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Biomedical subjects

T Peters

Publications and source records attributed to T Peters.

334 records · Page 19Linked to original sources
PubMedDate not supplied

Studies on the mechanism of the positive inotropic effect of ATX II (Anemonia sulcata) on isolated guinea pig atria.

The basic polypeptide ATX II (MW 4,770) isolated from the sea anemone Anemonia sulcata evokes a pronounced and dose-dependent positive inotropic effect in different mammalian heart preparations. The mechanism of this effect is so far unknown. (a) Investigations on isolated guinea pig atria indicate that changes of the steady state cellular Na, K and Ca concentrations cannot account for the positive inotropic effect. (b) An increase of the surface pressure of phospholipid monolayers was observed only at cardiotoxic ATX II concentrations. However, the 45Ca binding to phosphatidylserine, as the essential Ca-binding phospholipid, was not changed even at cardiotoxic ATX II concentrations. (c) Neither the enzymatic activity nor the ouabain inhibition kinetic of an isolated Na/K-ATPase preparation was affected by ATX II. (d) In intact electrically stimulated (1 Hz) guinea pig atria the binding of [3H]ouabain increases by about 50% at a positive inotropic ATX II concentration. The results suggest that the positive inotropic effect of ATX II is not caused by an unspecific membrane damaging action or by a direct interaction with the Na/K-ATPase. The increased binding of [3H]ouabain to intact heart muscles indirectly reflects an increased pump activity of the Na/K-ATPase, which is caused by an elevated Na transient due to the electrophysiologically well-established mechanism of the ATX II action on fast Na channel, i.e., delayed inactivation of the fast Na flux. However, the exact mechanism of the ATX II induced positive inotropic effect remains unknown.

Animals↗
PubMedDate not supplied

Plasmalemmal calcium in cardiac excitation-contraction coupling.

1. Mammalian heart muscle is extremely sensitive to the external calcium concentration. It reacts to alterations of the external calcium concentration with an immediate adaptation of contractile force. 2. In mammalian heart there is a network of large transverse tubules throughout the cell. These structures are regularly arranged at the level of the sarcomeric Z- and I-lines and increase the cell surface by a factor of ten. 3. Experimental evidence favours the assumption that the plasmalemma could be the site of a loosely bound superficial Ca fraction which becomes ionized upon depolarization and is again bound upon repolarization of the cardiac cell membrane. 4. A mechanism is discussed which bases the excitation-contraction coupling process on a physicochemical interaction of calcium with membrane phospholipids. The degree of interaction is thought to be governed by the transmembrane electric field, the induced dipole moment of membrane constituents, and proton activity within the membrane.

Animals↗
PubMedDate not supplied

Veratridine-induced intoxication: an in vitro model for the characterization of anti-ischemic compounds?

Due to the complexity of ischemia-induced cellular dysfunction many different pharmacological approaches have been tested to improve cellular ischemia resistance. However, despite the importance of [Na+]i for ischemia-induced dysfunction, only very few studies have investigated the contribution of the Na+ channel to ischemia-induced failure of intracellular ion homeostasis. Since an activation of Na+ channels by veratridine also results in a failure of intracellular ion homeostasis, the veratridine- and ischemia-induced alterations of cellular function were compared. Moreover, despite the difference in the electrophysiological changes induced by veratridine and ischemia, the possible involvement of a slowly inactivating, less selective Na+ channel in both veratridine- and ischemia-induced cellular dysfunction is discussed. As a conclusion it is suggested that veratridine intoxication could be a helpful in vitro method for the characterization of putative anti-ischemic compounds.

Action Potentials↗
PubMedDate not supplied

Elastosis and cancer.

Recently we have shown that the autofluorescence within or just outside of a malignant tumor is rather small or large resp. in comparison to healthy tissue when excited at 365 nm. Studies with unfixed, unstained cryosections of skin with melanomas have revealed bulky fiber-like structures with a high fluorescence intensity just outside of a malignant tumor. Using polarized light, the structures could be identified as elastic fibers. This was also confirmed by studies on arterial walls.

Aged↗
PubMedDate not supplied

Medicine and management--so much for "science".

The French think. The Americans do. The British sit on their duffs. but it all turns out the same. What does this mean to business and management? Lots.

Cross-Cultural Comparison↗
PubMedDate not supplied

Interaction between R 56865 and alpha-adrenoceptors in the pithed rat.

In pithed normotensive rats, the benzothiazolamine derivative R 56865 in high doses exhibits a competitive antagonism of alpha 1-adrenoceptor-mediated vasoconstrictions. The absence of a depression of the maximum of the dose-response curve of ST 587 and the very moderate attenuation of the maximal B-HT 920-induced increase in diastolic blood pressure (BP) confirms the lack of major calcium entry blocking properties of R 56865 for alpha-adrenoceptor-activated calcium channels in vitro. In doses up to 10(-5) mol/kg, the interaction of R 56865 with the sympathetic neurotransmission can solely be explained by alpha 1-adrenoceptor blockade. This was confirmed by the comparable antagonism of the selective alpha 1-adrenoceptor antagonist prazosin in a concentration of 6 x 10(-8) mol/kg. In contrast to the isolated rat aorta, where R 56865 showed an allosteric interaction with the NA binding site on the alpha 1-adrenoceptor, R 56865 acts like an alpha 1-adrenoceptor antagonist of the competitive type in vivo.

Adrenergic alpha-Antagonists↗