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Biomedical subjects

G Lembo

Publications and source records attributed to G Lembo.

At least 73 records · Page 4Linked to original sources
PubMed1991

[131I-meta-iodobenzylguanidine scintigraphy in patients with a suspected pheochromocytoma. A comparison with CT and biohumoral parameters].

The results of 131I metaiodobenzylguanidine (MIBG) and Computed Tomography (CT) scans in a group of patients with clinically suspected pheochromocytoma were evaluated and compared with biohumoral parameters. We studied 24 consecutive patients (7 M and 17 F; age range 20-66 years). 131I-MIBG scintigraphy and CT were in agreement in 19 patients (79%): of them 7 cases were true positive, and 12 were true negative. Disagreement between the two imaging techniques was observed in 5 patients (21%). In this group, one patient, with positive CT scan, had false negative MIBG study, while 4 patients with negative MIBG scan, had false positive CT. MIBG showed significantly higher (p less than 0.05) specificity (100%), positive predictive value (100%), and accuracy (96%) than CT (75%, 67%, and 83%, respectively). 131I-MIBG scintigraphy is an accurate, noninvasive technique for localizing pheochromocytoma and providing direct tissue characterization, while CT provides more accurate spatial information. In conclusion, CT and MIBG studies are complementary in the evaluation of patients with suspected pheochromocytoma.

3-Iodobenzylguanidine↗
PubMed1991

[The early hemodynamic and hormonal changes in patients with left ventricular dysfunction].

The aim of this study was to highlight a different hormonal and hemodynamic pattern in patients with mild cardiomyopathy. For this purpose, we studied subjects with mild heart failure (CHF; NYHA class I and II; post-ischemic and idiopathic) who underwent an isotonic saline load (SL) (0.22 ml/kg/min of 0.9% NaCl for 120 min). A second group of age- and sex-matched normal subjects (C) was studied as a control. Basal hormonal and hemodynamic values of the 2 groups differed only in atrial natriuretic factor (ANF), left ventricular end-diastolic diameter and ejection fraction (EF). There were, on the contrary, no differences in basal plasma renin activity (PRA) and plasma aldosterone (PA) values. After SL, in C, percent changes in EF, cardiac output and ANF values were significantly higher than in CHF while total peripheral resistances increased only in CHF but not in C. In both groups there were decrements of PRA and PA, but these responses were significantly higher in C than in CHF. In conclusion, our results show that hormonal, renal and hemodynamic responses to salt/volume load are compromised in the early asymptomatic phase of heart failure. These abnormalities may predict the progressive deterioration of cardiac function, and may indicate appropriate therapeutic interventions since the early phases of the disease.

Aldosterone↗
PubMed1991

[The effects of atrial natriuretic peptide on left ventricular function in subjects with heart failure].

The effects of atrial natriuretic peptide (ANP) infusion was evaluated in 11 patients with congestive heart failure undergoing cardiac catheterization. Data were obtained at rest and during steady-state phase of alpha-human (1-28) ANP infusion (1 microgram/kg bolus dose, 0.1 microgram/kg/min iv for 30 min). Mean blood pressure decreased from 104 +/- 20 to 89 +/- 21 mmHg (p less than 0.05) 15 min after ANP infusion, as well as left ventricular end-diastolic pressure (from 27 +/- 6 to 14 +/- 11 mmHg, p less than 0.05) and wedge pressure (from 22 +/- 5 to 13 +/- 7 mmHg, p less than 0.05). Left ventricular ejection fraction increased significantly after ANP infusion from 39 +/- 7 to 47 +/- 2%, p less than 0.01. The ANP infusion significantly increased cardiac output from 4.9 +/- 0.8 to 5.8 +/- 1.41/min, p less than 0.05, and decreased the relaxation constant from 69 +/- 17 to 48 +/- 18, p less than 0.05. These results demonstrate that in patients with congestive heart failure ANP infusion decreased wedge pulmonary pressure, left ventricular end-diastolic pressure and increased cardiac output and left ventricular ejection fraction.

Adult↗
PubMed1990

The use of laboratory methods in contact dermatitis induced by composite materials.

Thin-layer chromatography, column chromatography, mass spectrometry and nuclear magnetic resonance were used to investigate the chemical constituents and haptens responsible in 2 different circumstances where allergic contact dermatitis from composite materials was suspected. In an aircraft factory where epoxy resins were used, tetraglycidyl-4,4'-dimethyl dianiline and phenylglycidyl ether were identified as the haptens responsible for an outbreak of contact dermatitis. The role of abietic acid as the main sensitizer in colophony was confirmed in a case of contact dermatitis occurring in a sportsman with an acute eczematous reaction due to a leg bandage. Identification of the chemical sensitizers was possible only by using the aforementioned laboratory methods.

Adolescent↗
PubMed1990

Prolonged duration of myocardial ischemia in patients with coronary heart disease and impaired cardiopulmonary baroreceptor sensitivity.

To investigate the potential contribution of cardiopulmonary reflexes in myocardial ischemia, the coronary vascular response to cardiopulmonary baroreceptor unloading and the number and the duration of spontaneous episodes of symptomatic and asymptomatic myocardial ischemia were evaluated in 23 patients with coronary heart disease. Lower-body negative pressure at -10 mm Hg, which causes selective deactivation of cardiopulmonary receptors, reduced left ventricular filling pressure in all patients, but calculated coronary vascular resistance increased in only 14 patients (from 0.846 +/- 0.1 to 1.07 +/- 0.1 mm Hg/ml/min, p less than 0.01) (group 1). In the remaining nine patients, coronary resistance did not change during cardiopulmonary receptor unloading (group 2). A 60-mm Hg increase in neck tissue pressure, which induces arterial baroreflex-mediated sympathetic activation, caused comparable coronary vasoconstriction in the two groups. Clinical characteristics of the two groups were similar, except that a lower ejection fraction was measured in group 1 (45 +/- 2% vs. 56 +/- 1%, p less than 0.01). In the 14 patients in group 1, 24-hour electrocardiographic monitoring showed 151 episodes of myocardial ischemia (average individual value, 10.8 +/- 1), 137 of which were asymptomatic, with an individual daily ischemic period of 62 +/- 6 minutes. In contrast, the nine patients in group 2 had only symptomatic episodes of myocardial ischemia, and the daily ischemic period in these patients was longer than in patients of group 1 (104 +/- 10 minutes, p less than 0.01). After a 3-day treatment with digitalis, the patients of group 2 showed 38 asymptomatic episodes of myocardial ischemia and a shorter daily ischemic period (85 +/- 6 minutes, p less than 0.01 vs. control conditions). In contrast, no change in number and duration of the ischemic episodes was detected in group 1. The effects of acute administration of digitalis (Lanatoside-C 0.02 mg/kg body wt e.v.) on the coronary vascular response to cardiopulmonary receptor unloading were assessed in a separate group of patients with ischemic heart disease. Digitalis treatment did not significantly modify the magnitude of the coronary vascular response induced by -10 mm Hg lower-body negative pressure in the patients showing in control conditions an increase of coronary vascular resistance greater than 20% of the basal value during cardiopulmonary receptor unloading. On the contrary, digitalis potentiated the coronary reflex response to -10 mm Hg lower-body negative pressure in the patients with impaired cardiopulmonary responsiveness (delta percent increase in coronary vascular resistance: 1 +/- 1% in control conditions; 23 +/- 3.9% after digitalis, p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary Angiography↗
PubMed1990

Converting enzyme inhibition prevents the effects of atrial natriuretic factor on baroreflex responses in humans.

The aim of this study was to assess the influence of atrial natriuretic factor (ANF) on arterial baroreflex chronotropic responses and to investigate whether this effect of ANF is affected by angiotensin converting enzyme inhibition (CEI). For this purpose, in 13 normal volunteers, the reflex chronotropic responses to arterial baroreceptor stimulation (phenylephrine, 25-100 micrograms i.v.) or deactivation (nitroglycerin, 25-100 micrograms i.v.) were evaluated in control conditions and during the steady-state phase of a sustained infusion of ANF (50 ng/kg/min) or placebo, before and during prolonged treatment with the converting enzyme inhibitor enalapril (20 mg p.o. for 5 days). ANF infusion, which raised plasma ANF levels from 48 +/- 19 to 1,765 +/- 203 pg/ml, was associated with a slight decrease in systemic blood pressure and no change in heart rate. In addition, it caused a significant increase of the regression slope obtained with phenylephrine (from 11.3 +/- 2 to 18.5 +/- 2 msec/mm Hg) and a significant reduction of slope of the nitroglycerin-produced regression line (from 9.3 +/- 1 to 5.6 +/- 0.6 msec/mm Hg). After sustained CEI, which raised plasma renin activity from 1.4 +/- 0.4 to 19.9 +/- 5 ng/ml/hr, ANF infusion induced an increase in plasma ANF levels and a reduction in blood pressure comparable to those observed in control conditions. During CEI, however, ANF infusion had no significant effect on the chronotropic baroreflex responses produced by phenylephrine or nitroglycerin. Chronotropic and pressor responses to cold exposure were unchanged after CEI and during ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Coronary effects of left ventricular hypertrophy associated with hypertension].

Left ventricular hypertrophy secondary to hypertension has been associated with a reduction of maximum coronary flow per unit mass as shown by the increase in the minimal threshold of coronary vascular resistance per gramme. This phenomenon has usually been attributed to an increase in muscle mass with absent or inadequate vascular compensation. However, chronic hypertension may induce a function reduction in coronary flow. In particular, it has been recently shown that coronary vascular resistances are influenced by a cardio-cardiac reflex involving the baroreceptor response. Left ventricular hypertrophy could alter the function of the ventricular receptors and favourise myocardial ischemia by preventing the adaptation of coronary flow to myocardial metabolic demands.

Cardiomegaly↗
PubMed1990

[Hormonal control of the endocrine function of the heart].

Previous studies demonstrate that high doses of angiotensin II (Ang II) increase the release of ANF from atrial cells but it is not known whether this is a direct effect of Ang II or due to the induced hemodynamic changes. We report the effects of low doses of Ang II (1, 2.5, 5, 10 ng/kg/min) in anesthetized, instrumented dogs after volume load (2.5% body weight) and converting enzyme inhibition. During Ang II infusion we found an increase in mean blood pressure (from 147 +/- 3 to 160 +/- 3 mmHg, p less than 0.05) and arterial ANF (from 32 +/- 6 to 80 +/- 23 fmol/ml, p less than 0.05), while left and right atrial pressures did not change significantly. In a second group of dogs (n = 4) that underwent a similar protocol with the infusion of vehicle alone we failed to find any statistical difference in the above mentioned parameters. The Ang II induced ANF release was not related to the hemodynamic changes. Changes in plasma ANF levels were, in turn, related to the effects of Ang II on hormones and kidney, thus suggesting a role for endogenous ANF. In a separate study we found an increase of ANF production (+129 +/- 18, +176 +/- 46, +210 +/- 66% basal value) from isolated atrial minces exposed to Ang II concentration of 1, 10, and 100 nM, respectively.

Aldosterone↗
PubMed1989

Cardiac effects of atrial natriuretic peptide in subjects with normal left ventricular function.

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization that did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 micrograms/kg bolus, 0.05 micrograms/kg/min intravenously for 10 minutes). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mm Hg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The ANP infusion reduced LV end-diastolic and end-systolic volume indexes from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. The LV ejection fraction increased insignificantly from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant increase (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) increased to 1,890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma ANP concentrations. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

Adult↗
PubMed1989

Influence of volume expansion on hemodynamic effects of atrial natriuretic factor in rabbits.

We investigated the influence of acute volume expansion on the hemodynamic and renal responses to the constant infusion of atrial natriuretic factor (ANF) (alpha-human ANP, 2 micrograms/kg bolus, 0.2 microgram.kg-1.min-1) in rabbits anesthetized with ketamine and acepromazine. The effects of the peptide were evaluated in 12 euvolemic rabbits and in 15 rabbits during the steady-state phase of volume expansion (0.9% NaCl 4.5 ml/min for 60 min). In the euvolemic animals, ANF caused an increase in natriuresis and a reduction in blood pressure (BP), which was associated with a decrease in cardiac output (CO), stroke volume (SV), and no significant changes in central venous pressure (CVP), peripheral hematocrit (Hct), and heart rate (HR). When the peptide was infused in the volume-expanded animals, the effects of ANF on BP and HR were comparable with those observed in the euvolemic animals. However, in these animals the ANF-induced changes in CO, SV, CVP, and Hct were significantly greater than those observed in the euvolemic group. In addition, the percent increases in diuresis and natriuresis were significantly smaller than those obtained in the euvolemic animals. In conclusion, volume expansion with saline potentiates the effects of ANF on systemic hemodynamics and blood volume.

Animals↗
PubMed1989

Blunted sympathetic response to cardiopulmonary receptor unloading in hypertensive patients with left ventricular hypertrophy. A possible compensatory role of atrial natriuretic factor.

To investigate whether or not hypertension with left ventricular hypertrophy (LVH) modifies the mechanisms underlying the vascular adjustments to orthostatic stress, we evaluated the hemodynamic and hormonal effects of graded lower-body negative pressure (LBNP) (-10 and -40 mm Hg) before and after sympathetic blockade in 10 hypertensive patients with LVH and in five age- and sex-matched normotensive subjects. In control conditions, LBNP elicited comparable vasoconstrictor responses in the forearm in the two groups. In normotensive subjects, graded increases in plasma norepinephrine and plasma renin activity (PRA) and reductions in plasma immunoreactive atrial natriuretic factor (irANF) were recorded. In hypertensive patients, a significant increase in plasma norepinephrine and plasma renin activity was obtained only with the higher level of LBNP, whereas irANF plasma levels decreased progressively. In both groups, sympathetic blockade abolished the increase in plasma renin activity and did not modify the changes in plasma irANF induced by both levels of LBNP in control conditions. The vascular response to -10 mm Hg LBNP remained unchanged after sympathetic blockade in both groups. However, after sympathetic blockade, the vasoconstrictor response to -40 mm Hg LBNP in normal subjects was no longer different from that elicited by -10 mm Hg LBNP, whereas in hypertensive patients the vasoconstrictor response was still significantly higher than that induced by -10 mm Hg LBNP. Direct correlations between the percent changes in forearm vascular resistance and those in plasma norepinephrine and plasma renin activity were found only in normal subjects in control conditions but were not observed after sympathetic blockade. On the contrary, the inverse correlation between changes in irANF plasma levels and in forearm vascular resistance found in control conditions in both groups was still observed after sympathetic blockade. In a separate group of hypertensive patients with left ventricular hypertrophy, exogenous infusion of ANF induced an increase in venous irANF plasma levels of the same magnitude of the decrease evoked by LBNP and significantly reduced forearm vascular resistance. These data show that in hypertensive patients with left ventricular hypertrophy, sympathetic activation does not contribute to the vascular response to cardiopulmonary receptor unloading (-10 mm Hg LBNP). They also suggest that in these patients inhibition of ANF secretion may play a role in the response to a low level of LBNP so that the peripheral vasoconstriction induced by cardiopulmonary receptor unloading is comparable to that observed in normal subjects despite the lack of appropriate sympathetic reflex vasoconstriction.

Adaptation, Physiological↗