Monoaminergic innervation of the arteries and veins of the kidney observed using fluorescence reaction.
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Biomedical subjects
Publications and source records attributed to S Dolezel.
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Peculiarities in structure and deformability of epicardial conduit coronary arteries are described. The thin wall of animal coronary artery contrasts the human coronary artery in which the remarkable wall thickness is due namely by the intima thickness. Deformation in length and diameter of conduit coronary arteries, due to the left and right ventricle volume increase, has been defined in non-beating canine heart. Ramus interventricularis anterior being firmly tethered to the myocardium undergoes about 3 times larger deformation than ramus circumflexus. In anaesthetized dogs a 30% increase in blood pressure, elicited by aortic constriction, induces an increase in diameter of coronary artery, in segment length, in blood flow and consequently in shear stress which represents a load for circumferentially running smooth muscle bundles, longitudinally running smooth muscle bundles, as well as for the endothelium. The above load lasting 4 h is already reflected by an increase in total RNA content and [14C] leucin incorporation in the left ventricle myocardium in the wall of ramus interventricularis anterior, not in ramus circumflexus. The findings fit completely with the different range of deformation of both the above coronary branches and indicates an increase in proteosynthesis not only in myocardium, but in ramus interventricularis anterior as well. An increase in ornithindecarboxylase activity in coronary wall leading to an increase in biogenic polyamines, is present in the case only, when blood pressure increase is induced by infusion of noradrenaline.
In open-chest dogs, the left anterior descending coronary artery was ligated for 150 min. The heart was semiserially cut on a cryomicrotome and areas of ischemic damage were visualized by means of glycogen depletion (PAS reaction) and tissue acidosis (a "sandwich" technique with pH indicator dispersed in a layer of gel). The extent of myocardial damage was determined morphometrically. The mass of the glycogen-depleted heart muscle was greater than the mass of the ischemic tissue detected by means of decreased pH (p less than 0.01). The border zone was characterized by glycogen depletion without acidosis. Circulation studies using intravital fluorescein staining have shown that perfusion is partially retained in the border zone; it is assumed that the hypoperfusion triggers glycogenolysis. Nevertheless, the level of perfusion suffices to wash out the acidic end products. Comparison of contrapulsation-treated dogs and untreated dogs shows that the amount of damaged tissue comprising the border zone can be reduced by this therapeutic intervention (p less than 0.02) - in contrast to the acidotic tissue, the amount of which is not significantly influenced. Therefore the border zone contains damaged but still viable muscle cells.
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The purpose of this study was to evaluate contractility of the rabbit abdominal aorta 4 days after de-endothelialization by balloon catheter. The isometric tension of ring-segments in response to vasoactive agents was monitored. A significant enhancement of contraction to noradrenaline and serotonin was found in aortas 4 days after endothelium denudation as compared with controls with endothelium. The enhancement, however, did not differ from that found already in acutely denuded vessels (immediate denudation). No significant difference in contractility to potassium chloride was found in either group of denuded preparations as compared with controls. The sensitivity to all three vasoactive agents (EC50) was not influenced by denudation. These results indicate that changes in the contractility of denuded vessels are predominantly a consequence of lacking the endothelium as a producer of endothelium-derived relaxing factor. The access of mitogens to the media does not seem to interfere with the magnitude of contraction 4 days after denudation.
The authors present basic information about the technical development of the total artificial heart (TAH) and TAH drivers. Long-term experiments, in which the TAH TNS-Brno-II and VII and the Rostock hearts were implanted, are described. Long-term experiments were dedicated to analysis of specific pathophysiologic problems (venous hypertension, thrombogenesis, and calcification) in order to increase survival rates. Thrombogenesis has been partially solved in the TNS-BRNO-VII device by optimal TAH construction using an asymmetric driving diaphragm, the undulating motion of which produced excellent results. Two methods for prevention of increase in central venous pressure (CVP) are verified: administration of antihypertensive drugs and atrial electrical stimulation. Of 155 calves studied, 50 long-term experiments in calves and one in a goat were done. The survival of these animals extended from 31 to 293 days of pumping (average survival, 116.9 days). To prevent driving diaphragm calcification, we have incorporated exogenic inhibitors of calcification into the diaphragm biomaterial (polyurethane). A unique long-term experiment with intrathoracic TAH implantation in the goat is also described. In addition clinical use of the TAH as a bridge to transplantation is discussed. Parallel research with the left ventricular assist device (LVAD) system was studied experimentally, and twice used in patients. The TAH TNS-BRNO-VII/80/clin/ was used in four patients. It worked faultlessly for 22 hours to 10 days. More precise and specific indications for TAH implantation when used as a bridge to transplantation are needed.
The influence of previous pharmacotherapy or intra-aortic balloon counterpulsation (with thiamine infusion) on the effectiveness of reperfusion of the left anterior descending (LAD) coronary artery after 150 minutes of occlusion has been studied in dogs. The infarct size was determined by morphometric method 20 hours after the onset of ischaemia. Reperfusion 150 minutes after the occlusion of the LAD coronary artery resulted in a smaller infarct; however, no protective effect from pharmacological or mechanical heart support during the period of ischaemia was observed.