Apolipoprotein D (ApoD) constitutes an atypical lipoprotein in so far as it is predominantly found associated with HDL particles but belongs to the lipocalin structural family. Apart from its involvement in serum lipid transport it is abundant in various tissues, and differing physiological functions have been ascribed to it. We have now developed an E. coli expression system that permits the efficient production of biochemically homogeneous ApoD via secretion into the bacterial periplasm. Detailed ligand binding studies by fluorescence titration revealed that progesterone and arachidonic acid are complexed with dissociation constants both in the 1 microM range, whereas the presumed ligands pregnenolone, bilirubin and E-3M2H are not recognized by the recombinant protein. In contrast with previous reports it thus appears that ApoD discriminates well in its binding function between closely related compounds.

Apolipoproteins↗

PubMedDate not supplied

Left ventricular end-systolic pressure-volume relationships as a measure of ventricular performance.

The extent to which conclusions about myocardial performance may be drawn from end-systolic pressure-volume relations was investigated. Left ventricular isovolumetric and end-systolic pressure-volume relationships were measured in the rat, under acute impairment of contractility (hexobarbital), at chronic pressure overload (spontaneously hypertensive rats), and at chronic volume overload (aorto-caval shunt). Our results confirm the classic conception of Otto Frank where the curves of the isovolumetric maxima and the curves of the end-systolic pressure-volume relations follow separate courses. Acute alterations in contractility can be detected from shifts in the end-systolic pressure-volume relations. In chronic pressure or volume overloaded hearts the end-systolic pressure-volume relations do not render conclusions about ventricular or myocardial performance since in chronically altered hearts, the course of the end-systolic pressure-volume relations is primarily influenced by geometric factors.

Animals↗

PubMedDate not supplied

Myocardial elasticity and left ventricular distensibility as related to oxygen deficiency and right ventricular filling. Analysis in a rat heart model.

Hypoxia-induced changes in diastolic left ventricular (LV) pressure volume (P-V) relationships and myocardial elasticity as well as the extent to which diastolic right ventricular (RV) interactions are involved under hypoxia were analysed in male open-chest Wistar rats under isovolumetric conditions. Wall stress sigma and differential elastic modulus E were calculated for the midwall region, assuming a spherical model. LV end-diastolic P-V relationship shifted significantly to the left only 2 min after the start of pure N2 ventilation. The slope of the E-sigma curve did not change, corresponding to the "contracture type" of decreased myocardial distensibility. Identical changes occurred when filling of the RV was increased under O2 ventilation. Hypoxia, under emptied RV, led within 8 min to substantially lower, non-significant steepening of the end-diastolic P-V relationships. There was a significant change in the diastolic P-V curve along with a parallel increase in stiffness constant b, 45 min after N2 ventilation and under emptied RV. However, as a result of failure of cardiac function, ischemia was by now prevailing. These findings led to the following conclusions: In the early phase of hypoxia, i.e. within the first 20 min (in the model used in the present study) no substantial rigor occurs but the increase of LV end-diastolic P-V values is essentially due to augmented RV filling, even under opened chest and removed pericardium. The geometrical influence of the RV mimics the "contracture type" of decreased myocardial distensibility and cannot be recognized on the basis of the E-sigma relationship. Without knowledge of RV pressure it is not feasible to distinguish early "contracture" or rigor from extraventricular influences, caused by changes in the filling of the neighbouring ventricle.

Animals↗

PubMedDate not supplied

Morphological alterations of non-varicose and varicose veins. (A morphological contribution to the discussion on pathogenesis of varicose veins).

Venous valves do not play a role in pathogenesis of primary varicose veins. Their number remains constant during life time. In varicose veins their insufficiency is secondary. Intimal fibrosis is no prerequisite for the development of varicose veins. It is a frequent finding in non-varicose veins of all age groups. Fibrosis of media and adventitia is no early morphological alteration in varicose veins. Fibrotic replacement of smooth muscles represents a late stage of varicosis. Degenerative lesions of deep leg veins are rare even at old age. The deep veins are not influenced by sclerotic lesions of the adjacent arteries. Preexisting intimal fibrosis in autogenous graft veins may be one of several factors which induce an overshooting intimal proliferation. Degenerative alterations (fibrotic lesions of the wall layers, insufficiency of the valves) are secondary phenomena in pathogenesis of varicose veins which follow a functional deficiency of the smooth musculature.

Adolescent↗

PubMedDate not supplied

Temporary pulmonary vein stenosis during intraoperative transesophageal echocardiography in total cavopulmonary connection.

Two patients operated on by one of the authors (MK) developed hemodynamic instability after otherwise uneventful completion of total cavopulmonary anastomosis with an extracardiac tube. In both, a stenosis of the right pulmonary veins was demonstrated during routine intraoperative transesophageal echocardiography. The transesophageal probe was found to be the underlying problem. Apparently, the pulmonary veins became compressed between the probe and the extracardiac conduit.

Aorta, Thoracic↗