Search PubMed⌕ Search

Biomedical subjects

P Schnabel

Publications and source records attributed to P Schnabel.

71 records · Page 4Linked to original sources
PubMed1990

Myocardial beta-adrenoceptors and inhibitory G-proteins in myocardial biopsies and in explanted hearts from patients with dilated cardiomyopathy.

Cardiac beta-adrenoceptors and the alpha-subunits of the inhibitory guanine-nucleotide binding proteins (Gi alpha) were determined in myocardial biopsies and in larger samples of explanted hearts from patients with dilated cardiomyopathy. The myocardium of one non-failing heart was studied for comparison. There were fewer beta-adrenoceptors in right and left ventricular samples from hearts with dilated cardiomyopathy than in the non-failing myocardium. The number of beta-adrenoceptors determined by equilibrium saturation experiments closely correlated with their density as measured by a saturating concentration of the radioligand 125Iodocyanopindolol in myocardial biopsies. Using the 32P-ADP-ribosylation of a 40kDa membrane protein catalyzed by pertussis toxin, an increase of Gi alpha could also be shown in both myocardial biopsies and explanted hearts.

Biopsy↗
PubMed1989

Reduced effects of dopexamine on force of contraction in the failing human heart despite preserved beta 2-adrenoceptor subpopulation.

The results of the present study show that the reduction of the total number of beta adrenoceptors affected the beta 1-adrenoceptor subpopulation, whereas the beta 2 adrenoceptors were not detectably altered in the failing heart. Dopexamine had a 9.8-fold greater affinity to beta 2 adrenoceptors than to beta 1 adrenoceptors. In nonfailing myocardium, dopexamine increased force of contraction concentration-dependently. However, dopexamine alone had no effect in papillary muscle strips from moderately (NYHA II-III) and severely (NYHA IV) failing myocardium. However, in the presence of milrinone, it concentration-dependently increased force of contraction. Under this condition, the effectiveness was slightly less pronounced in NYHA IV than in NYHA II-III. Dopexamine concentration-dependently stimulated adenylate cyclase activity. Experiments with the beta 1-selective antagonist CGP 207.12 A and the beta 2-selective antagonist ICI 118.551 showed that both stimulation of adenylate cyclase and the increase of force of contraction are mediated by beta 2 adrenoceptors. It is concluded that although the number of beta 2 adrenoceptors is preserved in the failing myocardium, dopexamine alone does not increase force of contraction. However, the positive inotropic effect of dopexamine, which is observed in the presence of milrinone and the stimulation of adenylate cyclase activity by dopexamine are mediated by beta 2 adrenoceptors. Therefore, beta 2 adrenoceptors exist in the human myocardium, are coupled to adenylate cyclase, and are capable of increasing force of contraction. These results provide evidence for an impaired coupling of beta 2 adrenoceptors to mechanisms beyond receptor occupation in terminal heart failure.

Adenylyl Cyclases↗
PubMed1984

Lectin target cells in human central nervous system and the pituitary gland.

Peanut lectin (PNL), Concanavalin A (Con A) and Ulex europaeus lectin I (Ulex) were chosen to map their binding sites in different regions of formalin fixed and paraffin embedded human central nervous system tissue and pituitary gland tissues. An extended PaP method was used for PNL and Ulex, whereas a direct peroxidase technique was employed for Con A. In astrocytes, the cytoplasm as well as the delicate processes were stained by PNL and Con A; the most conspicuous binding of PNL was seen in the ependymal cells and on the surface of plexus epithelial cells; in the anterior part of the pituitary gland a selective population was PNL positive. Intracytoplasmic Con A acceptors could be demonstrated in neurons, in ependymal cells, and in plexus epithelial cells. Intracytoplasmic Con A receptors were finely granular in astrocytes, oligodendrocytes, and in some cells in the pituitary gland. Ulex binding was restricted to the vascular endothelial cells and a selective population of cells in the pituitary gland. Our results suggest that lectins may be good tools for the evaluation of their respective target cells in the central nervous system and in the pituitary gland.

Arachis↗
PubMed1983

Emphasis on peanut lectin as a marker for granular cells.

Peanut lectin (PNL) binding to a total of 13 granular cell tumours was examined by means of the peroxidase antiperoxidase technique. The tumours included six tumourettes of the neurohypophysis, one malignant granular cell tumour of the brain, and six peripheral tumours of distinct locations. Every tumour studied showed intracytoplasmic fine granular PNL binding; after pretreatment with neuraminidase, the weakly positive reaction was enhanced to a great extent. In all tumours simultaneous examination for the detection of lysozyme and glial fibrillary acidic protein (GFAP) was also carried out. Lysozyme was negative in all cases, whereas GFAP expression could be demonstrated at the periphery of the malignant granular cell tumour of the brain. The data presented clearly demonstrate that PNL can be used as a histochemical marker for granular cells regardless of their location. The fact that the presence of lysozyme could not be proved does not support the view of a histiocytic origin for granular cells, whereas the expression of GFAP in some immature granular cells of the brain tumour examined is considered to be an argument in favor of its glial origin.

Adult↗
PubMed1983

Immunohistochemical localization of peanut lectin binding sites on human brain tumors as determined by peroxidase-antiperoxidase technique in paraffin sections.

Peroxidase-antiperoxidase (PAP) technique was selected for visualizing the binding of peanut lectin (PNL) to the most frequent human brain tumors. The randomly selected material included neoplasms of neuroectodermal and mesenchymal origin. We employed 1--5 micrometers of routinely processed and paraffin-embedded tissues. PNL receptors were detected to a variable extent on the cell surface of astrocytoma, glioblastoma multiforme, oligodendroglioma, ependymoma, meningotheliomatous meningeoma, and plexus papilloma. In gliomas as increase in malignancy seems to be associated with a decrease in PNL binding. Except for the plexus papillomas, neuraminidase pretreatment had neither a qualitative nor a quantitative influence on the binding behavior of PNL. Intracellular PNL receptors could be detected in "granular cells" and in the perinuclear region of malignant gliomas.

Arachis↗
PubMed1981

[Experimental brain death].

There is described a method for cerebral circulatory standstill by means of an isolated intra vital sink of cerebral vessels with Kallocryl C and it is compared with other methods. This methods is the most suitable model. Indeed it is connected with only a single response of the circulatory system in contrast to the most frequent clinical progresses. The final condition, however, corresponds to the isolated brain death of the organ donor. Long time examinations are possible.

Animals↗
PubMed1979

[Perioral dermatitis and the atopic constitution].

Detailed allergologic investigations, allergy histories and skin tests in 80 patients with perioral dermatitis led to the conclusion that the disease has to be considered a manifestation of atopy. Thus another clinical entity would have to be added to the hitherto known manifestations of the atopic constitution. The findings reported by other investigators may thus be interpreted as conditional or aggravating pathogenetic factors.

Adolescent↗
PubMed1979

[Basic studies on the pathogenesis and treatment of fat embolism. I. Fracture mechanism and fat embolism].

We examined the amount of fat that can be forced into the circulation by compression of femora and of heads of the tibia in the very moment of injury. By fractures of diaphyses no considerable reduction of the intraosseous space was achieved and no fat was expelled through the foramina nutritia before the hard cortical bone was splintered. However, considerable amounts of fat were expelled into veins, when the epiphyses of the femora or when the head of the tibia was compressed from medially and from laterally. Even by a purely manual compression some fat was forced to leave the spongiosa by the foramina nutritia. This is explained by the higher elasticity of the spongious bone, permitting a marked space reduction by compression even before a fracture sets in. The mechanism resembles the procedure of opacification of veins by contrast media, injected into the bone cavity under pressure. The significance of these findings for the pathogenesis of clinical fat embolism is discussed.

Adult↗
PubMedDate not supplied

Beta-adrenergic signal transduction in the failing and hypertrophied myocardium.

A strong sympathetic activation has been observed in heart failure and is the cause of beta-adrenergic desensitization in this condition. On the receptor level there is downregulation of beta1-adrenergic receptors and uncoupling of beta2-adrenoceptors. The latter mechanism has been related to an increased activity and gene expression of beta-adrenoceptor kinase in failing myocardium, leading to phosphorylation and uncoupling of receptors. beta3-Adrenoceptors mediate negative inotropic effects, but alterations in these receptors are not known. In addition, an increase in inhibitory G protein alpha subunits (Gi alpha) has been suggested to be causally linked to adenylyl cyclase desensitization in heart failure. In contrast, the catalytic subunit of adenylyl cyclase, stimulatory G protein alpha and betagamma subunits, have been observed to be unchanged. Recent evidence shows that increases in Gi alpha also depress adenylyl cyclase in compensated cardiac hypertrophy both in monogenic and polygenic and in secondary hypertension. These increases of Gi alpha can suppress adenylyl cyclase in the absence of beta-adrenergic receptor downregulation. Since cardiac hypertrophy in pressure overload is a strong predictor of cardiac failure, these observations indicate that adenylyl cyclase desensitization by Gi alpha may be a pathophysiologically relevant mechanism contributing to the progression from compensated cardiac hypertrophy to heart failure.

Animals↗