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Biomedical subjects

G Losano

Publications and source records attributed to G Losano.

At least 37 records · Page 2Linked to original sources
PubMed1994

Control of coronary blood flow by endothelial release of nitric oxide.

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.

Animals↗
PubMed1994

Increases in coronary intravascular pressure during maximal coronary vasodilatation in the anaesthetized dog.

The present study was planned to investigate whether or not, after complete suppression of vasomotor tone, increases in intravascular blood pressure distend the coronary vasculature causing passive decreases in the resistance to the coronary arterial inflow during the diastole. In anaesthetized dogs, aortic and left ventricular pressures and flow in the left circumflex coronary artery were recorded. Coronary flow was derived using an electromagnetic flowmeter. Transient (10 s) increases in intravascular blood pressure in a range above 70 mm Hg were produced by mechanical constriction of the descending thoracic aorta. In the presence of a normal vasomotor tone the increase in blood pressure caused an autoregulatory increase in the mean diastolic coronary inflow resistance. After maximal vasodilatation by dipyridamole, no change in inflow resistance was induced by the increase in intravascular blood pressure. It may be argued that while a non-maximal vasodilatation is reported to increase coronary distensibility, at a blood pressure of 70 mm Hg the complete suppression of the vasomotor tone brings the vascular radius to a size which cannot be further distended by an increase in blood pressure.

Animals↗
PubMed1993

Tachycardia and coronary blood flow: non-invasive estimation during Valsalva manoeuvre and exercise.

Simultaneous changes in cycle length and coronary blood flow were studied during Valsalva manoeuvre and supine cycloergometer exercise test in 10 male patients (mean age 48 +/- 12 years) who had successfully undergone myocardial revascularization by surgical anastomosis of the left internal mammary artery on the left anterior descending coronary artery. Blood velocity curves in the left internal mammary artery were obtained by a non-invasive continuous-wave Doppler probe at rest, in the last phase of the expiratory effort of the Valsalva manoeuvre and at the maximum load attained during the exercise test. Mean arterial pressure by sphygmomanometer, and cardiac cycle length on the basis of Doppler recording were measured. Mean blood velocity, the length of the blood column entering the coronary bed at each cycle (cardiac cycle times mean velocity), an index of blood cell acceleration (the ratio of mean velocity to cardiac cycle), and an index of coronary resistance (the ratio of mean pressure to mean velocity), were calculated. For approximately the same change in cycle length, coronary resistance decreased in exercise, with an increased mean velocity, but increased in Valsalva, with no changes in mean velocity. The length of the blood column entering the coronary bed at each cycle was unchanged in exercise, with a marked increase in the acceleration index, while it decreased in Valsalva. Therefore, we hypothesize that tachycardia has a limiting effect on sympathetic coronary constriction in Valsalva when cardiac external work is decreased, and an additional vasodilatory effect on coronary bed in exercise when external work is increased.

Adult↗
PubMed1993

"Resistance" to left ventricular outflow studied in anesthetized dogs.

A simple method is proposed to determine resistance to left ventricular output from the evaluation of a parameter Z, given by the ratio of peak systolic pressure and the corresponding instantaneous blood flow. The method, derived from the basic equation of the Windkessel model, is applied to analyze pressure and flow data measured in the ascending aorta of anesthetized dogs. The Z values obtained in this way are found to be closely related to resistance calculated from the ratio of mean aortic pressure and mean flow over the cardiac cycle. Effects of abrupt changes of resistance obtained by removing an aortic constriction are also analyzed according to the same basic Windkessel equation and the results show the same close relationship to resistance.

Animals↗
PubMed1993

[The effect of maximal vasodilation on the distensibility of the coronary vascular bed].

This study aimed at investigating the changes in coronary vascular resistance induced by sudden increases in transmural pressure in the presence of a maximally vasodilated coronary bed. In anaesthetized open-chest dogs under artificial ventilation, aortic blood pressure, left ventricular pressure and the flow in the left circumflex coronary artery were recorded. The flow was derived by means of an electromagnetic flowmeter. Maximal vasodilatation was achieved by intracoronary infusion of dipyridamole (10-40 mg/h), increases in transmural pressure, starting from 70 mmHg, were obtained by constricting for 10 s the descending thoracic aorta with a plastic snare. While in the absence of vasodilatation the increase in pressure was accompanied with an increase in resistance because of an auto-regulatory response, when the coronary bed was maximally dilated the increase in pressure did not alter the coronary vascular resistance. These results seem to be in conflict with the observation that in the coronary circulation the distension of the vascular wall produced by increases in pressure is favoured by the reduction of the vasomotor tone. However, it may be argued that, while a reduction of the vasomotor tone can increase the vascular distensibility, a maximal vasodilatation, as it was seen in the resistance vessels of the skeletal muscles, brings the vascular diameter to such a size that no further distension can be induced when the transmural pressure is increased starting from a value of about 70 mmHg.

Animals↗
PubMed1992

Coronary flow and left ventricular pressure during diastole in the anaesthetized dog.

There is controversy about the effect of left ventricular pressure on resistance of the intramyocardial coronary vessels. In anaesthetized dogs the effect of left ventricular pressure on coronary flow during diastole was studied using an extracorporeal circulation and allowing the heart to contract and relax isovolumically. At constant coronary perfusion pressure of about 45 mmHg with maximal coronary vasodilatation, produced by dipyridamole, increases in diastolic left ventricular pressure to 22 mmHg, producing a volume of 50 ml, did not affect diastolic coronary flow. It is suggested that in the intact animal over the physiological range of left ventricular diastolic pressure the resistance in the coronary vessels is not affected.

Anesthesia↗
PubMed1992

Mechanical properties of the coronary vasculature: indirect evaluation.

Information on the mechanical properties of the coronary vascular bed can be obtained indirectly by modelling the vascular system. This indirect approach, unlike 'in vitro' measurements, allows to take into account the vasomotor conditions of the circulatory district as well as the effect of the surrounding embedding tissue on the vascular performance. An experimental manoeuvre of sudden occlusion and subsequent release of the thoracic descendent aorta on 5 anaesthetized dogs with open pericardium induces a step-like variation in the coronary perfusion pressure and the occurrence of oscillations in the mean coronary flow. Such a behaviour can be described using a second-order model ('windkessel'+inductance, which takes into account blood inertia in the large vessels). The value of the coefficients entering the equations have been obtained with a 'best-fit' procedure (minimum of the chi-squared variable) on the haemodynamical data. Coefficient variations are in agreement with the direct estimation of the myocardial compliance and volume, measured by Ultrasound Echocardiographic imaging (4-chamber projection mode).

Animals↗
PubMed1991

Relationship between hyperaemic response and viscoelastic properties in the coronary circulation of the dog.

A sudden reduction in perfusion pressure evokes a transient hyperaemic response in the coronary arteries of anaesthetized dogs; its characteristics depend on the vasomotor tone. A heuristic model, which mimics the vascular bed with a lumped second-order system on the lines of the well-known Windkessel model, but accounting for the blood inertia, is proposed to describe that response and to quantify the viscoelastic properties of the system.

Animals↗
PubMed1991

The mechanical effects of rhinoceros horned viper (Bitis nasicornis) venom on the isolated perfused guinea-pig heart.

In the guinea-pig Langendorff heart preparation, addition of 0.1 mg Bitis nasicornis venom to the perfusion solution caused transient increases in heart rate (HR) and left ventricular systolic pressure (LVSP) with peak increases at 2 min. With higher doses (0.6 and 1.4 mg), these increases were followed by the return of HR to normal, significant decreases in LVSP below control values and marked increases in left ventricular diastolic pressure. Histaminergic blockade with ranitidine reduced the positive responses. The results suggest that a venom component, possibly acting on intracellular calcium movement, could be responsible for both positive and negative effects.

Animals↗
PubMed1991

The myogenic contribution to coronary autoregulation.

It seems now, mainly from the results of the experiments carried out in the Department of Human Anatomy and Physiology of the University of Turin, Italy, that there is an active myogenic response in the coronary vessels. In response to changes in the transmural pressure, both increases and decreases, in the coronary vessels transient contractions and relaxations (respectively) of the smooth muscle wall can be demonstrated. Although this suggested mechanism can not be fully integrated into a hypothesis explaining autoregulation of blood flow in the coronary vessels it does seem a strong possibility that it takes part; but further investigation will be necessary to clarify all aspects of this kind of regulation.

Animals↗
PubMed1990

Coronary myogenic responses to abrupt changes in aortic blood pressure in anaesthetized dogs.

A transient increase in coronary transmural pressure was produced in anaesthetized dogs by occlusion of the descending thoracic aorta. Aortic blood pressure (ABP), left ventricular pressure and coronary flow were measured; coronary vascular resistance (CVR) was calculated. Results were similar in innervated and denervated hearts. Occlusion for 10 and 20 s resulted in no change in CVR for 15 s, followed by a metabolic dilatation attributable to enhanced oxygen demand; after release the fall in ABP resulted in an immediate increase in CVR, caused by vascular elastic recoil, followed by hyperaemia.

Anesthesia↗
PubMed1989

[Coronary vascular resistance during transitory variations in aortic pressure].

The present study was aimed at studying the interaction between elastic properties and myogenic responses of the coronary wall in regulating coronary vascular resistance (CVR) during and after sudden changes in perfusion pressure. Whilst the effects of transient reductions and recoveries of the aortic blood pressure (ABP) were previously considered, in the present study attention was paid to the changes induced in CVR by the reverse procedure, i.e., by transient increases followed by abrupt decreases of ABP. The experiments were performed in 6 anesthetized dogs after section of the vagi nerves and beta-adrenergic receptor blockade. The increase of ABP was obtained by a 10 or 20 s constriction of the descending thoracic aorta. During the experimental maneuver, coronary flow increased without any significant change in CVR. Only in the late part of the 20 s constriction a reduction of CVR was observed as a likely consequence of increased myocardial metabolism. Immediately after the release of the constriction, the fall of ABP below the control was accompanied by a significant reduction of coronary flow without any significant increase in CVR. About 10 s later, a remarkable increase in flow occurred together with a significant fall of CVR, while ABP was recovering towards the control. In each animal the exact timing of these changes was independent of the duration of the constriction. When, about 20-30 s from the end of the constriction, ABP was back to the control, the hyperemia was completely over.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of tachycardia and constriction of left circumflex artery on coronary flow and pressure in anaesthetized dogs.

1. The effect of graded changes in heart rate between 100 and 160 beats/min and constriction of the left circumflex coronary artery which reduced coronary blood flow was examined in seven anaesthetized and artificially ventilated dogs in the absence of significant changes in aortic blood pressure. Mean diastolic coronary blood flow, and the difference between the mean diastolic pressures in the coronary artery and the left ventricle were related to the increase in heart rate. 2. In all seven dogs diastolic coronary blood flow showed linear increases with heart rate increments with and without coronary narrowing which averaged 70 and 82% respectively. 3. A significant shift to the right in the relation between heart rate and mean diastolic coronary blood flow occurred with each grade of coronary constriction. Coronary blood flow became lower at any given heart rate. 4. The shift to the right in the relation between heart rate and coronary blood flow was associated with decreases in the difference between the mean diastolic pressures in the coronary artery and the left ventricle which accompanied the increase in heart rate. 5. The results suggest that increases in heart rate can enhance diastolic coronary blood flow despite coronary narrowing which reduced flow, possibly through dilatation in myocardial blood vessels.

Anesthesia, General↗