cardiac gene expression in cardiac biopsies. Using this method, we have analyzed changes in cardiac gene expression during induction and regression of triiodothyronine-induced heart hypertrophy, during development of heart atrophy secondary to starvation and protein depletion, in adriamycin cardiomyopathy, and in patients with mitral-valve diseases.

Animals↗
PubMed1979

[The regulation of protein synthesis in heart muscle. Biochemical data, stimulative and inhibitory factors and their clinical significance (author's transl)].

The regulation of protein synthesis in heart muscle has been investigated by many authors under both normal and pathological conditions. This review summarizes the evidence for the dependence of normal heart protein synthesis from normal serum levels of insulin, amino acids, fatty acids and glucose. A decreased serum concentration of these substances causes an inhibition of heart muscle protein synthesis by 30--60%. Various drugs and other chemical lead to similar impairments of heat muscle protein synthesis. The resulting imbalance between synthesis and degradation of myocardial proteins with their half-times of 5--12 days gradually leads to a decrease in their myocellular concentration with a consequent impairment of myocardial function. Finally, the biochemial sequences are described which represent the important pathogenetic mechanisms in the development of heart muscle hypertrophy and in the adriamycin-induced cardiomyopathy.

Amino Acids↗
PubMed1978

[Lactacidosis in biguanide therapy: diagnosis and therapy. 4 cases compared to 179 cases in the world literature].

In 4 out of 9711 (= 1:2400) patients, lactice acidosis due to biguanides was diagnosed. Serum lactate concentration averaged 18.2 mmol/l and the pH value 6.87. All patients showed signs of renal insufficiency and three had congestive heart disease. In addition to treatment with biguanides, other factors might have contributed to the lactice acidosis in these patients: prolonged fasting, severe dehydration due to persistent vomiting, acute bronchopneumonia, and acute pyelonephritis. On addmission, two patients were in shock and all patients were semi-conscious or comatose. All patients were treated with bicarbonate and glucose/insulin. One patient was hemodialysed. Two of our four patients died. Oour four patients are compared with 179 patients in the literature with respect to mortality and prognosis of lactic acidosis due to biguanides.

Acidosis↗