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Haemodynamic effects of withdrawal of efferent cervical vagal stimulation on anaesthetized dogs - relative importance of chronotropic and non-chronotropic mechanisms
No full textThe 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. © 1985
Short-term hemodynamic effects of intravenous propionyl-l-carnitine in anaesthetized dogs
No full textThe effects of intravenous administration of propionyl-L-carnitine (PLC) were investigated in anesthetized dogs instrumented for the analysis of general hemodynamic and electrocardiographic data, peripheral blood flows, coronary blood flow and oxygen consumption, urine flow, and renal function. PLC was administered in bolus (20, 60, and 200 mg/kg) or by infusion (20 mg/kg/min * 15 min or 30 mg/kg/min * 10 min). In some cases also L-carnitine (LC) and L-carnitine+propionate (LC + P) were administered in doses equimolar to those of PLC. PLC elicited dose-dependent, short-lasting enhancements of cardiac output, both in open- and closed-chest conditions. Arterial blood pressure, heart rate, and contractility varied slightly and unpredictably; the substance did not elicit electrocardiographic effects. These responses were not changed by alpha- or beta-adrenergic blockade, nor by the administration of a calcium antagonist, but they were abolished or reversed by the combination of such blocking interventions. Mesenteric and iliac blood flows were increased by both PLC and LC; LC + P increased these, and in addition increased renal blood flow. A strong diuresis obtained with PLC, LC, and LC + P was due to osmotic clearance following the administration of hyperosmotic solutions. PLC elicited coronary vasodilation with reduced oxygen extraction; this effect lasted longer than the general hemodynamic effects and was not seen with LC. All the cardiovascular actions of PLC can be attributed to its pharmacologic properties, rather than to its role as a metabolic intermediate
"Non chronotropic" mechanisms on withdrawal of efferent vagal stimulation in anesthetized dogs
No full textWithdrawal 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 pacing 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. © 1989
Cardiac alpha-1 adrenoceptors are not involved in heart rate control of the anaesthetized dog
No full textTo 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
Il Palladianesimo in Inghilterra
No full textCatalogo della mostrainternazionale celebrativa del quarto centenario della morte dell'architetto tenutasi a Vicenza nella Basilica Palladian
Isohemic blood volume expansion in normal and areflexive dogs
No full textThe hemodynamic and renal responses to rapid intravascular volume expansion (VE) were studied in normal and areflexive dogs. 'Isohemic' expansion was performed by infusion autologous blood (averaging 453 ml) thoroughly mixed with the circulating blood. In areflexive dogs cardiac output and arterial pressure doubled immediately after VE and fell back to control within 70 min; in normal dogs the circulatory response was less than one third as great, but arterial pressure failed to return to control within 120 min. In the areflexive dogs, water, electrolyte, and total osmolar urinary output rose three to fivefold after VE and declined thereafter, roughly following arterial pressure. In normal dogs the urine flow increased 40% immediately and rose further up to 70% in 60 min. No evidence for a natriuretic hormone was seen. It is concluded that mechanical factors are mainly responsible for the increased excretion of water and solutes after VE. Direct nervous reflexes to the kidney seemed to play a quantitatively minor role in the renal response
Pressure changes induced by whole body acceleration shocks
No full textIn 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..
Comparison between passive drag and drag during leg kicking of the crawl stroke in top level swimmers
No full textA body moving through water encounters a resistance called drag. Sixteen crawl swimmers (ten females and six males) and 11 breaststrokers (seven females and four males) were subjected to measurements of the force resisting towing in the prone position (Ft). Towing was performed in a 25-m swimming pool with a new device (Ben Hur, APLab, Rome) that measures Ft at a predetermined constant speed. Each crawl swimmer performed: I) six passive tows at constant speed (from 1.2 to 2.2 ms-1) in order to assess Ft1, which corresponds to passive drag; II) four tows at constant speed (from 1.6 to 2.2 ms-1) during leg kicking of the crawl stroke performed at maximum intensity for 8-12 s in order to assess Ft2. In breaststrokers, Ft1 was measured at the water surface and at a depth of 0.5 m. In eight swimmers (five females and three males), Ft1 was measured at the water surface twice to evaluate the reliability of the Ben Hur device. Ft1 was significantly higher in males than in females (p Ft1). We conclude that Ben Hur is a simple and effective measurement device for the evaluation of the individual passive drag in a common swimming pool. The effect of leg kicking on drag is very different among swimmers of the same technical level, especially in females. The individual comparison between Ft2 and Ft1 provides information about the effectiveness of leg kicking at race speed
Preservation of rabbit hearts with different cardioplegic solutions at low temperature.
No full textAn organ-preserving solution, including in its composition also organic molecules, prepared at the University of Wisconsin (UW), has been successfully used for preservation of liver, pancreas and kidney, and has recently been tested for long-term storage of isolated hearts. We have compared the effectiveness of the UW solution with that of a standard crystalloid cardioplegic solution (St. Thomas, ST) in the functional and structural preservation of isolated hearts. The hearts taken from 24 rabbits were mounted on a Langendorff preparation. After assessment of the left ventricular function by an intraventricular balloon, 40 ml of either cardioplegic solution were injected to arrest the hearts (12 UW and 12 ST), which were then immersed in the same solution for 4 h at 4 degrees C without perfusion. After this period, the hearts were normothermally reperfused with oxygenated Krebs-Henseleit solution for 30 min, and finally left ventricular function was assessed again. An electron microscopic evaluation was performed as well. Significantly higher recovery of left ventricular developed pressure (p < 0.01) and of negative dP/dt (p < 0.05), was observed after preservation with UW, while no difference on positive dP/dt was found. After reperfusion, left ventricular end-diastolic pressure significantly rose with ST (p < 0.01), but did not change with UW; the difference between ST and UW was significant (p < 0.01). Tissue water content was significantly lower in the hearts preserved with UW (p < 0.05). Electron microscopic examination revealed generally good preservation with no substantial difference between the two solutions.(ABSTRACT TRUNCATED AT 250 WORDS
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