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Biomedical subjects

V Regitz

Publications and source records attributed to V Regitz.

26 records · Page 2Linked to original sources
PubMed1987

Protection of the ischemic myocardium by propionylcarnitine taurine amide. Comparison with other carnitine derivatives.

The cardioprotective effect of the two synthetic carnitine derivatives, propionylcarnitine taurine amide (PCTA) and butyrylcarnitine taurine amide (BCTA), were studied in isolated perfused rat hearts. The protective effects of PCTA and BCTA were compared with those of chemically similar compounds, which have already been investigated in part and reported on; i.e. propionylcarnitine, carnitine, taurine and the combination of propionylcarnitine and taurine. The addition of either PCTA or BCTA significantly improved the recovery of cardiac function of ischemic reperfused hearts. PCTA (0.5 mM) treated hearts regained 75%, 91% and 89% of their preischemic values for cardiac output, left ventricular pressure and dp/dt after 90 min ischemia and 15 min reperfusion. These parameters of cardiac function remained impaired in control hearts which recovered only 38% of the initial preischemic cardiac output, 73% of initial intraventricular developed pressure and 64% of initial positive dp/dt. The cardioprotective effects of PCTA, BCTA and propionylcarnitine were in the same range. However, PCTA and BCTA acted in 20-fold lower molar concentrations compared to propionylcarnitine. Carnitine (11 mM), taurine (11 mM) as well as the combination of propionylcarnitine and taurine at low concentrations had no cardioprotective effect in these experiments. Myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were significantly higher in the PCTA or BCTA treated hearts than in controls, and lactate levels were reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Four years of experience in endomyocardial biopsy--an immunohistologic approach.

Left ventricular biopsies from 376 patients (including 78 patients undergoing bypass surgery) were analyzed by light microscopy (necrosis, infiltration with or without fibrosis) and by immunohistology (bound antibodies). Circulating antisarcolemmal antibodies (ASA) were determined at the time of biopsy using a double-sandwich technique. Circulating antimyolemmal antibodies were assessed in intact rat and human cardiocytes. Histologic findings, heart catheterization, and echocardiography together with the patient's history established the diagnosis of perimyocarditis, myocarditis, postmyocarditic dilated cardiomyopathy, healed myocarditis, and healed perimyocarditis. Both bound and circulating ASA were found in up to 100% of cases in acute inflammatory heart disease and postmyocarditic cardiomyopathy, indicating a secondary immunopathogenesis of the myocardial disease. Analysis of immunoglobulin subclasses revealed: IgG-binding does not discriminate between acute/healing/healed carditis and postmyocarditic dilated heart disease (61.1%-91.7% positive); IgM binding is diagnostic for acute or healing perimyocarditis but has a relatively low incidence (33.3%); IgA binding occurs in acute or healing myocarditis (45.5%), perimyocarditis (33.3%), and in postmyocarditic heart disease (39.4%), but not in controls; complement fixation was never seen in controls, but was seen in acute myocarditis (45.4%), perimyocarditis (25%), and postmyocarditic heart disease (46%). Pretreatment of cryostat sections with collagenase to avoid "nonspecific" binding of antibodies to collagen considerably reduced the sensitivity but increased the specificity. Thus, endomyocardial biopsy proved a safe and valuable method for the further analysis of patients with carditis and myocardial disease of unknown origin.

Acute Disease↗
PubMed1985

[Histologically detectable myocarditis in patients with impaired left ventricular function].

In patients with impaired left ventricular function in whom dilated cardiomyopathy is initially suspected after performance of comprehensive diagnostic studies, histologic evidence of myocarditis or status-post myocarditis is being documented with increasing frequency since the systematic use of endomyocardial biopsy has been incorporated into the work-up. This investigation was undertaken to analyze the histologic, clinical, hemodynamic and immunologic findings in these patients to delineate possible relationships between histologically-documented myocarditis and dilated cardiomyopathy. Incidence of histologically-documented myocarditis. In our patient population, 41 of 150 patients with impaired left ventricular function, the etiology of which had been unknown, histologic evidence of myocarditis was documented. In seven of eight in whom active myocarditis was diagnosed at initial biopsy, after a mean follow-up period of two years the histologic findings were consistent with dilated cardiomyopathy. In similar groups of patients comparable incidences of myocarditis have been reported by Parrillo et al. in 19 of 100 (19%) and Fenoglio et al. in 34 of 135 patients (25%). A higher incidence has been reported by Zee-Cheng et al. in 22 of 35 patients (63%). Accordingly, pooled data indicate that the overall incidence of histologically-documented myocarditis was 30% in 528 patients initially suspected to have dilated cardiomyopathy. The variances in the incidence reported by the respective authors may be attributable to differences in the histologic definition of myocarditis, number of biopsies obtained, size of the patient population and the epidemiologically-related incidence of viral disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1985

[Dilated cardiomyopathy: characterization by clinical and hemodynamic findings].

Dilated cardiomyopathy, a disease of the heart muscle of unknown origin, is characterized by impaired systolic function and dilatation of the left and right ventricles. In the Federal Republic of Germany, there are an estimated 4000 to 5000 new cases reported yearly [40]. Pathologic-anatomic studies have demonstrated that, in addition to an extent of dilatation of all heart chambers dependent on the stage of the disease, up to 60% of those who die can be found to have intracardiac thrombi [37]. Specific histologic changes are absent [34]. Disturbances of the microcirculation, a defect of autonomic innervation and biochemical alterations have been postulated as possible causes [7, 33, 35]. Circulating and bound antibodies against myocardial antigens and pathologic cellular immunoreactions have been reported in association with both myocarditis and dilated cardiomyopathy; this, in turn, has led to the hypothetical assumption of a secondary immunopathogenesis after myocarditis [6, 9, 12, 18, 26, 33]. Clinical and hemodynamic findings encompass a wide spectrum. With a mildly impaired ejection fraction to values between 40 and 54%, in our patients there was an associated enlargment of the end-systolic and end-diastolic ventricular volumes to 60 and 115 ml/m2 (upper normal limits 35 and 95 ml/m2), respectively. Those with increasing degrees of left ventricular function impairment to ejection fractions less than 40%, had additionally pathologic elevation of the filling pressures. In patients with marked impairment of the ejection fraction to values of less than 25%, cardiac output was reduced and systemic and pulmonary vascular resistances elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1981

Biochemical mechanism of infarct size reduction by pyruvate.

We have explored the biochemical mechanism of the infarct size reduction found after intracoronary pyruvate infusion. Using the double infarct model, we simultaneously produced in nine dogs a control- and a therapy-infarct and compared the infarct sizes in each dog after 90 min of occlusion and 90 min of reflow. Intracoronary pyruvate reached the therapy infarct only by way of collaterals but had no access to the control infarct. Tissue levels of reduced nicotinamide dinucleotide (NADH) were measured in control-normal-, therapy-normal-, control-ischaemic-and pyruvate-treated ischaemic areas. In all nine dogs we found a significant reduction in infarct size and NADH levels in the pyruvate-treated areas. Therapy-normal NADH levels fell to 30+/-10% (mean+/-SD) of control-normal levels and therapy-ischaemic NADH levels to 26+/-17% of control-ischaemic levels. We assumed that the infused pyruvate was converted to lactate and at the same time NAD was generated from NADH. Thereby the blockage of glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) by high NADH/NAD-ratios in ischaemic myocardium should be moderated, and ATP production by anaerobic glycolysis stimulated. These small amounts of ATP may be sufficient to guarantee membrane integrity over 90 min of ischaemia and so diminish its harmful effects on the myocardium.

Adenosine Triphosphate↗
PubMedDate not supplied

Identification of human myocard proteins separated by two-dimensional electrophoresis.

N-Terminal sequencing, internal sequencing and amino acid analysis were used to identify twelve proteins of the human myocard two-dimensional gel electrophoresis (2-DE) pattern. Amino acid analysis was shown to be a powerful tool in addition to sequencing. The identification of a disease-associated N-terminally blocked protein by internal sequencing was not successful. The twelve identified proteins are the basis of a human myocard 2-DE database.

Amino Acid Sequence↗
PubMedDate not supplied

Mitochondrial damage during myocardial ischemia.

The effects of 3 hours of ischemia and 1 hour of reperfusion on biochemical, physiological and ultrastructural parameters were studied in 12 dogs. In the ischemic subendocardium without reperfusion, mitochondrial losses of adenine (ATP + ADP + AMP) and pyridine (NAD + NADH) nucleotides far exceeded those observed in whole tissue. Adenine nucleotide translocator (ANT) was severely inhibited and seemed to be a sensitive indicator of a lesion of the inner mitochondrial membrane. Postischemic reperfusion led to a slight loss of adenine and pyridine nucleotides from the reversibly damaged subepicardium and to an enormous loss from the irreversibly damaged subendocardium. The washout of nucleotides from irreversibly damaged areas caused the negative para-Nitro Blue Tetrazolium ( pNBT ) staining of the infarcted tissue. Diagnosis of cell death with pNBT failed after the occlusion period without reflow because pyridine, although lost from the mitochondria, was still present in the tissue. In reversibly injured areas, mitochondrial function and ultrastructure were restored after reperfusion, although a significant nucleotide loss was found in the tissue. These studies suggest that mitochondrial ultrastructure and function may play a key role in cellular viability during recovery from ischemia.

Adenine Nucleotides↗