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Biomedical subjects

O Rimoldi

Publications and source records attributed to O Rimoldi.

43 records · Page 3Linked to original sources
PubMed1986

Power spectral analysis of heart rate and arterial pressure variabilities as a marker of sympatho-vagal interaction in man and conscious dog.

In 57 normal subjects (age 20-60 years), we analyzed the spontaneous beat-to-beat oscillation in R-R interval during control recumbent position, 90 degrees upright tilt, controlled respiration (n = 16) and acute (n = 10) and chronic (n = 12) beta-adrenergic receptor blockade. Automatic computer analysis provided the autoregressive power spectral density, as well as the number and relative power of the individual components. The power spectral density of R-R interval variability contained two major components in power, a high frequency at approximately 0.25 Hz and a low frequency at approximately 0.1 Hz, with a normalized low frequency:high frequency ratio of 3.6 +/- 0.7. With tilt, the low-frequency component became largely predominant (90 +/- 1%) with a low frequency:high frequency ratio of 21 +/- 4. Acute beta-adrenergic receptor blockade (0.2 mg/kg IV propranolol) increased variance at rest and markedly blunted the increase in low frequency and low frequency:high frequency ratio induced by tilt. Chronic beta-adrenergic receptor blockade (0.6 mg/kg p.o. propranolol, t.i.d.), in addition, reduced low frequency and increased high frequency at rest, while limiting the low frequency:high frequency ratio increase produced by tilt. Controlled respiration produced at rest a marked increase in the high-frequency component, with a reduction of the low-frequency component and of the low frequency:high frequency ratio (0.7 +/- 0.1); during tilt, the increase in the low frequency:high frequency ratio (8.3 +/- 1.6) was significantly smaller. In seven additional subjects in whom direct high-fidelity arterial pressure was recorded, simultaneous R-R interval and arterial pressure variabilities were examined at rest and during tilt. Also, the power spectral density of arterial pressure variability contained two major components, with a relative low frequency:high frequency ratio at rest of 2.8 +/- 0.7, which became 17 +/- 5 with tilt. These power spectral density components were numerically similar to those observed in R-R variability. Thus, invasive and noninvasive studies provided similar results. More direct information on the role of cardiac sympathetic nerves on R-R and arterial pressure variabilities was derived from a group of experiments in conscious dogs before and after bilateral stellectomy. Under control conditions, high frequency was predominant and low frequency was very small or absent, owing to a predominant vagal tone. During a 9% decrease in arterial pressure obtained with IV nitroglycerin, there was a marked increase in low frequency, as a result of reflex sympathetic activation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Neural control of vasomotor tone of large coronary arteries.

In man, the occurrence of constrictions of large coronary arteries accompanied by transient myocardial ischemia is now well established. However, the role of neural factors involved in such coronary artery spasms is still a matter of conjecture. A consistent reduction (9 +/- 2%) of the diameter of the large coronary arteries can be obtained in the conscious dog with alpha-adrenergic receptor stimulation with methoxamine in spite of the concomitant pressor rise (65 +/- 5%). Smaller reductions in coronary diameter can be obtained with electrical efferent sympathetic stimulation in anesthetized dogs. The diameter of a conduit artery such as the aorta can be reduced (5%) by reflex increases in sympathetic efferent activity: therefore it is not unlikely that similar neural influences might be exerted on the coronary tree as well. In normal life, stressful situations, such as emotion or exercise, will be accompanied by a drastic increase in sympathetic drive to the heart, together with a marked increase in coronary flow. The latter will induce an endothelial mediated vasodilation; however the net effect on coronary size of these two potentially opposite mechanisms is as yet unexplored. In the laboratory, intracoronary bradykinin and regional myocardial ischemia initiate a reflex increase in sympathetic activity to the heart; in the clinics acute myocardial ischemia can be accompanied by signs of sympathetic overactivity. The extent to which such increases in sympathetic activity, could play a role in the control of coronary tone and hence in the pathophysiology of coronary artery disease, is still under investigation.

Animals↗
PubMed1985

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↗
PubMed1984

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↗
PubMed1981

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↗
PubMedDate not supplied

Myocardial hibernation vs repetitive stunning in patients.

Myocardial hibernation is a state of persistently impaired left ventricular function in patients with coronary artery disease that was thought to be caused by a chronic reduction in resting myocardial blood flow in a segment subtended by a diseased coronary artery. However, recent studies using positron emission tomography have demonstrated that absolute myocardial blood flow (ml/min/g) to hibernating myocardium is within normal limits in most patients. If resting flow is not reduced, one must therefore suspect an alternative "trigger" for hibernation that is still a consequence of coronary artery disease and ischemia. We suspect that hibernating myocardium may be the result of repetitive myocardial stunning. Myocardial stunning is the reversible contractile dysfunction occurring after a period of myocardial ischemia that persists for a period of time despite the return of blood flow to normal. Myocardial stunning has been demonstrated in humans in the setting of thrombolysis, coronary angioplasty, coronary artery bypass surgery, and coronary artery spasm. Furthermore, stunning has been demonstrated after exercise in patients with coronary artery disease, and recent studies have provided evidence that repetitive episodes of exercise-induced ischemia can lead to cumulative and prolonged left ventricular dysfunction.

Coronary Circulation↗