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Biomedical subjects

A Morganti

Publications and source records attributed to A Morganti.

At least 19 recordsLinked to original sources
PubMed1992

Whole liver intraoperative irradiation after partial hepatectomy produces minimal functional and pathologic lesions.

Intraoperative radiation therapy (IORT) was delivered to remnant rat liver after partial hepatectomy to determine the chronic effects of treatment on survival, blood chemistry, liver weight, and histology. Survival at one year was 100%. Remnant liver weight was markedly increased in all animals. Liver function appeared to be unaltered in all groups and at all observation times. Inflammatory cell infiltration occurred immediately after treatment in all animals, showing a slight progression until day 45; by day 180 the values had returned to baseline. Vascular changes were seen early in all groups, then progressively decreased; the vascular score was back to baseline at days 180 and 365. Nuclear alterations were observed in both irradiated and nonirradiated hepatic cells; in all cases these were limited to isolated or focal areas of hepatocytes. There was little fibrosis formation and by day 180 all scores were back to baseline. We conclude that the chronic effects of whole liver IORT after one-third hepatectomy are minimal in the rat and are similar to those observed after surgery alone.

Animals↗
PubMed1992

Sympathomoderating influence of benazepril in essential hypertension.

OBJECTIVE: In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors. METHODS AND DESIGN: Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design. RESULTS: After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR. CONCLUSIONS: Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.

BACKGROUND: In humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however. METHODS AND RESULTS: In nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPT caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7 +/- 3.2%, p less than 0.01), CBF did not change and CVR increased (+12.2 +/- 4.0%, p less than 0.05). diving caused an increase in mean arterial pressure and a reduction in heart rate. RPP increased (+14.3 +/- 3.5%, p less than 0.01), but despite this increase, there was a reduction in CBF and a marked increase in CVR (+37.3 +/- 7.4%, p less than 0.01). Captopril did not modify the blood pressure and heart rate responses to both stimuli except for a slight accentuation of the bradycardia to diving. Despite the unchanged or only slightly reduced RPP response, the increase in CVR was markedly and significantly attenuated (p less than 0.01). CONCLUSIONS: ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone.

Angiotensin II↗
PubMed1992

Acute effects of cilazapril on coronary hemodynamics in patients with renovascular hypertension.

The effects of converting enzyme inhibition on coronary and systemic hemodynamics in the presence of a chronically activated renin-angiotensin system were investigated in five renovascular hypertensive patients with no ECG/echocardiographic evidence of left ventricular hypertrophy. Coronary blood flow (CBF, thermodilution technique), intra-arterial blood pressure, AVO2 difference (coronary sinus), heart rate, and coronary vascular resistance were measured at rest, during isometric exercise (handgrip to 50% of maximal effort for 3 min) before and 60 min after 2.5 mg of oral cilazapril. The drug induced a prompt, significant decrease in mean arterial pressure and a sustained increase in CBF. The performance of handgrip after cilazapril resulted in higher increases in CBF for a given increase in myocardial oxygen requirements. These observations suggest that angiotensin II (Ang II) maintains the ability to alter the control mechanisms of CBF even under long-term conditions and that converting enzyme inhibition reverses the Ang II-induced effects on coronary hemodynamics.

Adult↗
PubMed1991

Regulation of vasopressin release in moderately severe essential hypertension.

Vasopressin plasma concentrations have been measured in two groups of subjects, 13 moderate essential hypertensive patients without target organ damage and eight control normotensive subjects, before and after the assumption of the upright position, and intravenous infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h) and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in recumbent baseline conditions was not significantly different in the two groups. Upright posture and hypertonic challenge augmented, while hypotonic saline reduced plasma vasopressin levels, which were not significantly different between the two groups. Plasma renin activity increased in the upright position, was reduced by administration of hypotonic saline and unaffected by hypertonic saline, with no differences between the hypertensives and normotensives. After hypertonic saline, urinary flow rate and urinary sodium excretion in the hypertensive group increased to values significantly (p less than 0.05) higher than in normotensive subjects. In conclusion our study excludes significant alteration of vasopressin regulation in moderate uncomplicated hypertension. In hypertensives although the response of vasopressin to an osmotic load is preserved, the data suggest that the renal handling of the osmotic load may be altered.

Adult↗
PubMed1991

Plasma active and inactive renin and fetal complications in women with high risk pregnancies.

To examine whether the activation of the renin system, which occurs during pregnancy, may be relevant for the development and the outcome of the fetus, we measured active and inactive renin throughout gestation in 29 women having a pregnancy defined as "high risk" because of a clinical history of hypertension, nephropathy, and unexplained abortions. In 23 of these women who delivered full-term infants with normal weight and status, we found that active renin increased progressively from early pregnancy until the end of the second trimester and then declined slightly thereafter. In contrast, in the remaining six women who had fetal complications consisting of either signs of distress requiring cesarean section or growth retardation, the increase in active renin failed to occur. In all women the levels of inactive renin were more elevated throughout gestation than those observed in nonpregnant women, and were higher, although not significantly, in women without fetal complications than in those with fetal complications. Thus, a blunted activation of the renin system during pregnancy is associated with alteration in fetal development and may possibly contribute to it.

Adult↗
PubMed1990

Renal and humoral effects of ibopamine, a dopamine agonist, in patients with liver cirrhosis.

We investigated the renal and humoral effects of short-term administration of ibopamine, an orally active dopamine agonist, in patients with liver cirrhosis. The patients were divided into two groups on the basis of sodium excretion with a constant sodium intake of 40 mEq/d. We also compared the effects of ibopamine with those induced by intravenous infusion of dopamine hydrochloride (3 micrograms/kg per minute) in similar patients. Ibopamine caused significant increases in urine output, glomerular filtration rate, and sodium excretion throughout the 4 hours of the trial in patients with basal sodium excretion rate greater than 20 mmol/d. These renal effects were associated with a significant reduction in plasma aldosterone concentration. In contrast, only a transient increase in glomerular filtration rate and a diminution in plasma aldosterone concentration were observed after ibopamine in the patients with a basal sodium excretion rate less than 20 mmol/d. The infusion of dopamine had renal effects similar to those of ibopamine in both groups of patients. These results indicate that in cirrhotic patients with normal sodium excretion, ibopamine exerts a diuretic and natriuretic effect similar to that of dopamine infusion. However, these properties of dopaminergic agents are apparently lost in patients with avid sodium retention.

Adult↗
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

Time-course of the changes in blood pressure and in plasma renin activity during the first week after dilation of renal artery stenosis.

We measured arterial pressure and plasma renin activity throughout the first week after a technically successful percutaneous transluminal renal angioplasty (PTRA) in 12 patients with hypertension and unilateral renal artery stenosis. Mean arterial pressure fell from 126 +/- 4 to 105 +/- 3 mmHg within 1-2 days of PTRA and stabilized thereafter; in addition, plasma renin activity decreased sharply during the first 2 days after the angioplasty (from 5.2 +/- 2.3 to 1.3 +/- 0.3 ng/ml per h) but continued to decline, reaching 0.8 +/- 0.2 ng/ml per h at the end of the study. When the antihypertensive effect of PTRA was examined in relation to baseline values of plasma renin activity, the patients with low, intermediate and high plasma renin activity showed percentage decreases in mean arterial pressure of, respectively, 6%, 16% and 19% by the sixth day of observation after the angioplasty. No overall correlation was found between the changes in arterial pressure and those in plasma renin activity induced by PTRA. These data suggest that the beneficial effect of PTRA on blood pressure can be estimated within a few days and that the reduction in the activity of the renin system is the principal but not the sole mechanism responsible for it.

Adult↗
PubMed1989

Reciprocal changes in atrial natriuretic factor and aldosterone during angiotensin converting enzyme inhibition in man.

To investigate whether aldosterone responses to angiotensin converting enzyme (ACE) inhibition are affected by changes in atrial natriuretic factor, which is known to inhibit aldosterone secretion, we measured blood pressure, plasma renin activity, aldosterone, atrial natriuretic factor and plasma potassium before and after 1 week of treatment with fosenopril, a long-acting ACE inhibitor, in eight normotensive subjects. Fosenopril caused a slight fall in blood pressure and increased plasma renin activity in all subjects. In contrast, aldosterone and atrial natriuretic factor were, on average, unchanged. However, for both these hormones a wide range of individual responses was observed (aldosterone from -254 to +240 pmol/l, atrial natriuretic factor from +9.7 to -16.6 pmol/l) and a significant inverse correlation was found between the changes in aldosterone and those in atrial natriuretic factor (r = -0.73, P less than 0.05). Plasma potassium was unchanged after the fosenopril treatment. These findings suggest an inter-relationship between atrial natriuretic factor and the aldosterone responses to short-term treatment with an ACE inhibitor.

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↗
PubMed1988

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↗
PubMed1988

Dopaminergic control of aldosterone secretion is not mediated by atrial natriuretic factor in patients with essential hypertension.

Both dopamine and atrial natriuretic factor (ANF) are known to suppress aldosterone secretion. Since it is possible that dopaminergic mechanisms facilitate ANF release, we investigated the relationship between these two inhibitory systems by comparing the increases in aldosterone induced by metoclopramide, a dopaminergic antagonist, with decreases in ANF. Aldosterone, ANF, prolactin, plasma renin activity, cortisol and potassium were measured before and after the intravenous injection of 10 mg metoclopramide, blood samples being collected at 15-min intervals up to 2 h after the injection. These studies were performed in patients with essential hypertension who were maintained on a constant sodium intake (100 mmol/day), before and after 5 days of treatment with ibopamine, an orally active dopamine analogue. Before ibopamine metoclopramide induced the expected, marked increases in aldosterone and in prolactin, but only minimal, non-significant decreases in ANF. All other humoral parameters, as well as blood pressure and heart rate, were unaffected by metoclopramide. After ibopamine treatment, which caused a transient natriuretic effect, the responses of aldosterone and of ANF to metoclopramide were similar to those observed in control studies, whereas that of prolactin was enhanced. Thus, it appears that the suppressive effect exerted by the dopaminergic tone on aldosterone secretion is independent of ANF both before and after dopaminergic stimulation.

Aldosterone↗
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↗