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Biomedical subjects

G Schettler

Publications and source records attributed to G Schettler.

At least 73 records · Page 4Linked to original sources

[Modification of blood coagulation and fibrinolysis through physical activity].

Physical conditioning appears to protect against the development of vascular disease. Although physical training often evokes favorable alterations in established cardiovascular risk factors, such as plasma lipids and lipoproteins, the metabolic sequelae of regular exercise that mediate a reduction in the risk of cardiovascular disease remain incompletely understood. Studies in recent years have shown physical training to have beneficial effects on blood coagulation and fibrinolytic activity. On general the data support the concept that blood clotting is potentiated by exercise. Mechanisms involved are an increased release of thromboplastine of tissue, increased coagulation with lactate accumulation during exercise, increased concentrations of plasma proteins owing to hemoconcentration, increased concentrations of specific clotting factors, e.g., Factor VIII and fibrinogen, and an alteration in platelet count and platelet function. The acceleration in coagulation is less in the well-exercised individual. There is evidence that an epinephrine mediated mechanism is responsible for the difference between individuals who have a lot of exercise and those who do not. Fibrinolytic activity seems to increase with exercise in a linear relationship with the heart rate during physical activity. An enhancement of the plasma fibrinolytic activity, stimulated experimentally by thrombotic stress such as venous occlusion, could be an important mechanism in the beneficial effect of habitual physical exercise on the risk of cardiovascular disease.

Arteriosclerosis↗

[New aspects of the biochemistry and biology of the arterial wall].

Early lesions of arteriosclerosis are characterized by proliferating smooth muscle cells, macrophages,and foam cells. In addition, large amounts of connective tissue components and cholesterol esters are found. These changes are primarily located in the intima of the arterial wall. The initial mechanisms responsible for lesion formation are largely unknown. In recent years progress has been made particularly in fields of research related to the biochemistry of arterial wall cells in tissue culture. The findings obtained allow us to deepen our knowledge of the pathophysiology of arteriosclerosis. Of special interest are mechanisms involved in the maintenance of the thromboresistant endothelium, the factors triggering proliferation of intimal smooth muscle cells, and the transformation of macrophages to foam cells.

Animals↗

Solubilization and purification of an acetyl-LDL binding membrane protein from human leukocytes.

An acetyl-LDL receptor in the human leukocyte membrane might have some importance in the generation of foam cells in the atherosclerotic lesion. We show purification of a human leukocyte membrane protein which exhibits ac-LDL-specific binding. Our attempts to solubilize this protein from the leukocyte's membrane fraction involved the usage of the non-ionic detergents Triton X-114 and beta-D-Octylglucoside. Our scheme for the purification of the acetyl-LDL binding protein included ion exchange chromatography and affinity chromatography. Following solubilization the ac-LDL binding activity was assayed by ligand blotting, demonstrating polyvinylsulfate sensitive binding of ac-LDL to a single, acidic 280 000 D membrane protein in the crude membrane fraction.

Binding Sites↗

Acute influence of smoking on plasma lipoproteins.

This study was designed to investigate acute effects of smoking on plasma lipoproteins. Twelve fasting smokers inhaled the smoke of two cigarettes. Blood samples were taken before and 30 min after smoking. Triglycerides decreased in plasma from 136.8 +/- 39.8 to 108.0 +/- 34.9, in VLDL from 79.8 +/- 31.4 to 58.4 +/- 28.5 mg%. Cholesterol fell in HDL3 from 29.9 +/- 5.0 to 26.6 +/- 5.8 mg%. Determination of HDL-cholesterol with the phosphotungstic acid precipitation method revealed a reduction from 45.7 +/- 10.2 to 40.3 +/- 11.1 mg% after smoking. All C-apoproteins decreased in VLDL as an entity. Apoprotein A-I was diminished in plasma from 137.5 +/- 23.1 to 118.2 +/- 25.4, and in HDL3, from 97.1 +/- 12.1 to 85.0 +/- 13.1, apoprotein A-II in plasma from 28.6 +/- 8.9 to 24.7 +/- 6.9 and in HDL3 from 21.1 +/- 8.4 to 17.4 +/- 5.7 mg%. Zonal ultracentrifugation of D less than 1.063 g/ml lipoproteins confirmed the influence of smoking on VLDL. In LDL, an increase in cholesterol esters, mainly cholesterol linoleate, from 57.3 +/- 30.2 to 67.4 +/- 25.9 mg% was observed after smoking. The HDL2 subclass was shifted toward a slightly lighter hydrated density, but the major effect of smoking was seen in HDL3. Total cholesterol decreased from 30.5 +/- 7.3 to 22.3 +/- 6.6 mg%, due to a fall of all major cholesterol esters from 23.7 +/- 7.2 to 15.8 +/- 6.9 mg%. HDL3-phospholipids were reduced from 74.9 +/- 37.0 to 46.0 +/- 23.9 mg%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Lipoproteins and lipoprotein receptors and their significance for the pathogenesis of arteriosclerosis].

Plasma lipoproteins are macromolecular complexes which serve as vehicles for the transport of lipids in the blood in a soluble form. The protein components of lipoproteins are referred to as apoproteins. They apparently direct each lipoprotein to its site of metabolism. It is now evident that lipoprotein receptors on the surface of cells in the liver, extrahepatic tissues and perhaps in the RES mediate the uptake of lipoproteins by these tissues. Understanding the mechanisms of the uptake of atherogenic lipoproteins by the cells will lead to further insights of the etiology of atherosclerosis.

Apoproteins↗

[Effects of metoprolol on the peripheral circulation in patients with peripheral vascular disease].

Up to now betablockers were regarded as relatively contraindicated in patients with peripheral vascular disease (PVD). The effects of metoprolol were studied in hypertensive patients (stage I, WHO) with PVD of pelvic and thigh type (stage II according to Fontaine). An initial dose of 100 mg metoprolol followed by 100 mg 90 min after the first oral administration, twice a day was administered for 8 weeks. Blood pressure decreased from 181/105 to 163/96 mm Hg. Pulse rate was lowered from 72 to 68/min (p less than 0.001). Estimated doppler pressure in the posterior tibial artery decreased from 123 to 119 mm Hg. Venous occlusion plethysmography showed a slight but not significant decrease at rest and during reactive hyperemia. During long-term treatment the pain-free walking distance increased significantly from 225 to 348 m. No side effects were seen. Thus, metoprolol as a beta 1-selective betablocker is not contraindicated in patients with intermittent claudication.

Arterial Occlusive Diseases↗

[Peripheral arterial vasoocclusive disease: no absolute contraindication to beta receptor blockers (author's transl)].

An initial dosis of 40 mg followed by 40 mg propranolol (Dociton) t.i.d. for 4 weeks was administered to 16 hypertensive patients with manifest arterial vasoocclusive disease of the pelvic and thigh type (stage II according to Fontaine). Blood pressure decreased 90 minutes after the first oral administration from 174/106 to 155/93 mm Hg. Cardiac frequency was lowered significantly from 75 to 66/min. Occlusion plethysmography and Doppler pressure estimation were not changed significantly either in the acute nor in long-term assessment. The painfree walking distance remained constant 90 minutes after propranolol initially (baseline value 230 m, after 90 minutes 220 m). It rose to 330 m after two weeks and to 350 m after four weeks. Use of beta receptor blocker in arterial vasoocclusive disease is thus not contraindicated, at least as far as stage II is concerned.

Arterial Occlusive Diseases↗