1,721,215 research outputs found
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
"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
Which is the preferred substrate for pulmonary surfactant disaturated phosphatidylcholine (DSPC) synthesis in newborn infants?
No full textINTERVENTI AL LIMITE. BIOETICA DELLE TERAPIE INTENSIVE NEONATALI
No full textLe esperienze maturate dal Comitato di Bioetica del Dipartimento di Pediatria di Padova, le risposte alle domande che sorgono in materia di intervento medico e mortalità infantile, rianimazione dei neonati e patologie procurate dalle stesse tecniche impiegate per supportare le funzioni natali dei prematur
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