[Adenomyomatosis of the gallbladder. Remarks on 30 cases].
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Adult↗
Biomedical subjects
M Volpe
Publications and source records attributed to M Volpe.
Cardiac function in systemic hypertension before and after reversal of left ventricular hypertrophy.
In 3 age- and sex-matched groups of subjects--15 normotensives, 15 hypertensives without left ventricular (LV) hypertrophy and 15 hypertensives with LV hypertrophy--the slopes of the regression line obtained by plotting the individual values of LV fractional shortening against the corresponding values of echocardiographic end-systolic stress were compared. The first 2 groups were studied only in control conditions while the third group was restudied after a 20% reduction in LV mass index induced by a long-term antihypertensive treatment and after a 3-week washout period. A significant relation between fractional shortening and end-systolic stress was found in all instances. The slope of this correlation was higher in normotensives (-0.251) and in hypertensives without LV hypertrophy (-0.232) (both p less than 0.01) than in hypertensives with ventricular hypertrophy (-0.079). In this latter group, the slope increased after the reversal of LV hypertrophy (-0.230, p less than 0.01) and remained unchanged (-0.202) at the end of the washout period. No difference was detectable between the slopes obtained in these patients after reversal of LV hypertrophy, both with the antihypertensive treatment on and off, and those of normotensives and hypertensives without LV hypertrophy. Thus, LV hypertrophy attenuates the influence of changes in afterload on LV function. Reversal of LV hypertrophy restores a fractional shortening end-systolic stress relation quite comparable to that found both in normotensives and in hypertensives before the development of LV hypertrophy.
Cardiomegaly↗
[Surgical treatment of liver injuries. Considerations on a series of 32 cases].
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Adolescent↗
Effects of chronic antihypertensive treatment with ketanserin versus metoprolol on blood pressure and large arteries' compliance in humans: a cross-over double-blind study.
The antihypertensive efficacy of a serotonin-receptor antagonist, ketanserin, was compared with that of a well-established antihypertensive drug, metoprolol, and their cardiac and forearm hemodynamic effects were investigated using echocardiography and bidimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive subjects completed a double-blind, cross-over, randomized study using ketanserin and metoprolol. Two 5-week courses with ketanserin or metoprolol were preceded by a placebo period; the total duration of the study was 15 weeks. Despite a comparable efficacy in reducing systolic and diastolic blood pressure (about 10% of the basal value), the two drugs showed quite different effects on forearm hemodynamics. Ketanserin increased forearm blood flow and induced a significant decrease in forearm vascular resistance (from 141 +/- 16 to 75 +/- 11 mm Hg/mL/sec, P less than .01). Furthermore, this treatment was able to improve brachial artery compliance (from 1.89 +/- .3 to 3.2 +/- .3 cm4/dyne 10(-7), P less than .01). On the contrary, metoprolol did not modify forearm hemodynamics. Both drugs did not significantly modify cardiac performance, as evaluated by left ventricle circumferential fiber shortening. Cardiac output was increased by ketanserin (from 5.9 +/- .3 to 6.6 +/- .5 L/min, P less than .05) and fell during treatment with metoprolol (from 5.9 +/- .4 to 4.9 +/- .3 L/min P less than .01). Thus, the two drugs reduce blood pressure through different hemodynamic mechanisms and the effects of ketanserin on systemic and peripheral circulation seem more favorable.
Adult↗
Clonidine hyperphagia: neuroanatomic substrates and specific function.
Recent studies have indicated that the alpha 2-noradrenergic agonist clonidine (CLON), when peripherally and centrally administered, potentiates feeding in satiated rats in a manner similar to that observed following injection of norepinephrine (NE) into the hypothalamic paraventricular nucleus (PVN). The present experiments examined the effects of CLON on meal patterns and macronutrient selection and compared these findings to earlier NE-stimulated feeding studies. Administration of CLON (25 nmoles), directly into the PVN (n = 5), similar to PVN injected NE, produced an increase in meal size (190%) and feeding duration (164%), with no change in meal frequency. Additional tests were conducted in rats with PVN electrolytic or 6-hydroxydopamine lesions. In Sham rats (n = 16) peripheral CLON (0.05 mg/kg), like NE, produced an increase in food intake and particularly potentiated carbohydrate ingestion. Discrete electrolytic lesions of the PVN (n = 5) abolished this CLON-induced feeding and carbohydrate preference, suggesting that the PVN may be a primary site for CLON-stimulated hyperphagia. Neurotoxin lesions of the PVN (n = 17), which reduced PVN NE levels by 75%, failed to alter peripheral CLON-induced feeding. This and other evidence indicates that this agonist may be acting via postsynaptic alpha 2 receptors in the PVN to potentiate carbohydrate intake, rather than via presynaptic release of NE from nerve endings in the PVN.
Animals↗
Reflex control of coronary vascular tone by cardiopulmonary receptors in humans.
To examine whether cardiopulmonary receptors participate in the reflex control of coronary vascular resistance, systemic and coronary hemodynamics were assessed before and during -10 mm Hg lower body negative pressure in eight normal subjects and eight hypertensive patients with left ventricular hypertrophy. In both study groups, lower body negative pressure induced a significant decrease in right atrial pressure, left ventricular filling pressure and cardiac output, an increase in systemic vascular resistance and no change in mean arterial pressure and heart rate. In normal subjects, there was also a significant increase in plasma norepinephrine concentration (from 294 +/- 39 to 421 +/- 47 pg/ml, p less than 0.01). This increase was accompanied by a reduction in coronary blood flow, assessed by the continuous thermodilution method (from 101 +/- 5 to 79 +/- 4 ml/min, p less than 0.05). An increase in coronary vascular resistance (from 0.865 +/- 0.1 to 1.107 +/- 0.1 mm Hg/ml per min, p less than 0.05) and in myocardial oxygen consumption was detected in normal subjects during cardiopulmonary baroreceptor unloading. In contrast, in hypertensive patients, -10 mm Hg lower body negative pressure failed to induce any change in plasma norepinephrine, coronary blood flow or vascular resistance. Intravenous propranolol administration caused no significant change in the systemic hemodynamic response to -10 mm Hg lower body negative pressure in either study group, but it did abolish the decrease in coronary flow and the increase in plasma norepinephrine, coronary vascular resistance and myocardial oxygen consumption observed in normal subjects in control conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Stable improvement in large artery compliance after long-term antihypertensive treatment with enalapril.
In 12 patients with mild or moderate essential hypertension we assessed by 2-D pulsed Doppler flowmetry the influence of a 6-month effective treatment with enalapril or atenolol on peripheral hemodynamics. The patients were studied in control conditions, at the end of the 6-month pharmacologic treatment, and 2 weeks after the withdrawal of the therapy. In spite of a comparable fall in blood pressure, the effects of the two drugs on forearm hemodynamics were quite different. Enalapril induced a fall in vascular resistance and an increase in brachial artery diameter, flow, and compliance, while atenolol failed to modify all these parameters. In the enalapril group the improvement in forearm vascular resistance and brachial artery compliance persisted after the 2-week washout period. This latter observation raises the possibility that enalapril may reverse structural changes in the large arteries.
Antihypertensive Agents↗
Contribution of the renin-angiotensin system and of the sympathetic nervous system to blood pressure homeostasis during chronic restriction of sodium intake.
In a previous paper, we showed that during a long-term, moderate restriction in sodium intake, sympathetic nervous system activity was only transiently stimulated, whereas a sustained rise of plasma renin activity occurred. However, the contribution from stimulation of the renin-angiotensin system in the maintenance of blood pressure homeostasis during a low-salt diet is still unclear. To investigate this issue, in eight normal subjects blood pressure, heart rate, plasma catecholamines, renin activity, and aldosterone were measured during normal sodium intake (150 mEq/d), after converting-enzyme inhibition (enalapril 20 mg/d po), and during one month of sodium intake restriction (50 mEq/d) associated with chronic inhibition of converting-enzyme (CEI). During a low-salt diet with CEI, plasma renin activity rose significantly as a result of CEI. In addition, even in the presence of a marked and sustained increase in plasma norepinephrine and in upright heart rate, a decrease in blood pressure was observed in all the measurements performed during the course of the study as compared to the control values. Our findings support the hypothesis that renin-angiotensin system activation plays an important role in the maintenance of blood pressure homeostasis during a low-salt diet. In fact, in the presence of an effective blockade of angiotensin II formation, blood pressure is decreased, despite the concurrent, sustained stimulation of the sympathetic nervous system.
Adolescent↗
Atrial natriuretic factor potentiates forearm reflex vasoconstriction induced by cardiopulmonary receptor deactivation in man.
Previous evidence suggests that atrial natriuretic factor (ANF) interferes with the autonomic control of circulation. In the present study we investigated whether ANF modulates forearm vasoconstriction reflexly induced by cardiopulmonary receptor unloading in man. For this purpose, the hemodynamic response to -20 mm Hg lower body negative pressure (LBNP) was assessed under control conditions and during the constant infusion of alpha-human ANF (0.5 micrograms/kg bolus followed by 0.05 micrograms/kg/min) in seven normal subjects. ANF infusion resulted in a slight reduction in blood pressure and right atrial pressure, did not modify heart rate or forearm vascular resistance, but significantly potentiated the reflex increase in forearm vascular resistance during LBNP (+25 +/- 9% under control conditions vs +40 +/- 12% during ANF, p less than .05). In an attempt to clarify the mechanisms underlying the enhanced reflex vasoconstriction during infusion of ANF, in five additional subjects we demonstrated that there was a comparable vascular reflex response to LBNP under control conditions and during nitroglycerin infusion at a dose that induced a reduction in atrial pressure comparable to that observed during ANF. Finally, in seven additional subjects we found that ANF infusion did not alter the reflex hemodynamic responses elicited by carotid baroreceptor unloading induced by a +60 mm Hg increase in external neck pressure. We conclude that during the infusion of a pharmacologic dose of ANF the reflex forearm vasoconstriction in response to selective cardiopulmonary receptor unloading is potentiated. This effect does not seem to be related to the hemodynamic actions of the peptide or to interference with the sympathetic control of peripheral circulation.
Adult↗
Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.
The effects of endogenous activation of sympathetic nervous system on systemic and regional hemodynamics and on plasma levels of atrial natriuretic factor (ANF) were studied in subjects with essential hypertension. Stimulation of sympathetic nervous system was reflex-induced by a selective deactivation of carotid baroreceptors obtained by increasing external neck-tissue pressure (NTP) by means of a neck chamber. The effects of graded levels (+30, +45, and +60 mm Hg) and one single and sustained level (+45 mm Hg for 15 min) of NTP were studied. As expected, NTP caused reflex increases in blood pressure, heart rate, and forearm vascular resistance, whereas atrial pressures did not change significantly and cardiac output tended to increase. In the studies based on graded levels of NTP, immunoreactive ANF (irANF) progressively fell (from 31.7 +/- 10 to 13.3 +/- 4 fmol/ml; p less than .05) and the changes in irANF were significantly correlated with those observed in FVR (r = -.671, p less than .001). Both hemodynamic and irANF changes were prevented by adrenergic blockade (phentolamine + propranolol). During +45 mm Hg NTP for 15 min, the levels of irANF fell both in the pulmonary artery and in the inferior vena cava. The irANF arteriovenous difference also fell during this maneuver. These data show that, in hypertensive patients, factors other than atrial wall tension may influence ANF release. They also show that endogenous sympathetic activation may reduce ANF release.
Atrial Natriuretic Factor↗
Hemodynamic responses to atrial natriuretic factor in nephrectomized rabbits: attenuation of the circulatory consequences of acute volume expansion.
We investigated the hemodynamic responses to three doses of atrial natriuretic factor [human atrial natriuretic factor-(99-126)] (ANF) in nephrectomized rabbits anesthetized with ketamine and acepromazine. The influence of the different doses of the peptide on the hemodynamic consequences produced by acute volume expansion (0.9% NaCl, 1.4 ml/kg/min for 60 minutes) was also studied. All three dosages of ANF (0.001, 0.01, and 0.2 micrograms/kg/min for 20 minutes) significantly reduced blood pressure. With the lowest dose, the hypotensive effect was associated with reduction in systemic vascular resistance and no significant change in heart rate, stroke volume, central venous pressure, and hematocrit. In contrast, the intermediate and high doses, which resulted in markedly higher plasma levels, caused a significant decrease in heart rate, central venous pressure, and stroke volume; a slight rise in hematocrit; and no change in systemic vascular resistance. Volume expansion produced by saline infusion in an additional group of nephrectomized rabbits increased central venous pressure and decreased hematocrit. When ANF infusion was associated to volume expansion, each dosage of ANF was able to reduce the rise in central venous pressure, while only the higher dosage attenuated the progressive fall in hematocrit caused by volume expansion. Plasma volume, measured at the end of volume expansion was lower in the group treated with the highest dose of ANF than in the control animals (28.2 +/- 9 vs. 35.1 +/- 3 ml/kg, p less than 0.05). We conclude that 1) ANF induces significant hemodynamic effects independently from its renal action.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Efficacy of once-daily urapidil treatment in mild or moderate essential hypertension assessed by ambulatory 24-hour blood pressure monitoring.
The blood pressure-lowering effect and tolerability of urapidil 120 mg once daily versus urapidil 60 mg twice daily was compared in 36 outpatients with newly diagnosed mild to moderate essential hypertension. Patients were enrolled in the study if they showed a favourable response to urapidil 60 mg twice daily at the end of a 2-week run-in as revealed by a first non-invasive 24-hour blood pressure profile. The patients were then randomly allocated to a 6-week double-blind treatment with either urapidil 120 mg once daily or urapidil 60 mg twice daily. Blood pressure, heart rate and adverse reactions were recorded every 2 weeks in the morning before drug intake. A second 24-hour blood pressure profile was taken at the end of this treatment phase. Compared with the pretreatment value after placebo run-in, urapidil 60 mg twice daily lowered supine morning blood pressure from 159/103 to 138/89. Urapidil 120 mg once daily lowered blood pressure from 161/102 to 139/90. The decrease in blood pressure was statistically significant within (p less than 0.001) but not between the treatment groups. Similar results were obtained with standing blood pressures. Side effects were observed in 2 patients with urapidil 60 mg twice daily (dizziness, intermittent lack of ejaculation) and in 7 patients with urapidil 120 mg once daily (5 with dizziness, and 1 each with headache and palpitations). Thus, urapidil 120 mg once daily lowers elevated blood pressure throughout a 24-hour period as effectively as 60 mg twice daily. Therefore, during long term therapy, the tolerability but not the efficacy of urapidil appears to be directly related to its peak serum concentrations.
Adult↗
Long-term reduction of peripheral resistance with celiprolol and effects on left ventricular mass.
The antihypertensive efficacy of a new beta-blocker, celiprolol, was compared with that of a well established antihypertensive drug, metoprolol. Systemic and forearm haemodynamic effects were investigated using echocardiography and two-dimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive patients completed the double-blind crossover randomized study. Each 6-week active treatment period was both preceded and followed by 2 weeks of placebo treatment such that the total duration of the study was 18 weeks. Despite comparable efficacy in reducing systolic and diastolic blood pressures by approximately 10% of the basal value, the two drugs differed in their systemic and haemodynamic effects. Celiprolol significantly decreased forearm peripheral resistance and total peripheral resistance. Cardiac output remained unchanged and forearm blood flow was increased. Metoprolol reduced cardiac output through a reduction in heart rate, but stroke volume was unaltered. Neither drug significantly modified cardiac performance, as evaluated by left ventricular circumferential fibre shortening and left ventricular ejection fraction. Differences in the systemic and regional haemodynamic effects of the two drugs could account for the different blood pressure response seen in some patients. There was no observable change in left ventricular wall thickness or left ventricular mass. These results confirm previous reports which demonstrate that antihypertensive treatment with beta-blockers does not reduce left ventricular mass in patients with a left ventricle of normal size. It is generally accepted, however, that the ability of beta-blockers to reverse left ventricular hypertrophy is unrelated to the individual pharmacological characteristics of each agent.
Adrenergic beta-Antagonists↗
Acute hemodynamic effects of atrial natriuretic peptide in essential hypertension.
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Adult↗
[Splenectomy: elective therapy in hereditary spherocytosis].
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Child↗
[Mechanisms of regulation of arterial blood pressure: role of the sympathetic nervous system and of the renin-angiotensin system in patients on a low-sodium diet].
In order to discover more about the role of the sympathetic nervous and renin-angiotensin systems in the preservation of homeostasis during chronic reductions of salt intake, blood pressure, blood catecholamines and renin activity were measured in a group of healthy subjects in normal conditions and on a salt-free diet combined with blockade of the conversion enzyme by enalapril. The results confirmed the hypothesis advanced on an earlier occasion i.e. that both hormone systems contribute to pressure during salt depletion in the initial phase, while over the long term only the renin-angiotensin system is activated though when this is inhibited, the sympathetic nervous system will take over its function.
Adolescent↗
Effects of celiprolol on systemic and forearm circulation in hypertensive patients: a double-blind cross-over study versus metoprolol.
The antihypertensive efficacy of a new beta-receptor blocking agent, celiprolol, was compared with that of a well-established antihypertensive drug, metoprolol. Their systemic and forearm hemodynamic effects were investigated using echocardiography and two-dimensional pulsed Doppler flowmetry, respectively. Twenty hypertensive patients completed a double-blind, cross-over, randomized study using celiprolol and metoprolol. Two six-week courses with celiprolol or metoprolol were preceded and followed by a two-week placebo period; the total duration of the study was 18 weeks. In spite of a comparable efficacy in reducing systolic and diastolic blood pressure (about 10% of the basal value), the two drugs showed quite different systemic and regional hemodynamic effects. Celiprolol induced a significant decrease in forearm vascular resistance (from 157 +/- 17 to 113 +/- 13 mm Hg/mL/s, P less than .01) and total peripheral resistance (from 1596 +/- 90 to 1398 +/- 91 dyne.s.cm-5, P less than .05) whereas cardiac output remained unchanged and forearm blood flow increased. Metoprolol reduced cardiac output (from 6.5 +/- 3 to 5.7 +/- 3 L/min, P less than .05), through a reduction in heart rate, since stroke volume was unchanged. Both drugs did not significantly modify cardiac performance, as evaluated by left ventricle fractional shortening and ejection fraction. Thus, the two drugs seem to reduce blood pressure through different hemodynamic mechanisms.
Adrenergic beta-Antagonists↗
Beta blockers and left ventricular hypertrophy in hypertension.
It is now generally accepted that hypertension-induced left ventricular hypertrophy (LVH) represents a phenomenon of multifactorial origin. Antihypertensive therapy with beta-blocking drugs influences most of the factors involved in the control of left ventricular mass. Therefore, although initial animal experiments yielded conflicting results, it is not surprising that a great deal of evidence has been accumulated in clinical studies showing that successful long-term antihypertensive treatment with beta blockers induces regression of LVH in hypertensive subjects. Differences in molecular structure among various beta-blocking agents do not seem to influence this property. On the contrary, the question of whether reversal of LVH represents a beneficial or harmful byproduct of antihypertensive treatment with beta blockers is still unanswered. Animal and clinical studies suggest that left ventricular systolic function is unchanged or even improved after regression of LVH, whereas the ability of the heart to withstand recurrence of hypertension is slightly reduced. Furthermore, development of LVH in hypertensive subjects is associated with abnormalities in diastolic function which are not reduced by reversal of LVH induced by antihypertensive treatment with beta blockers.
Adrenergic beta-Antagonists↗