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Biomedical subjects

K Werdan

Publications and source records attributed to K Werdan.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Use of pseudomonas immunoglobulin. Indications and results].

In comparison with polyvalent immunoglobulins, Pseudomonas immunoglobulin (Psomaglobin) is enriched several times in antibodies to Ps. lipopolysaccharide antigens and exotoxin A as well as lipid A. The resulting protective action which is superior to polyvalent immunoglobulins in infections with Pseudomonas, was demonstrated both in cell culture (protection against cytotoxicity of Ps. exotoxin A in heart muscle cells) and in animal models of sepsis. In patients suffering from Ps. pneumonia and Ps.-sepsis clinical improvement is seen after application of this immunoglobulin and also in quantifiable by scoring systems, the unequivocal proof of lowering lethality by using this specific immunoglobulin in Pseudomonas infection is to be shown however.

Critical Care↗
PubMed1989

[Magnetic resonance tomography imaging of Botallo's duct--a case report].

In a female patient suffering from renal insufficiency in whom angiography could not be performed, it was possible to confirm the diagnosis of a ductus arteriosus (Botallo's duct) by magnetic resonance imaging. The present case report shows that it is possible to visualise this congenital heart disease by MRI. This can be of importance especially if angiography cannot be performed (as in this case) because of renal insufficiency or because of contrast medium allergy.

Adult↗
PubMed1989

[Echocardiography with angiotensin administration in the diagnosis of adriamycin-induced cardiomyopathy].

Noninvasive assessment of early cardiotoxicity of doxorubicin is still a problem of clinical concern. We studied whether echocardiography during afterload stress induced by angiotensin II (1,000-3,000 ng/min) allows earlier detection of left ventricular impairment than echo at rest. We compared 30 normals (N) to 30 patients with carcinoma, who had received doxorubicin at a cumulative dose of at least 360 mg/sqm. At rest echocardiograms of patients were either normal (P1; n = 24) or abnormal (P2; n = 6; fractional shortening less than 28%, distance of mitral E-point to septum greater than 7 mm). Best parameter for separation of P1 vs N was the slope K of the regression line of the relation between endsystolic diameter and systolic blood pressure (cuff-method). 38% of P1 and 100% of P2 had K-values below the range of N (less than 4.7 mm Hg/mm). Four of five patients with reduced ejection fraction assessed by scintigraphy (less than 55%) after continued therapy with doxorubicin have had, in previous echocardiographic studies, normal resting parameters but abnormal K-values. We conclude that afterload-stress increases the sensitivity of echocardiography in detecting cardiotoxicity due to doxorubicin.

Adolescent↗
PubMed1988

Homologous vs. heterologous desensitization of the adenylate cyclase system in heart cells.

Exposure of cultured heart muscle cells to noradrenaline led to a decrease in the effects of isoproterenol and prostaglandin E1 on cAMP formation and contraction velocity. However, heterologous desensitization, as measured by prostaglandin E1 stimulation, only occurred at higher noradrenaline concentrations than homologous desensitization (isoproterenol stimulation). As the defects of the adenylate cyclase system in heart failure are attributed to noradrenaline-induced desensitization, it is concluded from the results that, in comparison to the subsensitivity to beta-adrenoceptor agonists in failing human hearts, a decrease in the responsiveness to other receptor-dependent adenylate cyclase stimulators should also occur but only at higher degrees of heart failure.

Adenylyl Cyclases↗
PubMed1987

The role of endogenous noradrenaline in the beta-blocker withdrawal phenomenon--studies with cultured heart cells.

An in vitro model to evaluate the role of endogenous noradrenaline in the beta-blocker withdrawal phenomenon is described: Beating chicken heart muscle cells (5000 beta 1-adrenoceptors/cell) and heart nonmuscle cells (3000 beta 2-adrenoceptors/cell) were cultured in serum-free, hormone-supplemented medium. Basal state, subtype selective down-regulation of beta-adrenoceptors by endogenous noradrenaline (decrease in receptor number, beta 1 more than beta 2) was simulated by addition of noradrenaline to the culture medium; chronic beta-blockade was simulated by exposure of the cells for 3 days to various beta-blockers (propranolol, no ISA; timolol, slight ISA; pindolol, strong ISA). Beta-blocker withdrawal phenomenon--increased response in isoproterenol-induced cAMP production and positive inotropy--is correlated with the increase in the number of beta-adrenoceptors after withdrawal of the drugs. Propranolol induces a withdrawal phenomenon at every degree of noradrenaline-induced basal state down-regulation of beta-adrenoceptors; in contrast, a withdrawal phenomenon by pindolol is only seen at a higher degree of beta-adrenoceptor down-regulation. In the presence of physiological noradrenaline concentrations pindolol affects beta-adrenoceptor subtypes in a qualitatively different manner: the number of beta 1-adrenoceptors is increased, the number of beta 2-adrenoceptors is decreased. This finding demonstrates that the intrinsic sympathomimetic activity of nonselective beta-blockers can manifest itself only if the receptors are not strongly down-regulated. As beta 2-adrenoceptors are present in a much less down-regulated state than beta 1, ISA mainly acts on beta 2-adrenoceptor subtype, thus, presenting a beta 2-"pseudo-selectivity" of ISA.

Adrenergic beta-Antagonists↗
PubMed1987

Endogenous noradrenaline and beta-adrenoceptor regulation in cultured heart cells.

a) Cultured heart muscle cells from chicken embryos and neonatal rats possess about 5000 beta 1-adrenoceptors/cell, heart non muscle cells from these species about 3000 beta 2-adrenoceptors/cell. Agonist binding in heart muscle cells results in cAMP formation and in a positive inotropic effect. b) Beta 1- and beta 2-adrenoceptors of heart cells are downregulated to different degrees in the presence of physiological noradrenaline concentrations in the culture medium. c) Using chicken heart cells in culture, a cellular model of the beta-blocker withdrawal phenomenon in the heart has been established, elucidating the modifying action of endogenous catecholamines and the role of ISA (partial agonist activity) in this phenomenon and classifying the so-called "beta 2-pseudo-selectivity" of the ISA action. d) In the absence of added catecholamines, (-)propranolol exposure of the cells for 3 days increases the number of beta-adrenoceptors of chicken heart muscle cells up to 170% of control, while in rat heart muscle cells the receptor number remains unchanged. The mechanism of this "basal" receptor downregulation in chicken heart muscle cells is unclear. The data presented demonstrate the usefulness of heart cell cultures in the study of beta-adrenoceptor regulation of the heart.

Adenylyl Cyclases↗