Das Sulfonsäureamid CF3SO2NH2 (2a) reagiert mit S3N2Cl2 1, das aus Harnstoff und S2Cl2 hergestellt werden kann, unter Chlorwasserstoffabspaltung zu S3N3SO2CF3 3, während CH3SO2NH2 (2 b) unter Ringspaltung (CH3SO2NSN)2S 4 bildet. 1 und SO2(NH2)2 ergeben unter ähnlichen Bedingungen S4N4O2 5, dessen Struktur durch Röntgenstrukturanalyse bestätigt wird. Die Hydrolyse von 1 liefert mit wasserfreier Ameisensäure oder Acetanhydrid S3N2O 6. Fünfgliedrige S3N2-Ringe 9a–c lassen sich auch darstellen, wenn S4N4 mit den Anhydriden (FSO2)2O, (CF3CO)2O und (CCl3CO)2O umgesetzt wird. Easy Syntheses of Sulfur-Nitrogen Compounds The sulfonamide CF3SO2NH2 (2a) reacts with S3N2Cl2 1, which can be prepared from urea and S2Cl2, to yield S3N3SO2CF3 3 with formation of hydrogen chloride while CH3SO2NH2 (2b) yields (CH3SO2NSN)2S 4 under cleavage of the ring system of 1. Under similar conditions 1 reacts with SO2(NH2)2 to form S4N4O2 5. The structure of 5 is confirmed by X-ray analysis. The hydrolysis of 1 with anhydrous formic acid or acetic anhydride yields S3N2O 6. Five-membered S3N2-rings 9a–c are formed by the reaction of S4N4 with the anhydrides (FSO2)2O, (CF3CO)2O, and (CCl3CO)2O.
Einleitung: Arteriogenese – das Wachstum von pra-existenten Kollateralgefasen zu funktionellen Arterien – wird durch erhohte Schubspannung induziert. MicroRNAs (miRNA) sind in der post-transkriptionalen Regulation der Genexpression beteiligt. Eine schubspannungs-induzierte[for full text, please go to the a.m. URL]
Abstract Substituierte Schwefeldiimide werden durch Umsetzung von (CH 3 ) 3 SiNSNSi(CH 3 ) 2 mit CH 3 SO 2 Cl und CCl 3 SCl oder von P 2 O 3 F 4 mit (CH 3 ) 3 SiNSNSN(CH 3 ) 2 dargestellt. S 4 N 4 bzw. S 3 N 2 Cl 2 reagieren mit (CH 3 ) 2 Si[N(CH 3 ) 2 ] 2 zu (CH 3 ) 2 Si(N(CH 3 ) 2 )NSNSN(CH 3 ) 2 und (CH 3 ) 2 Si(Cl)NSNSN(CH 3 ) 2 . In der letzten Verbindung kann man das Chloratom durch Diäthylamin substituieren. Die neuen Verbindungen stellen Zwischenprodukte für die Synthese cyclischer Schwefel‐Stickstoff‐ Verbindungen dar. Sie wurden durch Massen‐, IR‐, 1 H‐NMR‐Spektren und Elementaranalysen charakterisiert.
We previously reported excessive growth of collateral vessels in the dog heart during arteriogenesis induced by implantation of an ameroid constrictor around the circumflex branch of the left coronary artery. In the present study, using histology and immunocofocal microscopy, we further investigated how these aberrant collateral vessels form. By comparison with mature collateral vessels the following findings were made: perivascular space was very narrow where damage of the perivascular myocardium occurred; the neointima was very thick, resulting in a very small lumen; elastica van Gieson staining revealed the absence of the internal elastic lamina and of elastic fibers in the adventitia, but abundant collagen in the adventitia as well as in the neointima; smooth muscle cells of the neointima expressed less α-SM actin and little desmin; expression of the fibroblast growth factors aFGF, bFGF and platelet-derived growth factor (PDGF)-AB was observed mainly in the endothelial cells and abluminal region, but transforming growth factor-β1 was only present in the adventitia and damaged myocardium; angiogenesis in the neointima was observed in some collateral vessels expressing high levels of eNOS, and cell proliferation was mainly present in the abluminal region, but apoptosis was in the deep neointima. In conclusion, these data for the first time reveal that the formation of the aberrant collateral vessels in the dog heart involves active extracellular proteolysis and a special expression profile of growth factors, eNOS, cell proliferation and apoptosis. The finding of a narrow perivascular space and perivascular myocardial damage suggests that anatomical constraint is most likely the cause for exacerbated inward remodeling in aberrant collateral vessels in dog heart.
The formation of collateral arteries in patients suffering from occlusive atherosclerotic vascular diseases has been frequently reported. The growth of these collateral arteries has been termed 'arteriogenesis'. Clinical observations and investigations using various animal models support the hypothesis that the mechanism of arteriogenesis is based on the remodelling of pre-existing collateral anastomoses. This process seems to be mainly triggered by fluid shear stress which is induced by the altered blood flow conditions after an arterial occlusion. Early arteriogenesis involves the activation of collateral endothelial cells, the attraction of leukocytes to the collateral vascular wall and subsequently their invasion into the perivascular space of the collateral vessel. In a second phase, proliferation of vascular cells is initiated by growth factors mainly released from accumulated leukocytes. Furthermore, tissue degradation and changes in the extracellular matrix are observed. Unravelling the mechanisms of arteriogenesis is crucial to the development of successful therapeutic approaches for the treatment of patients with ischemic vascular diseases.
Multiple chronic coronary artery occlusions were produced in dogs by implantation of ameroid rings on the circumflex branches of the left and right coronary artery. Sixty-five per cent of the animals survived. Seventy-seven per cent of the remaining animals had no detectable myocardial infarction. Myocardial blood flow distribution was studied 4 weeks after operation using the tracer microsphere technique. During control conditions myocardial blood flow was homogeneously distributed within the left ventricle. In one group of dogs, regional dilatory capacity was tested by intravenous infusion of dipyridamole. Four compartments of myocardial blood flow were found. The collateral dependent subendocardium with 114 ml/min-100 g-1 was the lowest perfusion rate. In another group of dogs myocardial blood flow distribution was examined during isoproterenol infusion and after beta-blockade with prindolol during continuous isoproterenol infusion. During isoproterenol infusion, a nonhomogeneous blood flow pattern was found when the heart rate increased to 200/min together with a slight fall in diastolic perfusion pressure. Under these conditions, the flow to the collateral dependent subendocardium was severely diminished, while the flow to the areas perfused by normal coronary arteries increased, reflecting compensatory vasodilation. After beta-blockade with prindolol 0.1 mg/kg, the myocardial blood flow distribution was also nonhomogeneous but in the opposite direction: the collateral dependent subendocardium was now the best perfused compartment. The flow to the areas perfused by normal coronary arteries decreased due to the reduced oxygen requirements, while the collateral dependent subendocardium remained maximally dilated. This phenomenon was explained as a postischaemic reactive hyperaemic response to the isoproterenol-induced ischaemia in the collateral dependent subendocardium.
Journal of Cardiovascular Pharmacology™ is a peer reviewed, multidisciplinary journal that publishes original articles and pertinent review articles on basic and clinical aspects of cardiovascular pharmacology. Appropriate subjects include new drug development and evaluation, physiological and pharmacological bases of drug action, metabolism, drug interactions and side effects, clinical results with new and established agents and novel methods. The focus is on pharmacology in its broadest applications, incorporating not only traditional approaches, but new approaches to the development of pharmacological agents and the prevention and treatment of cardiovascular diseases.
