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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 127 records · Page 7Linked to original sources
PubMed1983

[Significance of immunologic effector mechanisms in infectious endocarditis].

Whereas a number of investigations deals with extracardiac manifestations of immune reactions in infective endocarditis (e.g. circulating immune complexes), immunological effector mechanisms directed against the heart itself have not yet been analyzed. In 72 patients with infective endocarditis (41 patients with defined pathogen, 31 no pathogen isolated) humoral und cellular immunological effector mechanisms were investigated. Antibodies directed against the cytoskeleton of myocardial cells and against the endocardium were demonstrated in 60% to 100% depending on the infective pathogen and the clinical course. Whereas the antibodies were found in subacute and chronic courses regularly, they were found less frequently in acute lethal cases. Antibodies directed against connective tissue, endocardium and sarcolemma were indicative of, but not specific for the endocardial affection. Those antibodies which were directed against the inner parts of the sarcolemma, the myolemma, appear to be indicators of an additional myocardial affection, if they are cytolytic against vital cardiocytes in vitro. Circulating immune complexes are non-specific markers of an increased immunoreactivity. They were detected in 35 out of 41 patients with defined bacterial pathogen in the early phase of the disease. Both, their incidence and serum concentrations decreased significantly after antibiotic treatment. Cellular immune reactions directed against vital heart cells (e.g. cytotoxic reactions) can most likely be attributed to K- or NK-lymphocytes and were found in 48% of patients. Serum factors such as circulating immune complexes and/or antimyolemmal antibodies may enhance or block this cytotoxic reaction.

Adult↗
PubMed1983

[Left ventricular hemodynamics in acute alcohol intoxication in guinea pigs].

This study was undertaken to investigate to what extent the cardiodepression of acute alcohol intoxication is dose-dependent and to assess the validity of isovolumetric and afterload parameters in the latter condition. Isovolumetric and ejection phase parameters were measured in-situ in the intact heart of the guinea pig. The diastolic and systolic pressure-volume-relationships were calculated on the basis of direct measurements obtained at control conditions and during acuta alcohol intoxication at blood alcohol concentrations (BAC) of 160 and 280 mg/100 ml, respectively. Cardiodepression was dose-dependent; left ventricular isovolumetric pressure fell 13% at a BAC of 280 mg/100 ml, maximal rate of pressure rise (dp/dt max) decreased 33%. The changes in afterload parameters were less consistent: there was an increase in left ventricular isovolumetric pressure and dp/dt max in the group with BAC of 160 mg/100 ml, but both of these parameters decreased at BAC levels of 280 mg/100 ml. Stroke volume and preload decreased comparably in both groups. The divergent pattern of induced hemodynamic alterations may be due to peripheral effects of ethanol and/or counter-regulatory adrenergic mechanisms. The mortality rate associated with BAC of 160 mg/100 ml was 55% and that of 280 mg/100 ml was 75%.

Alcoholic Intoxication↗
PubMed1982

[Nifedipine in hypertrophic obstructive cardiomyopathy].

The effects of nifedipine on left-ventricular dynamics were assessed in 6 patients with hypertrophic obstructive cardiomyopathy (HOCM). After intravenous infusion of 3 mg nifedipine the mean aortic pressure decreased from 100 +/- 14 to 85 +/- 8 mm Hg (P less than 0.001). Heart rate increased from 70 +/- 5 to 93 +/- 5 beats per minute (P less than 0.001). This led to an increase of cardiac index from 3.0 +/- 0.5 to 3.8 +/- 0.9 l/min . m2 (P less than 0.01), whereas the stroke volume index decreased from an average of 49 +/- 11 to 42 +/- 12 ml/m2 (P less than 0.05). A marked diminution of outflow obstruction was demonstrable in 3 patients with intraventricular pressure gradients. The left-ventricular enddiastolic pressure rose from 14 +/- 3 to 18 +/- 6 mm Hg (P less than 0.02) in all patients. This effect was accompanied by a clear-cut coronary dilatation, evidenced by an increase of oxygen saturation in the coronary sinus from 29 +/- 4 to 54 +/- 9% (P less than 0.001). Thus nifedipine leads to diminished outflow obstruction and concomitant increase of cardiac output in hypertrophic cardiomyopathy. Inhibition of contraction does not seem to be compensated by peripheral effects. Coronary dilatation demonstrable in HOCM patients permits protection against coronary spasms and thus an additional antianginous effects.

Adolescent↗
PubMed1982

Immune reactions in tuberculous and chronic constrictive pericarditis. Clinical data and diagnostic significance of antimyocardial antibodies.

Humoral immune reactions were analyzed in 12 patients with exudative tuberculous pericarditis, 10 patients with constrictive pericarditis due to former tuberculosis, 10 patients with viral pericarditis, 20 patients with pulmonary tuberculosis, and 98 healthy donors. Pericarditis occurred in 12.5% of the patients with tuberculosis, whereas the incidence of tuberculosis in the 149 patients with pericarditis was 8%. Repeated pericardial puncture and pericardial effusions of greater than 500 ml with impending cardiac tamponade had to be performed in 4 patients. Clinical data indicated probable myocardial involvement in 4 of 12 patients. Antimyolemmal antibodies, which are a muscle-specific subtype of antisarcolemmal antibodies, were found in all patients with exudative tuberculous pericarditis and viral perimyocarditis, in only 1 of 12 patients with constrictive pericarditis, and in no patients with pulmonary tuberculosis. Antifibrillary antibodies--primarily of the antimyosin type--were missed in patients with viral heart disease but were demonstrated in 75% of patients with tuberculous pericarditis. Only sera with complement-fixing antimyolemmal antibodies of the IgG type in titers greater than 1:40 induced cytolysis of vital adult heterologous cardiocytes isolated and enriched by silica sol gradient centrifugation. These findings suggest not only that antimyolemmal antibodies are diagnostic indicators of perimyocardial involvement in tuberculous pericarditis, but also that they may play a significant role in its pathogenesis.

Antibody Specificity↗
PubMed1982

Antidiuretic hormone in congestive heart failure.

In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.

Adult↗
PubMed1982

Diagnostic relevance of humoral and cell-mediated immune reactions in patients with acute viral myocarditis.

Sera of 177 patients with acute myocarditis (10 coxsackie B 3/4, four influenza, four mumps, 15 cytomegalovirus, 144 undefined) were tested by indirect immunofluorescence for autoantibodies against heart and skeletal muscle and vital or air-dried adult cardiocytes. Antibody-dependent cytolysis, lymphocytotoxicity and antibody-dependent cellular lymphocytotoxicity were assessed using viral adult rat cardiocytes as target cells. Muscle-specific anti-sarcolemmal antibodies of the anti-myolemmal type--often associated with non-organ-specific anti-endothelial antibodies--were demonstrated in nine out of 10 patients with coxsackie B, in all patients with influenza and mumps and in 65 out of 144 patients with undefined myocarditis. In contrast, 13 out of 15 patients with cytomegalovirus myocarditis lacked anti-sarcolemmal antibodies but had low titre anti-inter fibrillary antibodies instead. In the presence of complement, anti-myolemmal antibodies induced cytolysis of vital cardiocytes, whereas hepatocytes remained unaffected. Titres of anti-myolemmal antibodies correlated with the degree of cardiocytolysis. The anti-myolemmal immunofluorescent pattern and the cytolytic serum activity could be absorbed with the respective viral antigens suggesting that these antibodies cross-react with moieties of the virus itself and may be both diagnostic and aetiological markers in acute viral myocarditis. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells could not be observed in our patients with myocarditis of proven viral aetiology. However, lymphocyte-mediated cytotoxicity was demonstrated in 10 ASA-positive and one ASA-negative patient with myocarditis of unknown origin. ASA-positive sera blocked lymphocytotoxicity in three of these patients.

Autoantibodies↗
PubMed1982

[Dose-dependent cardiodepression in acute alcohol intoxication in the rat].

Isovolumetric pressure-volume relations, parameters of contractility and the resting tension curve were recorded in Wistar rats prior and during acute intoxication with ethylalcohol. Parameters were recorded at blood levels between 6.0% and 2.0% of the intravenously infused alcohol. At the high blood alcohol level, maximal isovolumetric pressure is diminished by 24%, maximal rate of pressure rise by 42%, as compared with controls, whereas enddiastolic pressure increased by 32% and enddiastolic volume by 11%. Significant impairment of hemodynamics is also present at a blood alcohol level of 2.0%. These findings point to a dose-dependent cardiodepression in acute alcohol intoxication.

Alcoholic Intoxication↗
PubMed1982

[Effect of intracoronary nifedipine on coronary sinus blood flow and myocardial oxygen consumption in patients with coronary artery disease].

UNLABELLED: Reflex sympathetic nerve activation obscures the direct myocardial effect of Nifedipine after intravenous administration. Consequently, in 10 patients with coronary artery disease 0.1 mg of Nifedipine were injected into the left coronary artery to evaluate its specific effect on coronary sinus blood flow (CSF), coronary vascular resistance (CVR), and myocardial oxygen consumption (MVO2). One minute after Nifedipine, CSF increased from 115 +/- 15 to 193 +/- 47 ml/min (p less than 0.001), and CVR decreased from 0.92 +/- 0.16 to 0,54 +/- 0.12 mm Hg X min X ml-1 (p less than 0.001). Mean aortic pressure dropped from 107 +/- 5 to 99 +/- 3 mm Hg (p less than 0.01). MVO2 was reduced from 14.6 +/- 2.6 to 11.7 +/- 2.8 ml O2 X min-1 (p less than 0.05). After five minutes CSF (113 +/- 18) and MVO2 (14.9 +/- 3.1) had returned to their preinjection level. Additionally, CSF and MVO2 were measured during rapid atrial pacing (mean rate 118 +/- 6 min-1). Average CSF and MVO2 values were 172 +/- 63 and 19.8 +/- 5.0 before and 177 +/- 69 and 20.6 +/- 7.3 approximately 6 minutes after Nifedipine injection. CONCLUSIONS: Intracoronary Nifedipine results in coronary vasodilation and subsequently in an increase in coronary flow. The concomitant reduction in MVO2 provides evidence for an oxygen sparing, negative inotropic effect of Nifedipine, which, however, is of very limited duration. A sustained oxygen-saving effect during periods with increased oxygen demand could not be shown.

Angina Pectoris↗
PubMed1982

[Effect of alcohol consumption for a year on isovolumetric and auxotonic parameters in the rat heart].

Ethanol (20%) was given to wistar rats for 12 months, water to controls. In the intact heart in-situ parameters of pressure, volume, blood flow and contractility were recorded under control conditions as well as after dopamine given intravenously. Body weight of the ethanol-treated rats was diminished by 12.2%, heart weight by 12.7%, as compared with controls. A significant difference between controls and ethanol-treated rats was only found for isovolumetric left ventricular pressure. The increase in heart rate due to dopamine is less in the ethanol-treated rats. In all other parameters, no significant differences between both groups were observed.

Animals↗
PubMed1981

[Exercise tests during cardiac catheterisation in patients with mitral regurgitation (author's transl)].

Left-heart catheterisation with angiocardiography and right-heart catheterisation during exercise were performed in ten patients with pure chronic mitral regurgitation. Those patients who at rest had large normal haemodynamic parameters had a rise in pulmonary wedge pressure on exercise from 13.1 +/- 4.8 to 26.0 +/- 9.1 mm Hg (P less than 0.001), as well as subsequently an exercise-induced pulmonary hypertension with a rise in pulmonary arterial mean pressure from 20.9 +/- 8.9 to 36.5 +/- 10.3 mm Hg (P less than 0.001). In addition, there occurred abnormalities of right ventricular function in four patients during exercise, with a rise in right atrial mean pressure above 10 mm Hg. On the other hand, in 12 patients with pure mitral stenosis and higher pressures in the pulmonary artery on exercise (43.9 +/- 10.2 mm Hg) (P less than 0.1), there was no abnormal rise in right atrial pressure. In patients with mitral regurgitation associated with abnormal right ventricular function during exercise, left ventricular function at rest was impaired (ejection fraction under 51%). There was a reciprocal correlation (r = -0.86) between the left ventricular ejection fraction at rest and the level of pulmonary artery pressure on exercise. Exercise-induced pulmonary hypertension in chronic mitral regurgitation with largely normal pressure values at rest is thus less the result of volume overload of the pulmonary circulation than an expression of impaired left ventricular pumping action. Abnormal right ventricular function which occurs on exercise is not a secondary consequence of pulmonary hypertension but goes parallel with abnormal function of the left ventricle.

Adult↗
PubMed1981

Assessment of antibody mediated cytolysis of adult cardiocytes isolated by centrifugation in a continuous gradient of Percoll in patients with acute myocarditis.

Principal objections to conventional cytotoxicity assays in cardiac disease with myocytes as target cells are the use of fetal or neonatal myocardium, the cell-membrane of which does not express all antigenic determinants, and the use of trypsin as enzyme for isolation of the cells, since this alters the myolemmal membrane considerably. An improved and rapid procedure for the isolation of intact adult cardiocytes with collaggenase was developed. by means of a performed continuous self-generating silica sol and gradient centrifugation average enrichment of 81% vital myocytes was achieved by a single isopycnic procedure. The yield was improved to 94 +/- 3% vital cells by identical second centrifugation. Cardiocytes isolated by this method were used as target cells in an assay measuring the cytolytic activity of antibodies in the presence of complement: sera of patients suffering from acute viral myocarditis (Coxsackie B- and influenza-virus) with complement fixing antisacrolemmal antibodies (ASA) of the IgG- and IgM-type showed significant cardiocytolysis. ASA are postulated to play a role in the pathogenesis of acute Coxsackie B- and influenza-virus myocarditis.

Acute Disease↗
PubMed1980

[Variable acute effects of prazosin on left ventricular failure (author's transl)].

The effect of 2.5 mg prazosin orally was monitored for one hour by cardiac catheterisation in 11 patients with cardiac insufficiency as a result of primary cardiomyopathy. Mean pressures of the pulmonary capillary bed and pulmonary artery decreased on average by 9 mm Hg, of the right atrium by 2.5 mm Hg and systemically by 8 mm Hg. Judging by the increase of cardiac index patients were divided into a group of 7 "responders", all showing congestive cardiomyopathy, and a group of 4 "nonresponders" with various cardiomyopathies. During prazosin treatment cardiac index increased by 23% and pulmonary arteriole resistance decreased by 4% and pulmonary arteriole resistance increased by 41%. It is concluded that not all forms of left ventricular failure respond favourably to prazosin. Divergent effects of prazosin may possibly be caused by unequal effects on pre- and after-load of both ventricles and on variable behaviour of lung arteriole resistance.

Adult↗