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Biomedical subjects

G Losano

Publications and source records attributed to G Losano.

At least 55 records · Page 3Linked to original sources
PubMed1987

Simple physical model of coronary vasodilation.

The coronary diastolic pressure-flow relationship was studied in two groups of dogs; in one group coronary circulation was characterized by normal tone of vascular smooth muscle, while in the other group, complete relaxation of smooth muscle fibres was produced by intravenous infusion of dipyridamole. The coronary flow (CF) was measured in both groups for several values of mean aortic blood pressure (ABP), the variations being obtained by means of a 10 s arterial haemorrhage. The measured CF versus ABP data were found to be well represented by best fit curves calculated by power regression methods. These curves were quite different in the presence and absence of dipyridamole infusion. A simple physical model is proposed for analysis of these curves; the model is based on the Poiseuille equation, modified to take into proper account the variations of the vessel radii under different ABP values during ventricular diastole. These variations are expressed by means of Laplace and Hooke's laws by equating wall tension due to APB, to the sum of tensions due to elastic and smooth muscle forces. Analysis of CF versus APB curves, performed on the basis of this model, shows that to account for the large change of coronary bed conductance observed under dipyridamole infusion one must assume not only that the smooth muscle tone is absent but also that some relevant variations occur in the whole coronary bed, thus pointing to possible recruitment of new blood vessel paths.

Animals↗
PubMed1986

The effects of Gaboon viper (Bitis gabonica) venom on the electrical and mechanical activity of the guinea-pig myocardium.

The effects of Bitis gabonica venom were tested on guinea-pig heart, using both Langendorff preparations and isolated atrial strips or papillary muscles. In the self-paced whole heart, a single passage of 50 micrograms of venom per ml produced in sequence: irregularities of the A-V conduction and decrease of the contractile strength, progressive failure to relax and systolic arrest of the heart. Pretreatment with atropine reduced but did not abolish these effects. Venom recycled through the heart was effective at a much lower dose. The relationship between resting membrane potential and [K+]o was unaffected by envenomation, suggesting that the action of the venom cannot be ascribed to a loss of ionic selectivity of the cell membrane. The peak amplitude of action potentials declined in papillary muscle exposed to venom at physiological [K+]o, while in atrial cells it was affected only at higher [K+]o. Maximum upstroke rate of the action potential vs. resting potential at different [K+]o gave a sigmoid relationship, characterized by a higher upper asymptote as compared to controls, and by a shift of the curve towards more negative voltage values. A marked shortening of the action potential duration, paralleled by a decrease in time to peak tension, was recorded as well. 'Slow' action potentials, elicited in 20 mM K+ solution, were completely abolished within 10 min of perfusion with venom. These results are consistent with the hypothesis that the venom interacts with both transmembrane Ca2+ inflow and Ca2+ binding at the external side of the cell membrane. A transient positive inotropic effect induced by the venom was observed in papillary muscle and in atropinized atrium. This effect was abolished by previous administration of reserpine to the animal or by addition of propranolol to the perfusing solution, suggesting a venom-induced release of both adrenergic and cholinergic transmitters from nerve endings within the cardiac tissue.

Action Potentials↗
PubMed1986

The effect of the coronary vascular wall on the changes in the coronary vascular resistance during a sudden reduction and recovery of the aortic blood pressure.

To demonstrate the effect of elastic and myogenic properties of the vessel wall on the mean coronary vascular resistance during ventricular diastole (m.d.c.r.), this resistance was assessed in twenty dogs anaesthetized with sodium pentobarbitone during a 10 s period of arterial haemorrhage and 20 s of recovery from this haemorrhage. In a first stage of the study ten dogs were investigated following sectioning of the vagal nerves in the neck, beta-blockade, and ligation of the carotid arteries. During haemorrhage and reduction in aortic blood pressure (A.B.P.) in these dogs, there was an initial rise (at 2 s after the start of the haemorrhage) in m.d.c.r. which quickly decreased to a value similar to that obtained during the control period. After the abrupt cessation of haemorrhage, and a rise in A.B.P., there was an initial decrease in m.d.c.r. which eventually increased to the control levels. In the second stage of study identical patterns of changes were obtained in a group of five dogs in which the cervical vagi were not sectioned and beta-blocking agents not given. In another group of five dogs, during infusion of dipyridamole to force maximal coronary vasodilation, the increase in m.d.c.r. was maintained throughout the period of haemorrhage and reduction in A.B.P., and m.d.c.r. did not decrease below the control values following the abrupt cessation of haemorrhage and a rise in A.B.P. The findings in the dogs without dipyridamole infusion suggested that the pattern of changes in m.d.c.r. was due to changes in the perfusion pressure and their effect on the elasticity and myogenic properties of the coronary vascular wall. This suggestion was supported in the second stage of the study, when the reductions in m.d.c.r. were abolished by forcing coronary vasodilation using the infusion of dipyridamole.

Animals↗
PubMed1984

The effect of gaboon viper (Bitis gabonica) venom on cardiac stroke work in the anaesthetized rabbit.

The effect of Bitis gabonica venom administered intravenously in the rabbit at the dose of 0.125 mg/kg (approximately 10% of LD50) has been studied. Venom caused marked changes in cardiovascular parameters principally a precipitous but transient fall in total peripheral resistance and arterial blood pressure. Furthermore in the period occurring between 5 and 30 min after the injection of venom, a transient increase in stroke work was observed as a result of the ejection of an increased stroke volume against a blood pressure which had already returned to normal. Such a transient inotropic effect has also been observed in other small mammals and could be attributed to an adrenergic mechanism.

Animals↗
PubMed1983

Cardiac performance in the rabbit as affected by the venom of bitis gabonica. (A preliminary report).

The effect of the venom of Bitis gabonica administered intravenously in the rabbit at the dose of 0.125 mg/kg has been compared with that produced by the same dose of the compound in the dog. In the rabbit the effect on total peripheral resistance, aortic blood pressure and stroke volume is less marked and shorter than in the dog. Furthermore in a period included between 5 and 30 min after the injection, in the rabbit a transient increase of stroke work is observed as a result of the ejection of an increased stroke volume against a blood pressure which has already returned to normal. Such a transient inotropic effect of the venom was also observed in other small mammalians and might be attributed to an adrenergic mechanism.

Animals↗
PubMed1983

Changes in aortic blood pressure and cardiac output curves as induced by stenosis of the descending thoracic aorta.

In 9 anaesthetized open chest rabbits cardiac output and aortic blood pressure were recorded. Cardiac output was obtained by means of an electromagnetic blood flow transducer placed around the ascending aorta. When a 10 sec stenosis of the descending thoracic aorta was produced, an increase of mean, systolic, diastolic and pulse pressure was observed above the stenosis, with a remarkable delay of the peak systolic pressure with respect to the peak velocity of ventricular ejection. Moreover, it is note worthy that during the stenosis the deceleration phase of the ventricular ejection showed a slackening which was responsible for a longer ejection time. Owing to such a longer ejection time, in 4 experiments stroke volume and cardiac output increased above the control in spite of a high aortic impedance. It is probably that the changes observed in the contour of the ventricular ejection curve, depend on modifications of the gradient between left ventricle and aortic blood pressure as well as on the combined effects of the Starling's law and of the afterload.

Animals↗
PubMed1983

Autoregulation of the coronary vascular resistance after beta-adrenergic receptor blockade.

It was previously observed that at the beginning of a 10 sec multiple arterial haemorrhage, vascular elasticity induces an increase of coronary vascular resistance, which in the late part of the haemorrhage is counteracted by the relaxation of the vascular smooth muscle fibres. In the present study the effect of multiple arterial haemorrhage on the coronary vascular resistance was studied after beta-adrenergic receptor blockade. The results suggest that also in these circumstances an elastic mechanism precedes a myogenic mechanism in the regulation of coronary vascular resistance.

Adrenergic beta-Antagonists↗
PubMed1983

The effect of Bitis gabonica (Gaboon viper) snake venom on external iliac and mesenteric arterial circulation in the dog.

The effects of Gaboon viper (Bitis gabonica) venom on external iliac and mesenteric arterial blood flow and resistance were investigated in eight anaesthetized, close-chest dogs. Venom doses in the range 0.125-0.5 mg/kg produced a profound fall in external iliac and mesenteric arterial resistance, which recovered to control values after 30 min. After a third dose of venom, the mean arterial blood pressure failed to recover and the animals died after a period of severe hypotension. External iliac arterial blood flow rose concomitantly with the fall in external iliac resistance and decreased to a value significantly below control after 30 min. Paradoxically, mesenteric blood flow fell during the period of vasodilation. The results suggest that widespread vasodilation of muscle vascular beds (of which the external iliac circulation is representative) leads to shunting of blood away from the less-dilated mesenteric circulation. Venom-induced peritoneal haemorrhage caused a fall in blood volume and increase in viscosity. These undoubtedly contributed to the severe haemodynamic deterioration of the preparations after the third injection of the venom.

Animals↗
PubMed1981

The effect of the venom of Bitis gabonica on mesenteric and external iliac blood flow. - A preliminary study in the dog.

The activity of the venom of Bitis Gabonica on mesenteric and external iliac circulation was investigated in four anaesthetized dogs. Venom doses of 0.125, 0.25 and 0.50 mg/kg were injected intravenously with an interval of 30 minutes between two successive injections. Following the first and the second dose, a transient fall of the resistance was observed in the mesenteric and especially in the external iliac vascular bed. Then, mesenteric resistance returned to normal, whereas external iliac resistance increased noticeable above the control value. After the third injection the animals died in a state of severe hypotension. It is note-worthy that during the transient vasodilation, mesenteric flow did not increase proportionally to the reduction of the relevant resistance, owing to the fact that BP fell more than would have been expected from the mesenteric vasodilation. This discrepancy seemed to depend on a more conspicuous reduction of the resistance in other vascular beds as observed in the external iliac circulation.

Animals↗
PubMed1981

Haemodynamic effect of the suppression of ventricular tachycardia by atrio-ventricular captures.

In 10 anaesthetized open chest dogs, blood pressure, electrogram from the left auricular appendage or right atrium, peripheral ECG and cardiac output were recorded. Ventricular tachycardia was produced with aconitine and then suppressed by inducing atrial fibrillation or flutter-fibrillation either with aconitine or with electrical stimulation. After the capture of the ventricles by the supraventricular impulses, a haemodynamic improvement took place. This improvement is attributed to: I) beat to beat changes in the length of the cardiac cycles, whereby intermittent strong beats arise; II) restoration of the normal ventricular activation path and time course; III) the active contribution of properly timed atrial contractions, when present. The improvement was more evident when, after the capture, the ventricular rate was lower than during the ventricular tachycardia, because of a longer period available for the ventricular filling. It is believed that the reduction of the ventricular rate immediately after the capture is due to the suppression of the activity of the ventricular ectopic focus by the concealed conduction of high rate impulses coming from the atria.

Animals↗
PubMed1980

Vectorcardiographic analysis of prefibrillatory ventricular tachycardia in the rabbit.

In 10 urethan anaesthetized rabbits, VCG of acontine induced VT was studied. At the beginning of VT, both QRS and T loops arise and end regularly at the e point. Then, QRS loop opens and its end moves outside the E point, as a result of changes in ST segment. Later on, when ST segment disappears completely owing to an initial overlapping of the depolarization and repolarization processes, no arrest of the trace is observed between QRS and T loops. Lastly, immediately before the appearance of ventricular fibrillation, a progressive increase of the rate of VT above 400/min produces a fusion between the end of the T and the initial part ofn the next QRS loop. At this stage, no E point can be recognize. The results suggest that the transformation of VT into VF occurs through a delay and an overlapping of the depolarization-repolarization sequence.

Animals↗