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  • 1
    Electronic Resource
    Electronic Resource
    CONTROL OF CORONARY BLOOD FLOW BY ENDOTHELIAL RELEASE OF NITRIC OXIDE (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Nitric oxide (NO) is released from vascular endothelium following conversion of l-arginine to l-citrulline by calcium-calmodulin-dependent ‘constitutive’ NO-synthase.2. Nitric oxide release occurs under basal conditions, in response to chemical stimuli (acetylcholine, bradykinin, thrombin, prostacyclin, serotonin, etc.) and in response to changes in shear stress (effects of blood velocity on vascular endothelium).3. Analogues of l-arginine inhibit NO and are widely used to study the effects of NO on the cardiovascular system: in intact animals, these inhibitors cause vasoconstriction, leading to an increase in arterial blood pressure (ABP) and bradycardia.4. Bradycardia induced by NO inhibitors is due, in part, to baroreceptor activity following the increase in ABP and in part to a direct effect on the sino-atrial node.5. In the intact animals and isolated perfused heart, NO inhibitors cause coronary vasoconstriction and hence a reduction in basal coronary flow. This effect, however, is not seen in isolated coronary vessels.6. From experiments in which ABP did not change, NO does not appear to have an important role in regulating coronary vasomotor tone under basal conditions.7. Nitric oxide appears to be involved in the duration of reactive hyperaemia following coronary vascular occlusion but is not involved to any significant extent in the peak amplitude of hyperaemia.8. Responses to vasodilator stimuli which do not involve NO in the initiation of the vasodilation may be prolonged by the effect of increased blood flow (shear stress) which releases NO and potentiates hyperaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02447.x
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  • 2
    Electronic Resource
    Electronic Resource
    The role of nitric oxide in the initiation and in the duration of some vasodilator responses in the coronary circulation (1995)
    Springer
    Pflügers Archiv 430 (1995), S. 96-104 
    Details
    ISSN: 1432-2013
    Keywords: Nitric oxide ; Coronary circulation ; Coronary vasodilatation ; Coronary hyperaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the coronary bed vasodilatation can be mediated by several mechanisms including endothelium-produced nitric oxide. To examine the contribution of nitric oxide, three different techniques to cause vasodilatation in the coronary vessels were used in the anaesthetized dog: intracoronary injection of 1 μg; acetylcholine, sudden reduction of the aortic blood pressure inducing a myogenic response and transient occlusion followed by release of the left circumflex coronary artery causing reactive hyperaemia. Each manoeuvre was performed before and after intracoronary adminstration of 100 mg N-nitro-l-arginine, an inhibitor of the synthesis of nitric oxide. In contrast to previous investigations, the inhibition of nitric oxide synthesis was prevented from causing an increase in blood pressure by the use of a blood-pressure-compensating device. The results observed during each of the three techniques, suggest that the initial cause of the vasodilatation is not the result of the increase of the production of nitric oxide. However, subsequent to the initiation of vasodilatation, an increase in the shear stress can result in an increase in the release of nitric oxide from the vascular endothelium, thus prolonging the vasodilatation obtained using each technique.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373844
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of sudden reductions of the arterial blood pressure on the mean diastolic coronary resistance (1981)
    Springer
    Cellular and molecular life sciences 37 (1981), S. 488-489 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary At the beginning of a 10 sec arterial haemorrhage, vascular elasticity induces an increase of mean diastolic coronary resistance. Then, the increase is counteracted by the relaxation of the vascular musculature, which causes a coronary hyperaemia when, after the haemorrhage is arrested, the vascular wall is stretched by a sudden though slight increase of blood pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01986153
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  • 4
    Electronic Resource
    Electronic Resource
    Ventricular distension and diastolic coronary blood flow in the anaesthetized dog (1993)
    Springer
    Basic research in cardiology 88 (1993), S. 340-349 
    Details
    ISSN: 1435-1803
    Keywords: Coronary blood flow ; ventricular distension ; ventricular volume ; ventricular pressure ; coronary vasodilatation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary There appears to be no agreement as to whether or not an increase in diastolic left ventricular pressure and/or volume can cause a decrease in diastolic coronary blood flow. We investigated the problem in the anaesthetized dog using a flaccid freely distensible latex balloon inserted into the left ventricle with the animal on extracorporeal circulation and the coronary perfusion pressure constant at about 45 mm Hg. Maximal vasodilatation and suppression of autoregulation in coronary vasculature was obtained by the intracoronary infusion of dipyridamole (10–40 mg/h). Ventricular volume was changed in steps of 10 ml from 10 to 70 ml and back to 10 ml, whilst recording coronary blood flow and left ventricular pressure in the left circumflex coronary artery. Over a range of ventricular volumes from 20 to 50 ml and a concomitant rise in diastolic ventricular pressure to about 20 mm Hg there was no change in the diastolic coronary flow. Only when the ventricular volume was more than two times the control value (i.e. exceeded 50 ml) and left ventricular pressure was more than 20 mm Hg, was there a decrease in coronary flow. During the return of the volume to the control level there was a fall in diastolic flow and ventricular contractility with respect to the values obtained when the volume was increased; these two effects were transient lasting less than 10 min. It was not considered that any of the three models of the coronary circulation, waterfall, intramyocardial pump or varying elastance model could explain our results. The mechanisms suggested for the decrease in contractility are subendocardial ischaemia, a temporary damage of the endocardium or overstretch of the cardiac muscle. The lower contractility during the reduction of ventricular volume to control could explain, via the capacitive component of flow, the reduced diastolic coronary flow. The reduced coronary flow along with the reduced contractility could also result from incomplete recovery of the myocardium from the stress-relaxation where series elastic components are longer, sarcomeres shorter and muscle fibres thicker.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00800640
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  • 5
    Electronic Resource
    Electronic Resource
    Transient effects of quick changes in myocardial metabolism and perfusion pressure on coronary vasomotor responses (1994)
    Springer
    Basic research in cardiology 89 (1994), S. 341-353 
    Details
    ISSN: 1435-1803
    Keywords: Coronary blood flow ; myogenic responses ; coronary transmural pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of transient changes in coronary transmural pressure on the coronary vasomotor tone was studied in 23 anesthetized dogs. Increases and decreases of the coronary transmural pressure were obtained by constrictions of various duration (2 to 20 s) of the descending thoracic aorta. The maneuvers were performed in animals with intact cardiac innervation, with the vagi sectioned and with vagal section together with β-blockade. In the absence of β-blockade the increase in the transmural pressure caused a transient increase in the coronary vasomotor tone attributable to a myogenic contractile response and the extravascular compression. This contractile response was not observed when the transmural pressure was increased in the presence of high vasomotor tone after β-blockade. In all animals a transient hyperemia was seen with its peak 8 to 12 s after the release of the aortic constriction. Since its timing and amplitude were independent of the duration of the constriction, the metabolic effect of the increased ventricular afterload, although it may have contributed to the decrease of the coronary resistance, cannot be considered entirely responsible for the hyperemia, which was otherwise compatible with a myogenic vasodilatory response triggered by the sudden fall of the transmural pressure at the release of the constriction. It is concluded that, in the coronary circulation of the intact dog, transient changes in transmural pressure can induce vasomotor responses in which myogenic and metabolic mechanisms combine together in regulating the coronary flow. Changes in extravascular compression can also affect the flow when the experimental maneuver implies changes in the diastolic left ventricular pressure and volume. With the present experimental procedure the myogenic responses have been evidenced when the metabolic factors would have been expected to produce opposite changes in the vasomotor tone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00795202
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