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Biomedical subjects

C Giannattasio

Publications and source records attributed to C Giannattasio.

At least 91 records · Page 5Linked to original sources
PubMed1991

Left ventricular hypertrophy and the 'cardiogenic reflex' in man.

In man, cardiac receptors exert a continuous restraint on sympathetic activity. Reflexes originating from the heart also restrain renin and vasopressin secretion, thereby being involved both in blood pressure and in blood volume homeostasis. We have shown that these reflexes are markedly depressed in subjects with left ventricular hypertrophy (LVH) due to hypertension and that this is also the case when, in normotensive subjects, LVH is caused by prolonged physical training. In both instances, the cardiogenic reflex impairment is associated with derangement of blood pressure homeostasis. Either spontaneous regression of LVH by physical training cessation or antihypertensive treatment is followed by a marked improvement of the cardiogenic reflex. Thus, LVH also affects the 'afferent' function of the heart. 'Physiological', as well as pathological, hypertrophy has a similar adverse effect. This effect is reversible, however, and the reflex function can be restored by regression of hypertrophy.

Autonomic Nervous System↗
PubMed1990

Cardiogenic reflexes and left ventricular hypertrophy.

Studies performed in both animal and human species have shown that receptors anatomically located in the cardiac walls and in the pulmonary vascular bed exert a powerful influence on sympathetic vasoconstrictor tone and renin release from the kidney. This paper will review recent data collected by our group on the effects on this homeostatic reflex function of two different models of cardiac hypertrophy, i.e. that associated with arterial hypertension and that induced by prolonged physical training. It will also examine whether and to what extent cardiopulmonary reflex control of circulation can be restored after an effective antihypertensive pharmacological treatment has induced a regression of the structural alterations of the heart. The results of these studies suggest that cardiopulmonary reflex control of circulation is markedly impaired in the presence of cardiac hypertrophy, with (severe hypertensive subjects) or without (athletes) high blood pressure values. In hypertensives, furthermore, therapeutic regression of cardiac hypertrophy seems to restore, although not fully normalize, this reflex function. Taken together these findings suggest that cardiac hypertrophy, per se, is a condition characterized by the loss of the reflex functions exerted by cardiac receptors, with adverse consequences on cardiovascular homeostasis.

Adult↗
PubMed1990

Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction.

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.

Carotid Sinus↗
PubMed1990

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

Cardiopulmonary receptor control of the circulation is impaired in a variety of diseases having cardiac hypertrophy as a common feature. Whether this also occurs in the so-called "physiological" cardiac hypertrophy of the athlete, however, is unknown. We studied nine sedentary healthy subjects and 19 age-matched professional runners or hammer throwers who had trained at least 2 hours per day, 5 days per week for 7 years. The left ventricular mass index (echocardiography) was 99 +/- 7.4 and 135 +/- 5.9 g/m2 in the two groups, respectively. Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter for 5 minutes by leg raising and lower body negative pressure, keeping both stimuli at a level not affecting blood pressure and heart rate. In the sedentary healthy subjects, forearm vascular resistance (the ratio between mean arterial pressure and forearm blood flow) and plasma norepinephrine fell during leg raising (forearm vascular resistance, -7 +/- 1.7 units; norepinephrine, -57.4 +/- 1.4 pg/ml) and increased during lower, body negative pressure (forearm vascular resistance, 20 +/- 5.3 units; norepinephrine, 97.7 +/- 21.5 pg/ml). For similar or greater alterations in left ventricular end-diastolic diameter, the correspondent changes observed in the professional runners or hammer throwers were -5.3 +/- 1.3 units (forearm vascular resistance), -35.4 +/- 9.6 pg/ml (norepinephrine), 9.1 +/- 1.4 units (forearm vascular resistance), and 30.9 +/- 6.9 pg/ml (norepinephrine). This represented an attenuation of 25%, 38%, 55%, and 68%, respectively (p less than 0.01), of the control response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Effects of dilevalol on forearm circulation in essential hypertension.

In 6 patients with untreated hypertension of mild or moderate degree, dilevalol was infused in the brachial artery. Doses were calculated to produce plasma levels approximating those achieved after oral dosing (0.03, 0.07, 0.1, 0.3 micrograms.kg-1.min-1) and also to produce plasma levels exceeding oral dosing (0.5, 1.0, 2.0 micrograms.kg-1.min-1) without causing any blood pressure or heart rate changes. The effects of the infusion on forearm blood flow were assessed by venous occlusion plethysmography. Dilevalol caused a progressive increase in flow in all subjects up to the intermediate dose given, with the effect being attenuated when the dose was increased further. Simultaneous propranolol infusion reduced the increase in flow induced by dilevalol, shifting the dilevalol-induced vasodilation dose response curve to the right. Isoproterenol infusion caused a marked, dose-related increase in flow that was equally well reduced by simultaneous infusion of dilevalol or propranolol. These results indicate that dilevalol effectively blocks peripheral vascular beta receptors in humans. The drug also acts as a partial beta 2-receptor agonist, causing vasodilation which can be reduced by co-administration of propranolol.

Adrenergic beta-Agonists↗
PubMed1989

Investigation of reflexes from volume and baroreceptors during converting-enzyme inhibition in humans.

This article emphasizes the importance of testing baroreceptor and cardiopulmonary receptor control of circulation during angiotensin-converting enzyme (ACE) inhibitor treatment in hypertensives, because removal of angiotensin II-dependent stimulation of the sympathetic nervous system could impair reflex blood pressure homeostasis. In essential hypertensive subjects, the sympathetic vasoconstriction that occurs in skeletal muscle after deactivation of cardiopulmonary receptors was reduced after short-term or prolonged administration of the ACE inhibitor, captopril. However, another sympathetic target of the cardiopulmonary reflex, that is, renin release, was unaltered by both short-term and prolonged administration of captopril. Furthermore, the blood pressure and heart rate influences of arterial baroreceptors were preserved or even enhanced after administration of captopril. Thus important reflex mechanisms for cardiovascular homeostasis are not adversely affected by ACE inhibition, which preserves blood pressure levels during gravity challenges or exercise. Preliminary data suggest that this may be even more evident for benazepril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Cardiac hypertrophy impairs cardiac receptor control of circulation in man.

The cardiopulmonary reflex control of circulation (which, in man, depends largely on cardiac receptors) is impaired in hypertensive subjects who have left ventricular hypertrophy. To determine whether hypertension or cardiac hypertrophy per se is responsible for this, we studied nine sedentary normotensive subjects aged 23 +/- 1 years and nine age-matched normotensive weight-lifters with echocardiographic signs of left ventricular hypertrophy (left ventricular mass index for the weight-lifters: 134 +/- 7; for the sedentary subjects: 99 +/- 7 g/m2; P less than 0.01). Cardiac receptors were manipulated by increasing and decreasing the left ventricular end-diastolic diameter (LVEDD) by raising the leg and by reducing the lower-body negative pressure, respectively, and the reflex responses were assessed from the changes in forearm vascular resistance and plasma noradrenaline (high performance liquid chromatography assay). Forearm vascular resistance and the noradrenaline concentration were reduced by increasing the LVEDD, and were increased when the LVEDD was reduced. For a given change in the LVEDD, the responses were markedly less in the weight-lifters than in the non-athletes. In contrast, the haemodynamic effects of a cold pressor test were similar in both groups. Thus, the cardiopulmonary reflex is impaired in normotensive subjects in whom intense physiological training has led to an increase in left ventricular hypertrophy. This suggests that structural alteration of the heart per se is responsible for the phenomenon.

Adult↗
PubMed1989

Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension.

In order to investigate whether angiotensin II (Ang II) may contribute to cardiovascular regulation through facilitation of the adrenergic function, we examined the haemodynamic and humoral effects of the application of lower-body negative pressure (LBNP) in sodium-replete patients with essential hypertension before and after acute and chronic angiotensin converting enzyme (ACE) inhibition. We measured the changes in blood pressure, heart rate, central venous pressure, forearm blood flow, plasma noradrenaline, renin activity and Ang II induced by LBNP of two different magnitudes: a milder one deactivating predominantly the cardiopulmonary receptors (mild LBNP), and a greater one deactivating both the cardiopulmonary and the arterial baroreceptors (strong LBNP). We found that during mild LBNP systemic blood pressure was maintained after acute and chronic ACE inhibition, as in control studies; however, the decrements in forearm blood flow and the increments in forearm vascular resistance caused by LBNP were diminished after ACE inhibition (the latter by 69 and 67%, respectively, in acute and chronic studies), in spite of the fact that the falls in central venous pressure and the increases in noradrenaline (NA) were similar to those observed in control conditions. During strong LBNP, the fall in systemic blood pressure was greater after acute and chronic ACE inhibition than in control conditions and was associated with a reduction in the response of forearm vascular resistance similar to that observed during mild LBNP, while the increments in NA were again superimposable to those seen before ACE inhibition. These alterations in the haemodynamic responses to LBNP induced by ACE inhibition were associated with significant increments in basal plasma renin activity and with marked reductions in Ang II. These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses.

Adult↗
PubMed1989

Decreased cardiopulmonary reflexes with aging in normotensive humans.

Arterial baroreflex is impaired in the normotensive elderly. However, no information is available on the effects of aging on another major reflex mechanism of cardiovascular control, i.e., cardiopulmonary reflex. Three groups of normotensive subjects divided according to age were evaluated during leg raising, which increased central venous pressure, and during lower body negative pressures, which reduced central venous pressure without altering blood pressure and heart rate. These maneuvers stimulated and deactivated cardiopulmonary receptors with only little involvement of arterial baroreceptors. During lower body negative pressures, central venous pressure decreased similarly in three groups, but reflex increases in forearm vascular resistance, plasma norepinephrine, and plasma renin activity were smaller in elderly than in middle-aged and young subjects. Furthermore, during leg raising, comparable increases in central venous pressure caused reflex vascular and humoral responses that were smaller in elderly than in middle-aged and young subjects. Elderly subjects had smaller changes in left ventricular diameter in response to changes in central venous pressure. Blood pressure and vascular responses to cold pressor test were similar in the three groups, excluding a hyporeactivity of older subjects to neural stimuli. Thus aging is associated with an impairment of the cardiopulmonary reflex. This may originate from an impaired ability of cardiac receptors to sense alterations in central blood volume because of an age-dependent reduction in cardiac compliance.

Adult↗
PubMed1988

Cardiopulmonary receptor regulation of renin release.

Cardiopulmonary receptors have been shown to modulate renin release in animals. However, their involvement in reflex control of renin in humans has never been unequivocally established. This report reviews data on the effects on plasma renin activity of maneuvers (lower body negative pressure and passive leg raising) that reduce and increase central venous pressure and cardiac diameter without affecting blood pressure and heart rate, thereby deactivating and stimulating cardiopulmonary receptors with little or no involvement of the arterial baroreceptors. In normotensive subjects, reduction in central venous pressure was accompanied by an increase in plasma renin activity that was similar to the increase observed during tilt that reduced central venous pressure to a similar extent. Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity. The increase in plasma renin activity that followed the reduction in central venous pressure was drastically attenuated in four patients who had undergone cardiac transplantation, along with other reflex effects (changes in forearm vascular resistance and plasma norepinephrine) of cardiopulmonary receptor manipulations. There was a modest reduction in the overall reflex changes in plasma renin activity in patients with mild to moderate essential hypertension compared with normotensive subjects. However, patients with essential hypertension and cardiac hypertrophy showed marked attenuation of all reflex influences of the cardiopulmonary receptors. In five subjects, therapeutic regression of this structural alteration was associated with a clear improvement in the cardiopulmonary reflex. Thus, in humans, cardiopulmonary receptors exert an important reflex control of renin release. This control (which is due in part to receptors located in the cardiac walls) is moderately affected by a mild to moderate blood pressure elevation but is markedly impaired when the elevation produces structural alterations in the heart. Preliminary evidence, however, suggests that the cardiopulmonary reflex may be improved by a reduction in cardiac hypertrophy.

Animals↗
PubMed1988

Cardiopulmonary receptor reflex in hypertension.

Several studies have described the modifications of the arterial baroreceptor reflex in hypertension. Whether this condition alters the other major cardiovascular reflex (ie, that originating from receptors in the cardiopulmonary region) is less well known, however. Herein we describe the importance of the inhibitory control of sympathetic vasomotor and renin influences exerted by the cardiopulmonary reflex in normotensive humans as assessed by deactivating and stimulating heart and lung receptors through reductions and increases in central venous pressure respectively obtained via lower-body negative pressure and passive leg raising. Observations on this reflex obtained in experimental animal models are summarized. Finally, we report recent evidence showing that the cardiopulmonary reflex is only slightly affected by mild or moderate essential hypertension but impaired in hypertension with left ventricular hypertrophy in a fashion positively related to the degree of this cardiac structural alteration. This may further worsen the severity of hypertension. However, the impairment of the cardiopulmonary reflex is reversible with regression of hypertrophy obtained by antihypertensive treatment which is thus beneficial for cardiovascular homeostasis.

Humans↗
PubMed1988

Effects of ageing on the cardiopulmonary receptor reflex in normotensive humans.

This study examined the effects of ageing on the cardiopulmonary receptor regulation of vasomotor tone in skeletal muscle and renin release by the kidney. To this end, the changes in forearm vascular resistance (mean arterial pressure divided by plethysmographically measured forearm blood flow), plasma noradrenaline concentration and plasma renin activity were measured in eight young (23 +/- 2 years, mean +/- s.e.m.) and seven elderly healthy subjects (69 +/- 2 years) during manoeuvres which altered cardiopulmonary receptor activity. The cardiopulmonary receptors were stimulated by increasing central venous pressure through passive leg-raising and deactivated by reducing central venous pressure through non-hypotensive (-15 mmHg) and hypotensive (-40 mmHg) levels of lower body negative pressure. During either manoeuvre, central venous pressure changed by the same amount in both groups, but the reflex changes in forearm vascular resistance, plasma noradrenaline and plasma renin activity were significantly less in elderly subjects. Since the increase in forearm vascular resistance induced by a cold pressor test was comparable in young and elderly subjects, a non-specific depression of cardiovascular responsiveness to neural stimuli can be excluded. Thus, healthy normotensive elderly subjects show an impairment of both vascular and neurohumoral influences exerted by cardiopulmonary receptors. This may be involved in the decreased ability of the elderly to cope with gravity challenges.

Adult↗
PubMed1988

Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Cardiopulmonary reflex before and after regression of left ventricular hypertrophy in essential hypertension.

Studies that have examined the cardiopulmonary receptor control of circulation in hypertension have produced conflicting results. In 10 normotensive subjects and in age-matched essential hypertensive subjects without (n = 10) or with left ventricular hypertrophy (n = 12), as well as in seven subjects of the latter group restudied after 1 year of treatment that induced regression of cardiac hypertrophy, we examined the cardiopulmonary reflex by increasing central venous pressure and stimulating cardiopulmonary receptors through passive leg raising and by reducing central venous pressure and deactivating cardiopulmonary receptors through nonhypotensive lower body negative pressure. Reflex responses were measured as changes in forearm vascular resistance (mean blood pressure divided by plethysmographically measured blood flow), plasma norepinephrine concentration, and plasma renin activity. In hypertensive subjects without left ventricular hypertrophy, stimulation and deactivation of cardiopulmonary receptors caused changes in forearm vascular resistance, norepinephrine concentration, and plasma renin activity that were modestly reduced as compared with those in normotensive subjects. However, all these changes were markedly reduced in hypertensive subjects with left ventricular hypertrophy. Following regression of left ventricular hypertrophy, the changes in vascular resistance, plasma norepinephrine, and plasma renin activity induced by cardiopulmonary receptor manipulation all improved markedly. These results demonstrate that cardiopulmonary receptor regulation of peripheral vascular resistance and of neurohumoral variables is impaired in essential hypertension and that the impairment is much more pronounced when this condition is associated with cardiac structural alterations. Therapeutic regression of these alterations, however, leads to a marked improvement of this reflex, with consequent favorable effects on circulatory homeostasis.

Adult↗
PubMed1988

Reflex control of circulation and angiotensin converting enzyme inhibition in man.

Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.

Blood Pressure↗
PubMed1987

Calcium antagonists and neural control of circulation in essential hypertension.

Data from animals and from man suggest that calcium antagonists interfere with alpha-adrenergic receptors and that this mechanism may be responsible for some of the vasodilation induced by these drugs. However, alpha-adrenergic receptors play a primary role in baroreceptor regulation of the cardiovascular system and blood pressure homeostasis, which might therefore be adversely affected by calcium antagonist treatment. We addressed this question in 14 essential hypertensives studied before treatment, 1 h after 20 mg oral nitrendipine and 5-7 days after daily administration of 20 mg oral nitrendipine. Blood pressure was measured by an intra-arterial catheter, heart rate by an electrocardiogram, cardiac output by thermodilution and forearm blood flow by venous occlusion plethysmography. Total peripheral and forearm vascular resistances were calculated by dividing mean blood pressure by blood flow values. Plasma norepinephrine was also measured (high performance liquid chromatography) in blood taken from the right atrium. Compared with the pretreatment values, acute nitrendipine administration caused a fall in resting blood pressure, an increase in the resting heart rate and cardiac output, and a fall in resting peripheral and forearm vascular resistance. The resting hypotension and vasodilation were also evident during the prolonged nitrendipine administration, which was, however, accompanied by much less resting cardiac stimulation than that observed in the acute condition. Baroreceptor control of the heart rate (vasoactive drug method) was similar before and after acute and prolonged nitrendipine treatment. This was also the case for carotid baroreceptor control of blood pressure (neck chamber technique) and for control of forearm vascular resistance as exerted by receptors in the cardiopulmonary region (lower-body negative-pressure and passive leg-raising techniques).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗