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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 91 records · Page 5Linked to original sources
PubMed1988

Atrial natriuretic peptide in congestive heart failure in the dog: plasma levels, cyclic guanosine monophosphate, ultrastructure of atrial myoendocrine cells, and hemodynamic, hormonal, and renal effects.

In an animal preparation of congestive heart failure in the dog, during the development of cardiac failure due to rapid right ventricular pacing we observed significant decreases in cardiac output and arterial pressure and increases in pulmonary arterial and right atrial pressure. We also observed a related increase in right atrial pressure and increases in plasma levels of atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (c-GMP). Ultrastructure changes in the atrial myoendocrine cells indicated extreme stimulation of the secretory apparatus of ANP. The response of hemodynamic, renal, and hormonal variables was investigated after incremental infusions (0.01, 0.03, 0.1, 0.3, and 0.06 microgram/kg/min) of exogenous ANP. In healthy animals ANP significantly decreased mean arterial pressure, cardiac output, stroke volume, and right atrial pressure without changing heart rate or peripheral vascular resistance. As expected, we found a striking increase in urine flow and urinary excretion of sodium, chloride, magnesium and calcium and a smaller increase in potassium excretion. ANP suppressed renin secretion, and increased renal plasma flow, glomerular filtration rate, and filtration fraction. In dogs with heart failure ANP caused a small reduction in mean arterial pressure. No effect was seen on other hemodynamic variables or plasma renin concentration. The excretory effects on the kidneys were completely absent, and smaller increases in glomerular filtration rate and filtration fraction were observed. We found no difference between healthy dogs and animals with heart failure with respect to the secretion of c-GMP during ANP infusions in relation to the plasma levels of ANP. This suggests an intracellular defect that prevents the mediation of the hormonal signal into biological action in the presence of heart failure.

Animals↗
PubMed1987

Contribution of the renin-angiotensin-aldosterone system to development of tolerance and fluid retention in chronic congestive heart failure during prazosin treatment.

To determine the effects of the renin-angiotensin-aldosterone system on development of tolerance and fluid retention in patients with chronic congestive heart failure during long-term prazosin treatment, plasma renin concentration, aldosterone, norepinephrine and maximal exercise tolerance were measured during chronic therapy with digitalis and diuretics, to which prazosin, captopril or a combination of both drugs was added. Plasma renin concentration and aldosterone level decreased slightly during prazosin therapy and norepinephrine level increased significantly. When captopril was given, plasma renin concentration increased as expected, aldosterone level normalized and norepinephrine level decreased significantly. When prazosin was added to captopril therapy, norepinephrine level increased and plasma renin concentration and aldosterone level did not change. Exercise capacity did not increase during prazosin treatment, but was increased with captopril treatment. Prazosin treatment was associated with an increase in body weight even though the dose of furosemide was increased. Inhibition of the renin-angiotensin system did not prevent fluid retention induced by prazosin during combination therapy. These findings suggest that the renin-angiotensin-aldosterone system is not substantially involved in development of tolerance and fluid retention during prazosin therapy; stimulation of plasma norepinephrine may be of decisive importance.

Adult↗
PubMed1987

The effects of atrial fibrillation on coronary blood flow and performance of ischaemic myocardium in dogs with coronary artery stenosis.

1. Atrial fibrillation may impair coronary blood flow by tachycardia and reflex vasoconstriction. It has not been documented, however, whether in the presence of coronary stenosis atrial fibrillation exceeds the effects of rhythmic atrial tachycardia. 2. The effects of experimentally induced atrial fibrillation compared with atrial tachycardia, therefore, were tested in 22 anaesthetized dogs. Stenosis of the left anterior descending coronary artery was induced to reduce coronary blood flow by about 40%. 3. In the presence of coronary stenosis, atrial fibrillation (ventricular rate: 234 +/- 21 beats/min) reduced coronary blood flow from 58 +/- 7 to 44 +/- 8 ml min-1 100 g-1 (P less than 0.001, mean +/- SEM) and subendocardial segment shortening (ultrasonic crystals) from 12 +/- 2 to 4 +/- 2% (P less than 0.0025), and resulted in a lactate production of 30 +/- 11% (P less than 0.005 vs sinus rhythm). 4. Atrial tachycardia (heart rate: 216 +/- 21 beats/min, NS vs atrial fibrillation) did not significantly change coronary blood flow and reduced segment shortening to 7 +/- 3% (P less than 0.05 vs atrial fibrillation). Significant lactate production did not occur. 5. Since mean arterial pressure fell from 100 +/- 4 mmHg at sinus rhythm to 89 +/- 3 mmHg (P less than 0.01) during atrial fibrillation but not during atrial tachycardia, it was held constant in 13 dogs by a pressurized blood reservoir. Coronary blood flow, however, fell from 43 +/- 6 to 36 +/- 5 ml min-1 100 g-1 (P less than 0.0025). 6. Thus atrial fibrillation may reduce coronary blood flow and induce myocardial ischaemia in the presence of coronary stenosis in excess of atrial tachycardia.

Animals↗
PubMed1987

Nocardial endocarditis of an aortic valve prosthesis.

The organism responsible for endocarditis of a prosthetic aortic valve was identified as Nocardia asteroides. The patient was treated with intravenous amikacin (250 mg four times a day) and intravenous imipenem (1.5 g four times a day). The valve was replaced under this new antibiotic regimen. This is the first report of survival after prosthetic valve nocardiosis.

Amikacin↗
PubMed1987

Atrial natriuretic factor in acute and chronic cardiac failure.

Water, sodium, and potassium balance and urinary excretion of norepinephrine and aldosterone were investigated in rats with left ventricular failure due to left ventricular infarction, and measurements were obtained of plasma levels of atrial natriuretic factor (ANF). Increased plasma levels of ANF in relation to the size of the infarction and to the right atrial and left ventricular end-diastolic pressure were found. The augmented levels of ANF were not able to prevent an accumulation of sodium in the rats with myocardial infarction in which urinary excretion of norepinephrine and aldosterone was unchanged in comparison to control values. Plasma levels of ANF in the pulmonary artery, aorta, and renal vein of six conscious dogs were studied during the development of heart failure due to rapid right ventricular pacing. A threefold increase in ANF was found: ANF levels did not differ between the pulmonary artery and the aorta, but a reduction in ANF of about 30% was reported in the renal vein in comparison to the arteries. A close positive correlation between right atrial pressure and plasma levels of ANF was noted. No correlation could be demonstrated between mean pulmonary arterial pressure and ANF or between the stimulated plasma renin concentration and plasma ANF values.

Acute Disease↗
PubMed1987

[Initial experiences with pro-urokinase in acute myocardial infarct].

Pro-urokinase is a fibrin-specific, single-chain, high molecular form of urokinase that induces thrombolysis without fibrinogenolysis in experimental animals. Consequently, the potential advantage of pro-urokinase is that its activation can be limited to the site of a clot. Its efficiency was assessed in ten patients with acute transmural myocardial infarction. Reperfusion occurred in only two patients. In five out of seven patients with persistent complete coronary occlusion, clot lysis could be achieved by intracoronary streptokinase application within 30 min after completion of the pro-urokinase infusion. Fibrinogen and alpha 2-antiplasmin changed only moderately during pro-urokinase infusion. These preliminary data may indicate a limited thrombolytic efficiency of pro-urokinase in patients with acute myocardial infarction.

Adult↗
PubMed1987

Effects of a N(6)-disubstituted adenosine derivative on myocardial metabolism and ischemic stress following coronary occlusion.

The effect of N(6)-phenyl-N(6)-allyladenosine (PAA, BM 11.189) on myocardial ischemic stress was evaluated in six open-chest mongrel dogs during repeated coronary occlusions of 3 min. Whereas there was not significant change in hemodynamic parameters before and during coronary occlusions after treatment, PAA reduced significantly epicardial ST-segment elevations (-34%) during ischemia and myocardial release of lactate (-43%), phosphate (-44%), and potassium (-48%) in the early reperfusion period. PAA lowered significantly arterial non esterified fatty acids and converted oxidative myocardial metabolism from lipid to predominantly carbohydrate utilization, reflected by a shift of cardiac respiratory quotient from 0.81 to 1.01. The beneficial effects of PAA on myocardial ischemic injury could be explained by an improved economy of oxidative myocardial energy supply in the jeopardized border zone of the ischemic myocardium.

Adenosine↗
PubMed1986

Vasopressin, renin and norepinephrine levels before and after captopril administration in patients with congestive heart failure due to idiopathic dilated cardiomyopathy.

The effects of 4 weeks of captopril treatment were studied in 10 patients with chronic congestive heart failure (CHF). Acute administration of 50 mg of captopril resulted in an increase in cardiac index and significant decreases in arterial pressure, peripheral vascular resistance and pulmonary capillary wedge pressure. Before treatment, all patients had elevated vasopressin levels (17 +/- 4 pg/ml) relative to decreased plasma osmolality (274 +/- 15 mOsm/kg H2O), and these values were not initially affected by captopril administration (22 +/- 7 pg/ml). However, the relation between arginine vasopressin and plasma osmolality was restored to normal by long-term therapy with captopril (50 mg 3 times daily) (3.0 +/- 1.3 pg/ml; 283 +/- 166 mOsm/kg H2O), which also resulted in sustained improvement of cardiac function. Long-term captopril therapy increased plasma renin concentration from already elevated levels (11 +/- 4 to 32 +/- 8 ng AI/ml X hour) and decreased plasma norepinephrine from 1,054 +/- 244 to 488 +/- 101 pg/ml. Thus, nonosmolar stimulation of vasopressin secretion in CHF can be restored to normal by chronic converting enzyme blockade. The acute vasodilator effects of converting enzyme blockade are not mediated by a reduction of possible vasoconstrictor effects of vasopressin.

Arginine Vasopressin↗
PubMed1986

Effectiveness of converting enzyme inhibition (enalapril) for mild congestive heart failure.

The present study investigates the effectiveness of converting enzyme inhibition (CEI) on cardiac performance of patients with congestive heart failure (New York Heart Association functional class II). Outpatients (n = 12) were treated with enalapril, 5 to 10 mg twice daily, in addition to stable doses of digitalis and diuretic drugs. Before and after 4 and 12 weeks of treatment a treadmill exercise test and echocardiography were performed. Maximal oxygen uptake and exercise tolerance increased significantly and mean arterial pressure at rest and on exertion decreased significantly. Heart rate did not change. Left ventricular end-diastolic diameter decreased significantly. Serum angiotensin converting enzyme activity was reduced to nearly 0; plasma renin concentration, which was already elevated, increased further. Plasma norepinephrine levels did not change significantly. Treatment was tolerated well by all patients. CEI decreased preload and afterload, suggesting that they might have had an inappropriately elevated arteriolar and venous tone owing to a moderately stimulated renin angiotensin system and sympathetic nervous system. These conditions may lead to further deterioration of cardiac performance. By means of CEI one may be able to interrupt these pathogenetic mechanisms, relieving the already damaged heart from inappropriate elevations of preload and afterload and delaying or even preventing further deterioration of cardiac performance.

Adult↗
PubMed1986

Antibodies to human sinus node in sick sinus syndrome.

The incidence of autoantibodies against human conducting tissue was studied in 45 pacemaker patients with sick sinus syndrome (SSS), in 17 patients with bradyarrhythmia, and five patients with hypersensitive carotid sinus syndrome. Antibodies against the human sinus node were demonstrated in 29% of patients with SSS and in 24% of patients with bradyarrhythmia; a tenfold risk of SSS could be calculated in patients with this antibody as compared to age-matched controls. At least two subtypes of anti-sinus node antibodies were demonstrated: an antibody absorbable and another one not absorbable with ventricular myocardium. Patients with SSS and prior myocarditis of rheumatic fever have a threefold incidence of that antibody, demonstrating that anti-conducting tissue antibodies are etiologic indicators for former inflammatory heart disease. These antibodies may play a role in the secondary immunopathogenesis of sick sinus syndrome. This hypothesis emerges as an interesting new pathogenetic concept.

Aged↗
PubMed1986

Atrial natriuretic peptide in patients with severe heart failure.

Alpha atrial natriuretic peptide was measured in plasma in 7 patients with severe heart failure before and after the administration of the synthesized substance. An inverse correlation was found between basal plasma levels of alpha atrial natriuretic peptide and cardiac output. Incremental bolus injections of synthetic alpha atrial natriuretic peptide and the continuous infusion for 30 minutes resulted in a decrease of peripheral vascular resistance, an increase of cardiac output and a decrease of blood pressure. Plasma aldosterone was markedly reduced in each patient by the administration of atrial natriuretic peptide and a small but significant decrease of plasma cortisol was found. Diuresis, urinary sodium and potassium excretion were enhanced. No significant changes were observed concerning adrenocorticotropic hormone, plasma renin concentration, plasma norepinephrine and vasopressin and the plasma levels of 6-keto-prostaglandin F1-alpha and prostaglandin E2.

Atrial Natriuretic Factor↗
PubMed1985

[The atrial natriuretic factor in severe congestive heart failure. Plasma level, hemodynamic, hormonal and renal effects].

The effects of human alpha atrial natriuretic factor following bolus injection of increasing doses and during a continuous 30 minute infusion were investigated in 7 patients with severe congestive cardiac failure (NYHA III-IV). The natriuretic factor was measured in plasma before and after the bolus application or infusion. The plasma levels were raised in 6 patients. A significant inverse correlation was observed between the basal levels of the atrial factor and cardiac output. In addition, there was a dose-dependent fall in preload and afterload as well as in the peripheral vascular resistance and there was an improvement in cardiac performance. The alpha atrial natriuretic factor inhibited aldosterone and cortisol secretion and promoted diuresis and the urinary excretion of sodium and potassium. The plasma concentrations of renin, noradrenaline, vasopressin, 6-keto-prostaglandin F1 alpha, the stable metabolite of prostacyclin, and prostaglandin E2 remained unchanged.

Aldosterone↗
PubMed1985

Coronary hemodynamic and metabolic effects of nifedipine in patients with coronary artery disease treated with beta-blocking drugs.

In humans, reflex sympathetic nerve activation modulates the direct cardiac action of nifedipine after systemic administration and results in a positive chronotropic and inotropic response. The coronary hemodynamic and metabolic effects of nifedipine were evaluated after propranolol-induced acute beta-receptor blockade in 12 patients with angiographically documented coronary artery disease. The intravenous injection of propranolol led to a decrease in heart rate, coronary blood flow and myocardial oxygen consumption and an increase in coronary vascular resistance and the coronary arteriovenous oxygen difference. Mean aortic pressure did not change. The subsequent intravenous administration of nifedipine resulted in a transient increase in coronary blood flow and a reduction in coronary vascular resistance and the coronary arteriovenous oxygen difference and a sustained decrease in mean aortic pressure and myocardial oxygen consumption without significant changes in heart rate. Thus, in the presence of beta-receptor blockade, the positive chronotropic response to nifedipine is attenuated and nifedipine reduces myocardial oxygen consumption significantly. The vasodilatory effect of nifedipine is maintained and a potential propranolol-related inappropriate vasoconstriction may be reversed. The combination of nifedipine and beta-receptor blocking agents may be useful in the treatment of patients with both effort-induced angina and angina related to changes in coronary vasomotor tone.

Adult↗
PubMed1985

Deterioration of metabolic coronary regulation in hemorrhagic shock. Role of hypoxia and the renin-angiotensin system.

The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen (n = 7). A third group of dogs was ventilated with room air and bilaterally nephrectomized 5 h prior to starting the experimental protocol (n = 7). After control data had been obtained, dogs were bled from the femoral arteries into a pressurized reservoir which maintained blood pressure at 45 +/- 1 mmHg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 micrograms/kg per min). Coronary blood flow was reduced by hemorrhage, and no significant difference existed in coronary flow during hemorrhage among the three groups. Coronary sinus oxygen saturation was diminished in control animals during hemorrhage from 26% +/- 1% to 17% +/- 1% (P less than 0.05) but normal in 100% oxygen ventilated animals (30% +/- 3%) and in nephrectomized dogs (34% +/- 4%). Coronary oxygen extraction was reduced by saralasin in intact but not in nephrectomized dogs. In six additional experiments, in which blood pressure was not artificially held constant during saralasin infusion, saralasin still significantly improved coronary sinus oxygen saturation and thus reduced coronary oxygen extraction. The data suggest that both hypoxia and the renin-angiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.

Animals↗
PubMed1985

On the mechanism of renin release during experimental myocardial ischaemia.

An increase in plasma renin activity (PRA) following experimental coronary occlusion has previously been demonstrated in anaesthetized and conscious dogs. The purpose of the present study was to analyse the mechanism of this renin release. In two distinct models of myocardial ischaemia in anaesthetized dogs--i.e. occlusion of the left-anterior descending coronary artery (model A, n = 21) and atrial pacing in the presence of stenosis of the left-anterior descending coronary artery (model B, n = 23), an increase in arterial PRA was found from 1.68 +/- 0.43 to 3.06 +/- 0.63 ng ml-1 h-1 (model A, mean +/- SEM, P less than 0.025) and from 9.87 +/- 3.59 to 14.96 +/- 4.06 ng ml-1 h-1 (model B, P less than 0.05), respectively. The increase in PRA following coronary occlusion was not blunted by adrenergic beta-receptor blockade with propranolol (3 mg kg-1 i.v.; n = 4). Coronary sinus PRA was lower than arterial PRA and the increase in PRA did not occur in nephrectomized dogs (n = 5). The data suggest that myocardial ischaemia induces a release of renin from the kidney which is not mediated by adrenergic beta receptors.

Animals↗
PubMed1985

Immunological cellular regulator and effector mechanisms in myocarditis.

The diagnosis, pathogenesis and etiology of myocarditis are often difficult to establish with certainty. Consequently, we investigated cellular regulator and effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps) as well as other inflammatory heart diseases which could not be classified etiologically. In acute myocarditis there was an elevation of B- and activated T-lymphocytes (OKIa 1-positive) but, in contrast, no significant changes in the activity of peripheral suppressor T-cells (OKT 8-positive). The activity of cell-specific lymphocytic effector mechanisms against vital cardiocytes was unchanged or slightly elevated in myocarditis, while the activity of the less target cell specific natural killer cells, which were measured in vitro against K562 tumor cells, was diminished. These findings are indicative of increased activity of target specific cytotoxic effector mechanisms and a reduction in the activity of nonspecific cellular effector mechanisms in peripheral blood.

Animals↗
PubMed1985

[Humoral and cellular immunity in perimyocarditis and congestive cardiomyopathy].

In coxsackie B-, influenza and mumps-induced perimyocarditis the characteristic immunological features were cross-reacting cytolytic antimyolemmal antibodies, circulating immune complexes and no NK- or K-cell activity. Cytolytic antimyolemmal antibodies are markers of a secondary immunopathogenesis in perimyocarditis. In cytomegalovirus myocarditis antiinterfibrillary antibodies could be found and immune complexes were rarely observed. Postmyocarditic cardiomyopathy could be identified by circulating antimyolemmal and antisarcolemmal antibodies which also bind to the endomyocardial autopsy specimens. In these patients circulating immune complexes are more frequent than in normals and in dilated cardiomyopathy. In dilated cardiomyopathy antifibrillary and antiinterfibrillary antibodies were observed, the incidence of which correlated with the severity (NYHA) of the disease. A group of patients with dilated cardiomyopathy could be distinguished who demonstrated regardless of the severity lymphocytotoxic reactions against vital cardiocytes.

Antigen-Antibody Complex↗