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A Cevese

Publications and source records attributed to A Cevese.

At least 37 records · Page 2Linked to original sources
PubMed1991

The effect of distension of the urinary bladder on coronary blood flow in anesthetized dogs.

To determine whether distension of the urinary bladder reflexly affects coronary blood flow, experiments were performed in eleven dogs anaesthetized with sodium pentobarbitone. Both ureters were cannulated and the urinary bladder was distended with warm Ringer solution at a steady intravesical pressure. Arterial blood pressure was prevented from changing by a pressurized reservoir of warm Ringer solution connected to the femoral arteries. Coronary blood flow was measured with an electromagnetic flowmeter positioned around the origin of the left circumflex coronary artery. When the reflex increase in heart rate was prevented by atrial pacing in seven dogs, distension of the urinary bladder always caused a decrease in mean coronary blood flow. Similar results were obtained in all eleven dogs after administration of propranolol. The decrease in mean coronary blood flow was significantly reduced by atropine or bilateral cervical vagotomy, and was abolished by bretylium tosylate. The results showed that distension of the urinary bladder reflexly decreased mean coronary blood flow, a response involving efferent cardiac vagal and sympathetic pathways.

Animals↗
PubMed1991

Pressure changes induced by whole body acceleration shocks.

In the present paper pressure changes induced by sudden body acceleration are studied "in vivo" on the dog and compared to the results obtainable with a recently developed mathematical model. A dog was fixed to a movable table, which was accelerated by a compressed air piston for less than 1 s. Acceleration was varied by changing the air pressure in the piston. Pressure was measured during the experiment at different points along the vascular bed. However, only data obtained in the carotid artery and abdominal aorta are presented here. The results demonstrated that impulse body accelerations cause significant pressure peaks in the vessel examined (about + 25 mmHg in the carotid artery with body acceleration of g/2). Moreover, pressure changes are rapidly damped, with a time constant of about 0.1s. From the present results it may be concluded that, according to the prediction of the mathematical model, body accelerations such as those occurring in normal life can induce pressure changes well beyond the normal pressure value.

Acceleration↗
PubMed1991

The efferent mechanisms of reflex hemodynamic responses to distension of the descending colon in anesthetized dogs.

We have recently shown that distension of the descending colon in anesthetized dogs causes reflex increases in heart rate, aortic blood pressure and the maximal rate of rise of left ventricular pressure, involving afferent pathways in the hypogastric nerves. In this study we have examined the efferent mechanisms involved in those responses. The descending colon was distended using Ringer solution at constant pressure in 13 anesthetized dogs. As previously shown, distension of the colon caused an increase in aortic blood pressure, heart rate and the maximal rate of rise of left ventricular pressure. The increase in the aortic blood pressure was abolished by either bretylium tosylate or phentolamine. Propranolol or bretylium tosylate abolished the increases in heart rate when changes in the aortic blood pressure were prevented, and abolished the increases in the maximal rate of rise of left ventricular pressure when the increases in heart rate were also prevented. These results indicate that the reflex increases in heart rate, arterial blood pressure and the maximal rate of rise of left ventricular pressure involved efferent sympathetic pathways.

Animals↗
PubMed1991

Reflex effects of descending colon distension on coronary blood flow in anesthetized dogs.

To find out whether distension of the descending colon reflexly affects coronary blood flow, experiments were performed in nine dogs anesthetized with pentobarbitone. The descending colon was isolated between ligatures and distended with warm Ringer solution at a steady intraluminal pressure. Arterial blood pressure was prevented from changing by withdrawing blood from the left femoral artery. In two of the nine dogs the arterial blood pressure was also kept constant by tightening a plastic snare round the thoracic aorta. The reflex increase in heart rate was prevented by atrial pacing. Distension of the descending colon at constant heart rate and arterial blood pressure always caused a decrease in mean coronary blood flow, amounting to 2.44 +/- 1.8 ml/min (mean +/- SD), equal to a percent decrease of 14.3 +/- 10.5. This response was completely abolished by section of the hypogastric nerves, thus demonstrating that a reflex mechanism is involved.

Animals↗
PubMed1990

The effect of distension of the urinary bladder on left ventricular inotropic state in anesthetized dogs.

To decide whether distension of the urinary bladder reflexly affects the left ventricular inotropic state, experiments were performed in eight dogs anesthetized with pentobarbitone. After cannulation of both ureters the urinary bladder was repeatedly distended through a urethral catheter with warm Ringer solution at a steady intravesical pressure. The maximal rate of rise of left ventricular pressure (dP/dtmax) obtained at constant heart rate and cardiovascular pressures was used to assess changes in left ventricular inotropic state. Arterial blood pressure was prevented from changing by a pressurized reservoir containing warm Ringer solution and connected to the femoral arteries. Following prevention of the reflex increase in heart rate by atrial pacing, distension of the urinary bladder always increased the maximal rate of rise of left ventricular pressure in the eight dogs. There were no significant changes in left ventricular systolic or end-diastolic pressures. The increase in maximal rate of rise of left ventricular pressure was abolished following the administration of propranolol. The results indicate that a reflex increase in left ventricular inotropic state occurred in response to distension of the urinary bladder. This reflex response involved beta-adrenergic stimulation.

Animals↗
PubMed1989

'Non-chronotropic' mechanisms on withdrawal of efferent vagal stimulation in anesthetized dogs.

Withdrawal of the efferent vagal tone to the heart is an important factor of the increase of cardiac output (CO) and arterial blood pressure (ABP) in several conditions, such as exercise, emotion, postural changes. Vagal withdrawal enhances cardiovascular performance both by increasing heart rate (HR) and by other mechanisms, which were globally named 'non-chronotropic mechanisms'. The nature of these non-chronotropic mechanisms was studied in open-chest dogs under morphine-chloralose anesthesia. After cutting the cervical vagi and all the branches of the stellate ganglia except for the ansae subclaviae, the animals were prepared for recording HR, ABP, CO and left ventricular pressure (LVP). The experiments started during control vagal stimulations and consisted either in turning the vagal stimulators off (STOP), or in raising HR by atrial placing without withdrawing vagal stimulation (PACE), or in turning the vagal stimulators off while keeping HR constant by atrial pacing since the control vagal stimulation (STPA). Thus, STOP, PACE and STPA produced withdrawal of all vagal effects, of the chronotropic effects and of the non-chronotropic effects, respectively. Non-chronotropic mechanisms were evaluated both as the effects of STPA and as the difference between the effects of STOP and PACE. Experiments were repeated during stellate ganglion stimulation and during simultaneous atrio-ventricular pacing, to evaluate the role of vagosympathetic interactions and of atrial contractility. CO increased by 25% after STOP, by 20% after PACE and by 5% after STPA in the absence of sympathetic stimulation and by 30% after STOP, by 20% after PACE and by 10% after STPA during sympathetic stimulation. Stellate ganglion stimulation doubled non-chronotropic effects probably by potentiating vagal effects on myocardial contractility: after STPA the maximum LVdP/dt increased by 2% without sympathetic stimulation and by 7% with sympathetic stimulation. In all conditions, the increases in ABP after STOP, PACE and STPA were small and not statistically different between STOP and PACE. Simultaneous atrio-ventricular pacing in the absence of sympathetic stimulation nearly abolished non-chronotropic mechanisms, since CO increased to about the same extent both with STOP and with PACE. It is concluded that non-chronotropic mechanisms on vagal withdrawal consist mainly in the enhancement of atrial contractility and in the release of vagal restraint on the sympathetic effects upon the ventricles.

Analysis of Variance↗
PubMed1987

Cardiac alpha-1 adrenoceptors are not involved in heart rate control of the anaesthetized dog.

To study the possible role of cardiac postsynaptic alpha-1 adrenoceptors in heart rate control of the anaesthetized open-chest dog we injected a specific alpha-1 agonist (amidephrine) into the right coronary artery or stimulated electrically the right stellate ganglion. Reflex influences were minimized by bilateral cervical vagotomy and de-afferentiation of both stellate ganglia. Activation of alpha-2, beta- and muscarinic receptors was prevented by intravenous administration of yohimbine, propranolol and atropine, respectively. Since alpha-1 receptor stimulation could affect heart rate indirectly via coronary constriction, a continuous intracoronary infusion of adenosine (0.25 mg/kg/h) was given. Amidephrine did not affect heart rate at the lower dose (1-10 microgram). After the highest dose (100 micrograms) the maximum variation in heart rate was an increase of 2.2 +/- 1.1 bpm at 3 min after injection (mean +/- SEM; P less than 0.05). This slight cardioacceleration was simultaneous with an aortic pressure rise of 13.8 +/- 3.4 mm Hg and it was abolished by alpha-1 blockade with prazosin (1 mg/kg i.v.). After propranolol (1 mg/kg +0.5 mg/kg/h) the residual positive chronotropic effect of sympathetic stimulation (12.2 +/- 4.0 bpm) was not significantly altered (13.8 +/- 5.7 bpm) by prazosin administration. Similar results were recorded without adenosine infusion. We conclude that in the anaesthetized dog chronotropic effects directly mediated by alpha-1 adrenoceptors either do not exist or lack physiological significance.

Adenosine↗
PubMed1985

Role of the autonomic nervous system in the control of heart rate and blood pressure in the defence reaction in conscious dogs.

The present study was performed on conscious, chronically instrumented dogs, which underwent selective blockade of sympathetic adrenergic and vagal outflows. Excitements were performed on these animals in normal states (N), after chronic treatment with guanethidine, for sympathetic blockade (SB), after cold vagal blockade (VB), and after combined sympathetic and vagal blockade (SB + VB). Heart rate and arterial blood pressure were monitored in all the experiments, while a group of dogs was also tested with an electromagnetic flowmeter on the superior mesenteric artery. The role of the sympathetic and parasympathetic controls in the defence reaction was assumed from comparison of experiments performed in the presence or in the absence of each (or both) autonomic component(s). In the SB + VB condition, excitement was followed by sudden hypotension, without changes in heart rate. In VB experiments, a brief and transient hypotension appeared, followed by gradually developed hypertension, while heart rate progressively rose in about 5 s; there was no sudden increase in mesenteric vascular resistance, which contrasted with the very marked reaction in N experiments. Under vagal control alone (SB), the stimulus elicited prompt tachycardia and hypertension, followed by a period of moderately reduced blood pressure. We conclude that, while the defence reaction leads to a sudden fall of arterial blood pressure, in the absence of compensatory mechanisms, both branches of the autonomic nervous system play a protective role against hypotension. In addition, the modulation of the vagal outflow, leading to sudden changes in the heart performance, seems to be responsible for the initiation of the overall haemodynamic adjustments following excitements. The possibility that withdrawal of the parasympathetic outflow to the heart may raise arterial blood pressure was verified in a special experiment in which artificial vagal stimulation in a conscious (vagal blocked) dog, was turned off for brief periods, before and after guanethidine. This led to changes in blood pressure and heart rate very similar to those seen at the onset of the defence reaction, both in N and SB conditions.

Aggression↗
PubMed1985

Haemodynamic effects of withdrawal of efferent cervical vagal stimulation on anesthetized dogs--relative importance of chronotropic and non-chronotropic mechanisms.

The aim of the present work was to study changes in cardiac output (CO) and arterial blood pressure (ABP) following either interruption of artificial efferent vagal stimulations (STOP), or suppression of negative chronotropic effects, during uninterrupted vagal stimulations (PACE). Experiments were performed on 7 anesthetized, open-chest dogs. A computerized data acquisition system was used to record CO (electromagnetic flowmeter), ABP, right atrial pressure and electrocardiogram; 9 parameters were automatically elaborated. The peripheral stumps of both vagus nerves, sectioned at the neck, were stimulated for long control periods (at least 3 min) with brief trains of stimuli triggered by atrial P waves. Records were started during steady-state vagal stimulations, and consisted of paired trials: in the first step the vagal stimulators were turned off (STOP); in the second step the heart was paced at the same rate reached at the end of the preceding step, but vagal stimulation was continued (PACE). Observations lasted two min after each step. Results indicate rapid rise in CO and ABP after STOP, up to 30% and 10%, respectively, in 10 s, followed by slow reduction in CO and further increase in ABP (22% and 15%, respectively, at 120 s). Thus STOP caused rapid and sustained improvements in the cardiac performance. After PACE changes in CO and ABP were smaller and followed a slower time-course. The greater effects of STOP with respect to PACE were attributed to non-chronotropic mechanisms, accounting for about 50% of the overall haemodynamic consequences of vagal withdrawal. Since peak aortic flow velocity and acceleration were increased after STOP, stroke volume was reduced much less than after PACE, despite equal rise in heart rate, and similar shortening in the ejection time. Evidence was presented of enhanced atrial and ventricular contractility after STOP. Experiments performed after beta-blockade in 5 dogs substantially confirmed the results. It is concluded that vagal withdrawal, which is an important aspect in many physiological situations, constitutes a rather powerful strategy for rapid enhancement of the cardiovascular performance, through different mechanisms, in addition to cardioacceleration.

Anesthesia↗
PubMed1984

Cervical efferent vagal stimulation related or unrelated to cardiac cycles: comparison of negative atrial inotropic effects.

Efferent cervical vagal stimulations were performed in 4 anesthetized dogs, either with trains of stimuli of constant frequency (CONT), or with brief trains, triggered by the atrial electrical activity (TRIG). Heart rate was increased by cardiac pacing during vagal stimulations. Negative inotropic effects of vagal stimulations, evaluated as changes in atrial contractility, were partially inhibited by cardiac acceleration during CONT, but were unaffected during TRIG. It is concluded that the number of stimuli per cycle, not the number of stimuli per second, is the critical factor for parasympathetic heart regulation.

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

Heart rate variability at the onset of efferent vagal stimulations in the rabbit.

Vagal stimulations were performed in 6 anesthetized rabbits for single cardiac cycles. The distribution of effects over 6 consecutive cardiac cycles was described as a function of varying intervals between P waves and stimuli (P-St): the response on the first couple of cycles is affected by P-St whilst the effects decline regularly over successive cycles. Stimulation of 6 consecutive cycles showed rapid rise and subsequent slow increment of the response. Results interpreted as evidence for intracellular accumulation of a restraining factor for heart rate due to vagal stimulation.

Animals↗
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↗