Biomedical subjects

B Pasche

Publications and source records attributed to B Pasche.

22 records · Page 2Linked to original sources

PubMed1989

Influence of high and low wall shear rates on the inhibition of factor Xa and thrombin at surfaces coated with immobilized heparin.

The thromboresistant function of a surface with end-point attached heparin is based upon interaction among the immobilized heparin, antithrombin, and at least factor Xa or thrombin. Heparinized arteriovenous shunts were implanted in dogs. By compressing a segment of the shunt, high and low wall shear rate regions were obtained in each shunt. After removal, the tubings were tested for their factor Xa and thrombin inhibitory capacity. It was found that on a molar basis, the factor Xa and thrombin inhibitory capacity were similar in low wall shear rate segments. In high wall shear rate segments, the thrombin inhibitory capacity was decreased, thus indicating that the AT-mediated inhibition of the serine protease is dependent on the wall shear rate.

Animals↗

PubMed1987

Antithrombin III binding to surface immobilized heparin and its relation to F Xa inhibition.

The mode of F Xa inhibition was investigated on a thromboresistant surface with end-point attached partially depolymerized heparin of an approximate molecular weight of 8000. Affinity chromatography revealed that one fourth of the heparin used in surface coating had high affinity for antithrombin III (AT). The heparin surface adsorbed AT from both human plasma and solutions of purified AT. By increasing the ionic strength in the AT solution the existence of high and low affinity sites could be shown. The uptake of AT was measured and the density of available high and low affinity sites was found to be in the range of 5 and 11 picomoles/cm2, respectively. Thus the estimated density of biologically active high and low affinity heparin respectively would be 40 and 90 ng/cm2. The heparin coating did not take up or exert F Xa inhibition by itself. With AT adsorbed on both high and low affinity heparin the surface had the capacity to inhibit several consecutive aliquots of F Xa exposed to the surface. When mainly high affinity sites were saturated with AT the inhibition capacity was considerably lower. It was demonstrated that the density of AT on both high and low affinity heparin determines the F Xa inhibition capacity whereas the amount of AT on high affinity sites limits the rate of the reaction. This implies that during the inhibition of F Xa there is a continuous surface-diffusion of AT from sites of a lower class to the high affinity sites where the F Xa/AT complex is formed and leaves the surface. The ability of the immobilized heparin to catalyze inhibition of F Xa is likely to be an important component for the thromboresistant properties of a heparin coating with non-compromised AT binding sequences.

Animals↗

PubMed1986

Thrombin inactivation on surfaces with covalently bonded heparin.

About 8000 Daltons porcine mucosa heparin fragments were covalently bonded by end-point attachment to polyethylene. The interaction between the immobilized heparin, added thrombin, and antithrombin III [AT] was investigated. The heparin surface was adsorbed with either albumin, AT dissolved in albumin or Tyrode, or platelet free plasma. Irrespective of the pre-treatment procedure, exposure of the surface to thrombin resulted in the same substantial decrease of thrombin in solution and the same degree of surface-confined thrombin activity. It was concluded that the heparin surface has a large capacity to bind thrombin and that the thrombin inhibitory capacity of high affinity heparin fragments is limited. On exposure of the thrombin-loaded surfaces to defibrinogenated plasma or AT, the surface-confined thrombin was inhibited within 30 seconds. Successive dilutions of plasma or AT decreased the inhibition rate but not the inhibition capacity. It is concluded that inhibition of thrombin adsorbed on the heparin surface occurs as follows: Added AT adheres to high affinity heparin fragments on the surface whereupon adsorbed thrombin migrates in the hydrophilic heparin coating towards the reaction site of AT and becomes inhibited. The inactivated thrombin-AT complex leaves then the surface, thus enabling the process to be repeated.

Antithrombin III↗

PubMedDate not supplied

Electroencephalographic changes following low energy emission therapy.

Low energy emission therapy (LEET) is a novel approach to delivering low levels of amplitude-modulated electromagnetic fields to the human brain. The sleep electroencephalogram (EEG) effects of a 15-min LEET treatment were investigated in a double-find cross-over study to assess sleep induction. Fifty-two healthy volunteers were exposed to both active and inactive LEET treatment sessions, with a minimum interval of 1 week between the two sessions. Baseline EEGs were obtained, and 15-min posttreatment EEGs were recorded and analyzed according to the Loomis classification. A significant increase in the duration of stage B1 sleep (0.58 +/- 2.42 min [mean +/- SD], p = 0.046), decreased latency to the first 10 sec epoch of sleep (-1.23 +/- 5.32 min, p = 0.051) and decreased latency to sleep stage B2 (-1.21 +/- 5.25 min, p = 0.052) were observed after active treatment. Additionally, establishment of slow waves with progression from stages B to C was significantly more pronounced after active LEET treatment (p = 0.040). A combined analysis of these results with those of an identical study performed in Denver showed that LEET had a significant effect on afternoon sleep induction and maintenance with shorter sleep latencies (decreased latency to the first 10 sec epoch of sleep; -1.00 +/- 5.51 min, p = 0.033; decreased latency to sleep stage B2; -1.49 +/- 5.40 min, p = 0.003), an increased duration of stage B2 (0.67 +/- 2.50 min, p = 0.003), an increase in the total duration of sleep (0.69 +/- 4.21 min, p = 0.049), and a more prominent establishment of slow waves with progression to a deeper sleep stage (p = 0.006). It is concluded that the intermittent 42.7 HZ amplitude modulation of 27.12-MHz electromagnetic fields results in EEG changes consistent with shorter sleep latencies, longer sleep duration, and deeper sleep in healthy subjects.

Adult↗