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Biomedical subjects

A U Ferrari

Publications and source records attributed to A U Ferrari.

At least 37 records · Page 2Linked to original sources
PubMed1994

Alterations in neural cardiovascular control mechanisms with ageing.

AGEING AND MECHANISMS OF BLOOD PRESSURE CONTROL: Ageing is associated with functional and structural alterations to the cardiovascular system. Evidence is accumulating, however, that ageing also determines major changes in the effectiveness of mechanisms involved in blood pressure control and that this represents an important determinant of the cardiovascular changes that can be observed in the elderly. DIFFERENCES SEEN IN ELDERLY SUBJECTS: It has been observed that compared to young subjects, in the elderly (1) baroreceptor control of the heart rate and cardiac function is impaired; (2) baroreceptor modulation of the sympathetic drive to the peripheral circulation is impaired, particularly the speed of reflex adjustments to normal and abnormal stimuli; and (3) cardiopulmonary stretch receptors, which tonically inhibit sympathetic tone, the renal release of renin and vasopressin secretion, are impaired. These three factors may account, at least in part, for the raised blood pressure and sympathetic activity in the elderly. They certainly explain the reduced ability of elderly people to maintain blood pressure and blood volume homeostasis, and their increased blood pressure variability over 24 h. ASSOCIATION WITH HYPERTENSION: All these problems are exacerbated if ageing is associated with hypertension, and are highly relevant to antihypertensive treatment. Care should be taken that any antihypertensive drugs selected for treatment in the elderly do not aggravate these basic homeostatic problems.

Aged↗
PubMed1993

Vascular effects of lacidipine: a review of animal and human data.

AIM: To compare the vascular effects of lacidipine with those of other calcium antagonists. METHODS: A review of published studies. RESULTS: Experimental studies have shown that for a similar fall in blood pressure, lacidipine increased cardiac contractility while verapamil decreased cardiac contractility. In the rat aorta, the dose of lacidipine required to reduce a calcium-induced contraction by 50% was lower than that of all other calcium antagonists tested except nisoldipine. In human studies, especially, there are inherent limitations in the techniques available to measure regional blood flows under physiological conditions, making it difficult to compare the effects of different antihypertensive drugs. A recent study showed that renal blood flow was increased by lacidipine without any reduction in renal function. As in animals, vital organ perfusion was either preserved or increased. Further, maximal coronary vasodilation was associated with lower coronary resistance values during lacidipine treatment compared with pretreatment values. Another lacidipine study showed increased brachial artery compliance, while a study on the radial artery showed that lacidipine increased the compliance of this artery also. CONCLUSIONS: Lacidipine has vascular selectivity. Although regional blood flows are difficult to measure, due to inherent limitations in the techniques available, the evidence suggests that lacidipine produces vasodilation in essential hypertensive subjects while maintaining or even increasing vital organ perfusion. This appears to be due to a regression of the structural changes that characterize hypertension.

Animals↗
PubMed1993

Spontaneous variability of regional haemodynamics in unanaesthetized rats.

AIM: To study the spontaneous variability in regional haemodynamics. METHODS: Twenty normotensive Wistar-Kyoto rats were chronically instrumented with an arterial catheter and with pulsed Doppler flowmeters on the distal aorta, and the superior mesenteric and left renal arteries. After surgical recovery, the rats were monitored in unrestrained conditions. The recorded signals were analysed beat-to-beat to obtain means and coefficients of variation for mean arterial pressure, heart rate, regional blood flow velocity (consecutive 0.8-s periods) and indices of regional vascular resistance (0.8-s ratio of mean arterial pressure to mean blood flow velocity). RESULTS: Muscle and splanchnic blood flow velocities were markedly variable, with coefficients of variation of 12.8 +/- 0.8 and 12.2 +/- 1.7% (means +/- SEM), respectively, about twice as large as the coefficient of variation for mean arterial pressure (6.2 +/- 0.3%). The renal blood flow velocity was slightly less variable than the muscle and splanchnic blood flow velocities, with a coefficient of variation of 10.4 +/- 0.8%, but still markedly and significantly more variable than systemic arterial pressure. A contingency analysis of paired variations in any two given parameters (arterial blood pressure, heart rate, blood flow velocities and indices of vascular resistance) showed a concordant pattern, the only exception being a distinctly discordant trend for the covariations in muscle and splanchnic blood flow velocities. CONCLUSIONS: Regional blood flow velocity and vascular resistance have a larger degree of spontaneous variability than systemic arterial pressure. Renal blood flow velocity is also highly variable, suggesting that short-term stimuli that affect the renal blood vessels are not countered by autoregulation to any great degree. We conclude that while central factors may drive concordant regional haemodynamic variations, some opposing changes in regional blood flow velocity may cancel each other out, thereby reducing the variability in systemic blood pressure.

Animals↗
PubMed1993

Modulation of parasympathetic and baroreceptor control of heart rate.

The heart rate is modulated from beat to beat by efferent vagal and sympathetic fibers, the former being the predominant mediators of the chronotropic influence of arterial baroreceptors and respiration and the latter being important in the cardiac responses to physical and mental stress. Cardiac vagal influences are modulated by a number of factors. These can be grouped as: 1) neural factors, such as the wakefulness-sleep cycle, the alerting reaction, and exercise; 2) humoral-pharmacological factors, such as angiotensin II, atrial natriuretic factor, cardiac glycosides; 3) normal aging; 4) a number of cardiovascular and other diseases, such as arterial hypertension, coronary artery disease, congestive heart failure and diabetes mellitus. The mechanisms underlying modulation of cardiac vagal control are not completely understood, the range of the possibilities including structural or functional alterations in baroreceptor afferents, in central and efferent vagal pathways and in cardiac responsiveness to neural stimuli. Irrespective of the mechanisms involved, the modulation of cardiac vagal control may have important implications for normal cardiovascular homeostasis, as well as for the pathophysiology, diagnosis and prognosis of various diseases.

Aging↗
PubMed1992

Age-related modifications in neural cardiovascular control.

Integrated cardiovascular responses to a range of different stimuli, as well as the overall, spontaneously occurring variability in blood pressure and heart rate, undergo complex changes with aging. A general trend is that homeostatic control mechanisms lose part of their ability to modulate heart rate and to buffer the concomitant blood pressure variations; the two phenomena are possibly linked by a cause-effect relationship. A detailed analysis of the age-related changes in the major reflex systems reveals a clear-cut impairment in arterial baroreceptor control of the heart rate, but much less pronounced changes in its control of blood pressure, on the other hand, both the hemodynamic and humoral components of the cardiopulmonary reflex appear to be markedly attenuated. The experimental evidence of the mechanisms underlying these changes is still largely incomplete, and it appears that the gaps will have to be filled by a systematic, detailed analysis, i.e., that no generalizations or extrapolations will be possible. Indeed, the data available so far indicate that the age-related alterations are highly non-uniform, some functions undergoing a definite impairment but others being much better preserved and some being even enhanced; thus aging is by no means associated with a generalized decline in cardiovascular functions and should instead be viewed as a complex, highly selective process. These peculiar biological features of the aging phenomena merit further investigation in both the cardiovascular and the other organ systems, in order to verify the possibility that currently unrecognized homeostatic potentials in the elderly subject may be exploited to advance his/her clinical management in health and disease.

Aging↗
PubMed1992

Cardiac parasympathetic hyperresponsiveness in spontaneously hypertensive rats.

The bradycardic response to baroreceptor stimulation is impaired in human and experimental hypertension. Because this bradycardia mainly depends on the vagus, this may reflect a reduced cardiac parasympathetic responsiveness, which would parallel the reduced cardiac adrenergic responsiveness observed in hypertension. To test this hypothesis, 12-week-old spontaneously hypertensive rats (n = 12) and normotensive Wistar-Kyoto rats (n = 11) were anesthetized with ketamine and underwent bilateral vagotomy. Cardiac parasympathetic responsiveness was assessed from the bradycardia induced by 1) graded electrical stimulation of the right efferent vagus (1-16 Hz) and 2) graded intravenous injections of methacholine (1-8 micrograms.kg-1). The slope of the linear regression between the bradycardiac response and the applied stimulus was taken as the measure of cardiac parasympathetic responsiveness. To identify the onset of possible alterations in cardiac parasympathetic responsiveness in hypertension, the study was extended to younger (8-week-old) spontaneously hypertensive (n = 11) and Wistar-Kyoto (n = 13) rats. With vagal stimulation, cardiac parasympathetic responsiveness was greater in 12-week-old spontaneously hypertensive rats than in 12-week-old Wistar-Kyoto rats (24.8 +/- 5.4 versus 10.1 +/- 1.2 beats per minute per hertz, mean +/- SEM, p less than 0.035). This was also the case with methacholine (18.8 +/- 3.5 versus 13.1 +/- 4.4 beats per minute per microgram per kilogram, p less than 0.045). In contrast, cardiac parasympathetic responsiveness was similar, with both vagal stimulation and methacholine, when tested in the younger spontaneously hypertensive and Wistar-Kyoto groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Reflex control of circulation in the elderly.

Baroreceptor control of heart rate is markedly reduced in elderly subjects. However, the effects of aging on baroreceptor control of blood pressure and on the vascular and neurohumoral influences of volume cardiopulmonary receptors are unknown. In this paper we report evidence that in both conscious rats and humans aging is associated with a fall in the baroreceptor ability to rapidly cause blood pressure changes, but that the more long-term carotid baroreceptor control of blood pressure remains similar to that observed in younger individuals. Early and late cardiopulmonary receptor modulation of vascular resistance is impaired by aging, which also reduces the influence of this reflex on renin secretion. These dynamic and steady-state alterations in reflex cardiovascular control account for several hemodynamic abnormalities of the advanced age.

Aged↗
PubMed1991

Differential effects of aging on the heart rate and blood pressure influences of arterial baroreceptors in awake rats.

The effect of aging on arterial baroreceptor control of heart rate and blood pressure was evaluated in unanesthetized normotensive rats aged 5-6 (young), 12-16 (adult) and 75-90 (old) weeks. Each rat was chronically implanted with arterial and venous femoral catheters and with bilateral balloon-in-cuff occluders around the common carotid arteries. Baroreceptor control of heart rate was assessed by the bradycardic and tachycardic response to intravenous boluses of phenylephrine and nitroprusside, respectively. Carotid baroreceptor control of blood pressure was assessed by a 12-s bilateral common carotid occlusion (CCO). All baroreflex responses were similar in young and adult rats. Compared with the young group, old rats showed a marked reduction of the bradycardic and tachycardic baroreflex response (-42% and -46%, respectively, P less than 0.05). The initial pressor responses to CCO were also impaired in the old animals (3 s: -63%, 6 s: -54%; both P less than 0.01), whereas the peak pressor response (9 and 12 s) was virtually identical in the young and old groups. The preservation of the peak pressor response to CCO in old rats was independent of chemoreceptor activation, aortic baroreceptors or cerebral ischemia. Thus, aging impairs baroreceptor control of heart rate but alters baroreceptor control of blood pressure, as assessed by the pressor response to CCO, only in its fast-developing component, leaving its longer-term component unaffected.

Aging↗
PubMed1991

Alterations in cardiac parasympathetic function in aged rats.

Aging impairs sympathetic and parasympathetic cardiac control. Although the reduced sympathetic responses are known to depend on an age-related cardiac beta-adrenoceptor dysfunction, the hypothesis of a parallel cardiac muscarinic receptor dysfunction underlying the reduced parasympathetic responses has never been tested. We therefore measured the bradycardic responses to graded electrical stimulations of the right efferent vagus and to graded bolus intravenous injections of acetylcholine in anesthetized, vagotomized rats of young (16 wk) and old (103 wk) age. Unexpectedly, the bradycardia was markedly larger (greater than 2-fold) in old than in young rats with both the electrical and the pharmacological stimulus. This indicates that at variance with its effects on beta-adrenergic receptor responsiveness, aging not only fails to impair but actually enhances cardiac muscarinic receptor responsiveness. It also suggests the more general conclusion that aging has complex and diversified effects rather than simply and uniformly depressing biological functions.

Acetylcholine↗
PubMed1991

Role of sinoaortic afferents in modulating BP and pulse-interval spectral characteristics in unanesthetized cats.

Sinoaortic denervation (SAD) is accompanied by an increase in blood pressure (BP) and a reduction in pulse-interval (PI) variance. Little is known, however, about the effect of SAD on the complex BP and PI variability pattern, which is identified by spectral analysis. In nine unanesthetized cats in which intra-arterial BP was monitored before and 7-10 days after SAD, spectral powers (estimated by fast Fourier transform) were calculated for the low frequency (LF, 0.025-0.07 Hz), midfrequency (MF, 0.07-0.14 Hz), and high frequency (HF, 0.14-0.60 Hz) band. The very low frequency (VLF) BP and PI components (VLF less than 0.025 Hz) were also estimated. SAD increased systolic BP variance and decreased PI variance. The reduction of PI variance was paralleled by significant and marked reductions in all PI powers including the VLF components. In contrast, the increase in systolic BP variance was accompanied by a marked increase in LF power, a decrease in MF power, and no change in HF power. The VLF BP components increased after SAD for frequencies between 0.025 and 0.0012 Hz, whereas a sudden marked reduction was observed below 0.0012 Hz. Similar results were obtained for diastolic BP powers. Thus the reduction in PI variance induced by SAD is paralleled by a reduction in all PI fluctuations identified by spectral analysis. This is not the case for the SAD-related increase in BP variance, which is accompanied by an increase, no change, or even a reduction in the different BP spectral components.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1991

Potentiation of the baroreceptor-heart rate reflex by sympathectomy in conscious rats.

In both animals and humans, stimuli leading to sympathetic activation are accompanied by an impairment of the baroreceptor-heart rate reflex. To determine whether sympathetic activity normally interferes with this reflex function we examined in conscious Wistar-Kyoto (WKY) rats the effect of chemical sympathectomy by 6-hydroxydopamine on the bradycardic response to baroreceptor stimulation induced by raising blood pressure via intravenous phenylephrine boluses; control rats received vehicle. Spontaneously hypertensive rats were also studied because in these animals there is both a baroreceptor reflex impairment and a sympathetic overactivity. Baroreceptor reflex sensitivity, calculated as the ratio of the peak increase in pulse interval to the peak increase in mean arterial pressure, was 75% greater in sympathectomized WKY rats than in control WKY rats (1.28 +/- 0.15 versus 0.73 +/- 0.10 msec/mm Hg, mean +/- SEM; p less than 0.01). The sympathectomy-induced increase in sensitivity was even larger in spontaneously hypertensive rats (SHR) (1.26 +/- 0.12 versus 0.44 +/- 0.06 msec/mm Hg in sympathectomized SHR versus control SHR, +186%; p less than 0.01) so that the impaired baroreceptor reflex sensitivity observed in control SHR as compared with control WKY rats (-40%, p less than 0.01) was no longer detectable in the sympathectomized groups. To establish whether the sympathectomy-induced potentiation of the reflex was due to an increase in cardiac responsiveness to vagal stimuli, we subjected separate groups of anesthetized, vagotomized SHR and WKY rats to graded electrical stimulation of the right efferent vagus. The bradycardic effects of vagal stimulation, however, were similar in sympathectomized and control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Intra-arterial pressure alterations during tail-cuff blood pressure measurements in normotensive and hypertensive rats.

The heating and restraint inherent to tail-cuff measurement of systolic blood pressure (SBP) in rats may alter SBP and introduce a 'biological' error in its estimation by this technique. This problem was examined in unanesthetized normotensive and hypertensive rats fitted with an arterial catheter. All SBP values recorded in unrestrained rats during a 2 h period were averaged by computer and compared with intra-arterial SBP measurements observed while the rat was being subjected to the tail-cuff procedure. With the latter procedure, SBP was 16 +/- 2 mmHg lower in normotensive rats (P less than 0.001) and 7 +/- 3 mmHg higher in hypertensive rats (P less than 0.05) than when the rats were unrestrained. The effects of heat and restraint, both separately and in combination, on SBP were evaluated during four additional 30-min monitoring periods. In both groups of rats, restraint failed to alter SBP and heat lowered it slightly. The two stimuli, combined, lowered SBP in normotensive rats, but raised it by 12 +/- 2 mmHg in hypertensive rats (P less than 0.01). Thus, tail-cuff SBP measurements represent under- and overestimates in normotensive and hypertensive rats, respectively, since the two groups respond to the procedure in opposite manners.

Animals↗
PubMed1990

Atrial natriuretic factor and arterial baroreceptor reflexes in unanesthetized rats.

The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. In group 2, right common carotid occlusion was performed in rats with their aortic and left carotid sinus baroreceptors denervated to assess the baroreceptor control of blood pressure; the reflex response was quantitated as the peak blood pressure rise observed during the maneuver. The reflex studies were performed before and during atriopeptin III infusion (0.15-0.20 micrograms/kg/min for 60 minutes). ANF augmented the bradycardic response to phenylephrine by 102.5 +/- 29% (p less than 0.01), reduced the tachycardic response to nitroprusside by 67.7 +/- 6.4% (p less than 0.01), and failed to modify the pressor response to carotid occlusion (-6.8 +/- 2.1%, p = NS). In a separate group of rats infused with low dose nitroprusside, no change in the baroreceptor-heart rate reflex was observed. ANF infusion (0.20 micrograms/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480 +/- 58 fmol/ml. Values in control vehicle-infused rats were 50 +/- 8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaortic-denervated rats) was only minimally reduced by ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Age-related alterations in cardiac parasympathetic responsiveness: a preliminary report.

Baroreceptor control of the heart rate is reduced by ageing in animals and man. This has been ascribed to an age-related reduction in beta-adrenergic receptor density and cardiac responsiveness to sympathetic modulation. However, the baroreceptor-heart rate reflex largely depends on the vagus and the age-related changes in cardiac parasympathetic responsiveness have never been tested directly. We examined the heart rate responses to acetylcholine in six young (3-5 months) and six old (22-24 months) ketamine-anaesthetized, bilaterally vagotomized Sprague-Dawley rats instrumented with arterial and venous catheters. The acetylcholine was given as 2, 4 and 8 micrograms/kg intravenous bolus injections. Linear regressions between each dose of acetylcholine and the ensuing bradycardia were calculated. The acetylcholine-induced bradycardia was strikingly larger in old than in young rats, amounting to 20.9 +/- 4.4 and 8.6 +/- 1.5 beats/min per microgram per kg, respectively (P less than 0.05). Thus cardiac muscarinic receptor responsiveness is increased rather than reduced by ageing. Therefore not all functions involved in cardiovascular regulation show an age-related impairment, and some may even be enhanced as age progresses. It is also clear that mechanisms other than attenuation of cardiac responses to autonomic stimuli (central and/or afferent) account for the age-related impairment in the baroreceptor-heart rate reflex.

Acetylcholine↗
PubMed1988

Effect of atrial natriuretic factor on arterial baroreceptor control of heart rate and blood pressure in conscious rats.

The effects of atrial natriuretic factor (ANF) on arterial baroreceptor control of heart rate and of blood pressure were examined in conscious normotensive rats chronically instrumented with arterial and venous catheters, by measuring (1) the pulse interval responses to four intravenous boluses of phenylephrine and four intravenous boluses of nitroprusside, reflex sensitivity being calculated as the slope of the linear relationship between pulse interval and mean arterial pressure (nine rats); (2) the pressor response to right common carotid occlusion (balloon-in-cuff occluder) in eight rats with aortic and left carotid baroreceptor denervation. The study was performed before and during a non-hypotensive infusion of ANF. Atrial natriuretic factor increased the bradycardic responses to phenylephrine by 90% but reduced the tachycardic response to nitroprusside by 67% (P less than 0.01 for both) and left the pressor response to carotid occlusion unaffected (-7%, NS). It is concluded that ANF modulates the arterial baroreceptor reflex in a complex fashion, with opposite responses to arterial baroreceptor stimulation and deactivation, and different responses for the cardiac and vascular component of the reflex.

Animals↗