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Biomedical subjects

A Malliani

Publications and source records attributed to A Malliani.

At least 163 records · Page 9Linked to original sources

Analysis of the pressor sympathetic reflex produced by intracoronary injections of bradykinin in conscious dogs.

The reflex hemodynamic effects of intracoronary bradykinin were tested in 20 conscious instrumented dogs. When the experiments were performed after full recovery from surgery and anesthesia, graded doses (10-300 ng/kg) of bradykinin always produced graded pressor responses, in the absence of any pain reaction. At the maximum pressor response obtained with 100 ng/kg, mean arterial pressure rose 28 +/- 3% from 89 +/- 4 mm Hg, left ventricular pressure 20 +/- 3% from 121 +/- 2 mm Hg, heart rate 30 +/- 4% from 88 +/- 5 beats/min, rate of change of left ventricular pressure 18 +/- 3% from 2812 +/- 65 mm Hg/sec (P less than 0.01). Higher doses of bradykinin did not produce greater responses. The magnitude of the response was similar when the injection was performed in either the left anterior descending (change in mean arterial pressure 29 +/- 3%) or circumflex (change in mean arterial pressure 27 +/- 2%) coronary artery. The reflex nature of the response was proved by its disappearance after appropriate pharmacological blockades; moreover, after vagotomy, the pressor rise was maintained, the heart rate response was reduced (change in heart rate 10 +/- 2%), and the inotropic response was enhanced (rate of change of left ventricular pressure 24 +/- 3%). This suggested that the afferent pathway of the pressor reflex was in the sympathetic nerves and that a subordinate vagal depressor reflex was also operative. No pain reaction was obtained even when injecting very large amounts (1000-2000 ng/kg) of bradykinin, which, instead, induced arterial hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗

Simultaneous analysis of beat by beat systemic arterial pressure and heart rate variabilities in ambulatory patients.

The analysis of power spectral density (PSD) or RR variability in the electrocardiogram (ECG) has suggested that, in the early phase of essential hypertension, sympatho-vagal interaction is characterized by a sympathetic predominance. Recently, we have developed a high fidelity, direct arterial pressure ambulatory recording system which allows a beat by beat computer analysis of arterial pressure and heart rate. A microminiature tip transducer (Millar, diameter 0.8 mm) is inserted percutaneously into the radial artery and connected to a Holter two-channel magnetic tape recorder. The tip transducer has a wide band pass (> 1 kHz), excellent stability (congruent to 2 mmHg/24 h) and does not require a perfusion line. The overall frequency response of the entire recording-reproducing system is better than 20 Hz (-3 dB). The ECG and pressure signals are analysed with automatic autoregressive modelling algorithms to provide a quantitative estimate of blood pressure and heart rate variability through the computation of the PSD. In seven hypertensive patients, systolic arterial pressure and variance were higher during the day (157 +/- 9 mmHg and 122 +/- 9 mmHg2) than during the night (122 +/- 4 mmHg and 30 +/- 3 mmHg2). The PSD of RR and of systolic arterial pressure consisted of a predominant low frequency peak (congruent to 0.09 cycles/beat) during the day, and two peaks at low and high (congruent to 0.25 cycles/beat) frequency during the night. While RR variance was similar during both day- and night-time, a predominant low frequency peak was observed during the day.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Global versus regional myocardial ischaemia: differences in cardiovascular and sympathetic responses in cats.

The cardiovascular and sympathetic responses to occlusions of the left main ("global" ischaemia) or distal left anterior descending ("regional" ischaemia) coronary artery were studied in 19 anaesthetised cats with chronic sinoaortic baroreceptor denervation. "Global" ischaemia, before vagotomy, resulted in a significant reduction of mean arterial pressure (MAP), left ventricular pressure (LVP), and LVdP/dtmax while sympathetic efferent impulse activity was significantly augmented during the initial 15 +/- 2 s of occlusion (early phase) and, vice versa inhibited during the subsequent 20 +/- 2 s of occlusion (late phase). Vagotomy did not modify the haemodynamic responses, however, a significant increase in sympathetic discharge was detectable during the whole occlusion period (early and late phases). "Regional" ischaemia, before vagotomy, resulted in a significant increase in sympathetic neural discharge and MAP, with no changes in left ventricular function. After vagotomy the occlusion elicited a significant increase in MAP, LVP, LVdP/dtmax and efferent sympathetic neural activity. These excitatory responses were abolished after the interruption of a large part of the cardiac sympathetic afferents. Thus coronary artery occlusion induced haemodynamic and sympathetic reflex responses that were dependent upon the interaction of opposite influences mediated by the simultaneous activation of cardiac vagal and sympathetic afferents. The extent of "ischaemic myocardium" represented a determinant factor for the prevailing type of neural response.

Action Potentials↗

Power spectral density of heart rate variability as an index of sympatho-vagal interaction in normal and hypertensive subjects.

Instantaneous heart rate reflects sympatho-vagal influences on pace-maker activity. Hence computer analysis of heart rate variability might provide a quantitative index of that interaction. The power spectral density (PSD) estimate of heart rate variability was obtained in normal controls and in uncomplicated hypertensives, both at rest and during a non-hypotensive sympathetic stimulus (tilting). In normal controls PSD shows three major peaks of frequencies P1 = 0.07, P2 = 0.12, P3 = 0.25 cycles/beat. P1, which is associated with sympathetic activity, represents only a minor portion of total variability at rest, while becoming predominant with tilting. P2 and P3 are associated with vagal activity, and represent the major part of variability at rest, while they are reduced by tilting. In hypertensive patients PSD is altered, as P1 is already predominant at rest and increases only slightly with tilting. Thus PSD of heart rate variability is capable of detecting an early alteration in sympatho-vagal balance of cardiac control present in uncomplicated hypertension.

Adult↗

The role of the sympathetic nervous system in congestive heart failure.

Congestive heart failure is usually accompanied by cardiovascular signs of an increased sympathetic and a decreased parasympathetic efferent activity. A current hypothesis for these autonomic changes holds the baroreceptor mechanisms mainly responsible for this complex neural reflex pattern together with a decreased responsiveness of cardiac vagal afferent ffibers. An alternative hypothesis is proposed here. Afferent sympathetic fibers with sensory endings in the atria and in the pulmonary veins are progressively excited by volume load. In cats with a chronic spinal section at C8, breathing spontaneously, an infusion of saline induces a reflex tachycardia through a sympatho-sympathetic neural circuit. In chronic dogs with intact cardiovascular innervation, the stimulation of aortic or cardiac sympathetic afferent fibers elicits an excitatory sympathetic reflex leading to hypertension and tachycardia; in addition, the sensitivity of baroreflexes is markedly reduced. Therefore, in congestive heart failure, especially in the absence of hypotension, the reflex excitation of the sympathetic outflow and the inhibition of the vagal efferent activity directed to the heart could be due to reflex mechanisms mediated by sympathetic cardiovascular afferents.

Animals↗

A positive feedback sympathetic pressor reflex during stretch of the thoracic aorta in conscious dogs.

The role of pressor sympathetic reflexes in circulatory control was investigated in conscious dogs. Animals were previously instrumented with a 6- to 8-cm rigid core cannula covered by an inflatable rubber cylinder in the thoracic aorta, a pressure catheter implanted in the aorta above the cannula, and a second catheter inserted into the aorta below the cannula through a femoral artery. Two piezoelectric crystals were positioned at opposing adventitial sites to measure aortic distension with ultrasound techniques. After recovery from surgery, the diameter of the aortic segment surrounding the cannula was increased by 9.6 +/- 0.4% from 16 +/- 1 mm by inflating the rubber cylinder, without obstructing blood flow. Mean aortic pressure rose 31 +/- 3% from 100 +/- 3 mm Hg and heart rate 20 +/- 3% from 91 +/- 3 beats/min (P less than 0.01). The pressor response was abolished by alpha-adrenergic blockade (phentolamine 1 mg/kg, iv). The heart rate response was reduced either by beta-blockade (propranolol 1 mg/kg, iv) or muscarinic blockade (atropine 0.2 mg/kg, iv) and abolished by their combination. During aortic stretch, the sensitivity of the baroreflex was reduced 57 +/- 7% from 18 +/- 2 msec/mm Hg (P less than 0.01). The pressor response was increased by 49 +/- 8% after bilateral carotid sinus nerve section and vagotomy. These excitatory reflex responses were obtained in absence of any pain reaction. Thus, in the conscious dog, aortic distension within physiological ranges induces a potent pressor sympathetic reflex with positive feedback characteristics. Such a pressor reflex not only occurs in the presence of functioning baroreflexes, but is also capable of reducing their sensitivity.

Adrenergic alpha-Antagonists↗

The visceral nervous system as a mediator of psychosocial risk factors: therapeutic implications of its specific organization.

The visceral (autonomic) nervous system is one of the most important mediators between mind and viscera. Its organization has conventionally been attributed to the dominance of the brain, with the sympathetic and parasympathetic systems performing solely outflow functions. However, since the reflex arc appears to be the functional unit of these systems, their organization may be based on local reflexes, modulated by higher nervous structures. Visceral nervous activity therefore reflects both the central excitatory state and local input from the viscera. Moreover, the sympathetic and parasympathetic systems do not exert reciprocal control more or less independently, as used to be thought. In the heart, visceral afferent impulses carried by the vagus and sympathetic nerves each reflexly influence both sympathetic and vagal outflow. Recognition of this pattern of reflex control appears to have implications for beta-adrenergic blockade.

Animals↗

Functions of afferents in cardiovascular sympathetic nerves.

This paper contains data and discussion of the role of afferents in the sympathetic trunks from the cardiovascular complex that evoke autonomic reflex action. A description is given of these cardiovascular reflexes induced by afferents of the sympathetic trunks in neurally intact as well as spinal animals. A positive feedback hypothesis is also proposed.

Afferent Pathways↗

A sympathetic hypertensive reflex from the heart of conscious dogs.

1. The aim of the present experiment was to study in conscious animals the effect of chemical stimulation of cardiac sensory innervation by bradykinin, a physiological substance known to activate both vagal and sympathetic cardiac sensory nerve endings, at doses devoid of systemic haemodynamic effects. 2. In conscious dogs with implanted catheters bradykinin (100 ng/kg) injected into a cannulated branch of the left coronary artery induced significant (P less than 0.01, n = 5) reflex increases in mean arterial pressure and heart rate as well as increases in left ventricular pressure, left ventricular dP/dt max. and coronary blood flow. 3. These changes were obtained in the absence of pain reactions. 4. The concept, derived from experiments on anaesthetized animals, that chemical stimulation of the intact sensory supply of the heart always elicits a cardiovascular depressor reflex mediated by cardiac vagal afferents has to be modified, as pressor sympathetic reflexes may occur after an appropriate stimulus to the fully innervated heart of conscious dogs.

Animals↗

Effects of intracoronary administration of bradykinin on the impulse activity of afferent sympathetic unmyelinated fibers with left ventricular endings in the cat.

In anesthetized and artificially ventilated cats, we recorded the impulse activity of 23 afferent sympathetic unmyelinated fibers with left ventricular endings, dissected from the left sympathetic rami T3 and T4. All fibers displayed a spontaneous discharge at a rate of 0.79 +/- 0.2 (mean +/- SE) impulses/sec. During constriction of the thoracic aorta, the discharge increased to 1.92 +/- 0.2 impulses/sec. During myocardial ischemia, produced by interruption of left main coronary artery perfusion, supplied through an extracorporeal pump, the impulse activity increased to 1.73 +/- 0.3 impulses/sec. The mean latency for this excitation was 16.5 +/- 1.5 sec. The intracoronary administration of bradykinin (5 and 10 ng/kg) elicited a marked increase in impulse activity that, following 5 ng/kg, reached 2.06 +/- 0.2 impulses/sec, after a latency of 18 +/- 2 sec and in absence of significant hemodynamic changes. Myocardial ischemia and bradykinin never revealed the existence of silent afferent fibers included in the split nerve strand. The results obtained with this experimental model indicate that the ventricular endings of these afferent sympathetic unmyelinated fibers act as "polymodal" receptors. We hypothesize that the peripheral mechanism for cardiac nociception involves intensive excitation of fibers discharging spontaneously and not recruitment of silent fibers which are purely nociceptive in function.

Action Potentials↗