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Biomedical subjects

C Fiorentini

Publications and source records attributed to C Fiorentini.

At least 127 records · Page 7Linked to original sources
PubMed1990

Cardiac tamponade produced by a loculated pericardial hematoma simulating a right atrial mass.

We report a case of cardiac tamponade due to thrombosis of a loculated pericardial effusion which occurred after open heart surgery. The loculated hematoma was highly echogenic and mimicked a right atrial mass. Cross-sectional echocardiography, in association with color Doppler flow imaging, was extremely useful in identifying this rare complication of cardiac surgery and, therefore, in determining the subsequent surgical approach.

Cardiac Surgical Procedures↗
PubMed1990

Hemodynamic and renin responses to nifedipine in renovascular hypertension.

We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that "ischemic lateralization" could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 mm Hg to an average of 113 +/- 11 mm Hg), a 44% reduction of systemic vascular resistance (from 2162 +/- 540 dynes.sec.cm-5 to to 1205 +/- 279 dynes.sec.cm-5), a 33% rise in cardiac index (from 2920 +/- 970 ml/min/m2 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Interaction of Clostridium difficile toxin A with cultured cells: cytoskeletal changes and nuclear polarization.

Experiments done on in vitro-cultured cells exposed to toxin A from C. difficile showed a series of cytopathologic changes leading to cell retraction and rounding accompanied by the marginalization of the nucleus, which localized at one pole of the cell. Cytoskeleton appeared to be strongly involved in such modifications. In particular, the microfilament system seemed to be involved in cell retraction, while microtubule network integrity and function seemed to be necessary for the nuclear displacement. The carboxylic ionophore monensin completely blocked the cytopathic effect when added with the toxin. The serine protease inhibitor chymostatin appeared to be protective also upon addition long after the end of the binding step. The Ca2(+)-dependent cytosolic protease inhibitors antipain and leupeptin were uneffective in protecting cells. Thus, our results suggest the involvement of an acidic compartment and the action of a serine protease in toxin A-induced cytopathic effect.

Animals↗
PubMed1989

Effects of Clostridium difficile toxins A and B on cytoskeleton organization in HEp-2 cells: a comparative morphological study.

A comparative study on the effects of toxin A and toxin B from Clostridium difficile on HEp-2 cells was carried out. Both toxins caused cell retraction and rounding and seemed to exert their effect on cell morphology via a rearrangement of actin and alpha-actinin microfilaments. Such a rearrangement occurred at an early stage, when no change in microtubular and cytokeratin systems was detectable. Nevertheless, several structural modifications accompanying the cytopathological process induced by toxins A and B appeared to be quite different. In particular, toxin B-treated cells showed an arborized phenotype as a result of cell retraction and rounding, whereas toxin A caused cell rounding without arborization. Moreover, nuclear polarization following disorganization of the microfilament system was only observed in toxin A-treated cells. The structural features distinguishing intoxication processes induced by the two toxins probably reflect a different mechanism of action and suggest the presence of a distinct subcellular component as a primary target for each toxin.

Bacterial Proteins↗
PubMed1989

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure.

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Adult↗
PubMed1989

Enhanced hypoxic pulmonary vasoconstriction in hypertension.

In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.

Adrenergic alpha-Antagonists↗
PubMed1989

Accessory thyroid tissue in the right ventricle.

In an asymptomatic 66-year-old woman presenting a systolic murmur in the pulmonic area, echocardiography evidenced a voluminous mass in the right ventricular outflow tract resembling a cardiac tumor. Histologic finding was that of aberrant normal thyroid. Although the occurrence of ectopic thyroid tissue in the heart is rare, it should be considered in the differential diagnosis whenever a mass is located at the level of the interventricular septum and encroaches on the right ventricular outflow tract. In these cases, a thyroid scintiscan may avoid an unnecessary surgical intervention.

Aged↗
PubMed1989

[Multicenter, double-blind study comparing rilmenidine 1 mg and hydrochlorothiazide 25 mg in 244 patients].

The efficacy and acceptability of Rilmenidine (RIL) were assessed in a multicentre, controlled, double-blind trial versus hydrochlorothiazide (HCZ) in patients with mild to moderate hypertension. After an initial 4 week washout period on placebo, patients with diastolic BP of between 90 and 110 mmHg were administered in monotherapy either RIL 1 mg or HCZ 25 mg for four weeks (Day 0-Day 28). In the following four weeks (Day 28-Day 56), those with diastolic BP of over 90 mmHg were given, in association, the antihypertensive agent that they had not received initially. The other patients continued the trial with single daily doses of monotherapy. Two hundred and fourty four patients (48.4 +/- 0.6 years) with supine systolic and diastolic BP of 155.86 +/- 0.96 mmHg and 101.02 +/- 0.28 mmHg respectively were randomly allocated to two comparable treatment groups (RIL, n = 120 and HCZ, n = 124). The systolic and diastolic BP decreased significantly between Day 0 and Day 28, as much at Day 14 as at Day 28 in both treatment groups. The antihypertensive effect was comparable: at Day 28 the mean fall in systolic/diastolic BP was 16/10 mmHg in the RIL group and 15/9 mmHg in the HCZ group (NS). The clinical acceptability was equivalent in the two groups: secondary effects were responsible for one patient's withdrawal in each group and their incidence was 5% on average, 10% for the most common.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

[Circulatory and renin response to the administration of nifedipine in renovascular hypertension].

In 12 severe (diastolic values averaging 114 mmHg) hypertensives with unilateral renal artery stenosis (angiography) and hyperreninemia, we investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics. Plasma renin activity was determined on blood samples withdrawn from the aorta and both renal veins, so that "ischemic lateralization" could be evaluated through appropriated derived indexes. Nifedipine promptly and significantly lowered the aortic pressure in all patients. At 30 min maximal circulatory responses were recorded, which consisted of 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 to an average of 113 +/- 11 mm Hg), 44% reduction of systemic vascular resistance (from 2162 +/- 540 to 1205 +/- 279 dynes.S.cm-5), 33% rise of cardiac index (from 2920 +/- 970 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 min continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in primary hypertensives with similar levels of blood pressure. After nifedipine, renin activity of the systemic blood significantly rose, due to a potentiated release from the kidney with arterial stenosis. This effect, that was interfered as a due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all of cases. It is suggested that nifedipine may not only be regarded as an additional diagnostic tool, but also as an effective antihypertensive agent in this disorder, al least in the short term. This contrasts with the previous suggestion of nifedipine as substantially more effective in low-renin rather than high-renin hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Anomalies of diastolic filling common to both ventricular cavities in hypertension].

In a population of 43 primary hypertensive patients we investigated the mitral and tricuspid valve flow in order to test whether: a) hypertension, as compared to normotension (Group 0, 10 normotensive subjects), alters the ventricular filling; b) changes are shared by the left and the right side of the heart; c) the structural characteristics (ultrasounds) of the left ventricle (LV) correlate with these changes. Hypertensives were divided into: Group 1, 11 patients in whom thickness (th) of both the ventricular septum (VS) and LV posterior wall (PW) was within a normal range (mean +/- 1 SD of values derived from 145 normal subjects); Group 2, 8 patients whose VSth exceeded normal values by more than 1 SD; Group 3, 24 patients in whom both VSth and PWth exceeded normal values by more than 1 SD. Groups 0, 1, 2 and 3 were homogeneous regarding gender, age, heart rate, LV cavity dimensions and systolic function. Blood pressure was slightly increased from Group 1 to Group 2 to Group 3. Mitral peak flow velocity in early diastole (PFVE) was similar in the 4 groups; in late diastole peak flow velocity (PFVA) through the same valve in each of the 3 hypertensive groups was significantly higher than in Group 0; as a consequence, PFVE/PFVA and E'/A' areas in hypertensives were significantly smaller than in normotensives. The flow pattern through the tricuspid valve was quite similar to this in each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Combined hemodynamic overload of the left and right ventricles as a possible cause of interventricular septum preponderance in high blood pressure.

We tested whether overload of the two ventricles may be associated with a preponderance of interventricular septum in patients with high blood pressure. The rationale is that the septum is shared by the greater and lesser circulation and that in hypertension the latter shows the same qualitative hemodynamic alterations as the former. Among 65 hypertensive patients, 40 (group 1) showed (echo) posterior wall thickness within the mean +/- 1 SD of 62 normal subjects, and 25 (group 2) had a posterior wall thickness exceeding the mean + 1 SD of the normal population. Both groups were subdivided into subgroups A and B, which included patients whose ventricular septum was similar to (within the mean + 1 SD) and thicker than (exceeding the mean + 1 SD) the posterior wall thickness in the corresponding group, respectively. Resting differences in systemic and pulmonary pressure and vascular resistance among subgroups 1A, 1B, and 2A were not significant; however, in subgroup 2B these variables exceeded those in the other subgroups to a significant extent. During cold pressor testing (CPT) the levels reached and the changes in pressure and resistance from baseline values in both circuits were much greater in subgroups B than in subgroups A. The baseline plasma norepinephrine value showed a trend toward an increase from subgroup 1A to 1B and from subgroup 2A and 2B; during CPT norepinephrine invariably changed and in subgroups B it rose significantly more than in subgroups A. It was not determined whether this caused the hemodynamic overload in subgroups B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cytoskeletal changes induced in HEp-2 cells by the cytotoxic necrotizing factor of Escherichia coli.

The effect of the cytotoxic necrotizing factor of Escherichia coli on HEp-2 cells was studied by fluorescence and scanning electron microscopy. This cytotoxin, known for inducing the formation of giant multinucleated cells in several cell lines, caused changes in actin and tubulin organization. The presence of membrane ruffles at the cell border and of numerous thick bundles of actin crossing the cell body, suggests that the factor promotes cell spreading; this probably interferes with cytokinesis, ultimately leading to the formation of very large flattened multinucleated cells. Moreover, the nuclear segmentation observed in treated cells seems to be associated with a rearrangement of actin in the perinuclear region and with the presence of tubulin bundles in proximity to nuclear clefts. Although the primary target is still unknown, these findings suggest that the cytoskeleton is affected accounting for the multinucleation process induced by the factor.

Bacterial Toxins↗
PubMed1988

Left ventricular systolic function in relation to withdrawal of different pharmacological treatments in hypertensives with left ventricular hypertrophy.

We evaluated the left ventricular mass index (LVMI) and the functional response to cold pressor and handgrip tests in 74 untreated essential hypertensive patients and 26 age and sex-matched normals. The same measurements were repeated in 22 essential hypertensives after 6 and 12 months of treatment (captopril or nitrendipine, plus diuretic or beta-blocker in a few cases) and in 21 essential hypertensives after withdrawal of treatment, a reduction in the LVMI and a further increase in blood pressure. Left ventricular systolic function was evaluated by the relationship between left ventricular end-systolic stress and fractional shortening. Highly significant negative correlations, with similar slopes and intercepts, were found between end-systolic stress and fractional shortening under basal conditions, after regression of left ventricular hypertrophy and after withdrawal of treatment, both at rest and at the peak of stress tests. An examination of each point of the relation between end-systolic stress and fractional shortening showed that very few points were beyond the 95% prediction limits of the correlation obtained in normal volunteers. These results indicate that left ventricular systolic function is normal in most untreated essential hypertensives, and is usually well maintained after regression of left ventricular hypertrophy during long-term treatment as well as after withdrawal of treatment, both at rest and during an acutely induced afterload increase.

Adult↗
PubMed1987

Changes in systemic and pulmonary vascular reactivity in hypertension following nifedipine and verapamil.

Excessive vascular tone and overresponsiveness to adrenergic stimuli characterize the hemodynamics of the greater and the lesser circulation in hypertension. We tested whether calcium entry blockade with verapamil (11 cases) or nifedipine (11 cases) may improve the vascular regulation in high blood pressure. Mental arithmetic and cold were used as adrenergic activators. The former stimulus produced obvious elevation of epinephrine plasma concentration, increase of cardiac output (CO), slight systemic vasodilatation, pulmonary vasoconstriction, and rise of blood pressure in both circuits. After calcium antagonists, the epinephrine reaction to the arithmetic test was significantly attenuated, variations in CO and systemic blood pressure were unchanged, pulmonary vasoconstriction was abolished, and the pressure rise in the lesser circuit was halved. The cold pressor test increased norepinephrine plasma concentration (NE pc), systemic and pulmonary blood pressure, and vascular resistance and did not alter CO. The attained NE pc during cold was unvaried after verapamil and significantly enhanced after nifedipine; pressure and resistance responses of the two circuits were almost unchanged after the former, whereas systemic and pulmonary vascular resistance rises were importantly attenuated after the latter compound, resulting in much lower pressure reactivity. A modulation of the sympathoadrenal reaction, per se, can explain changes in the systemic and in the pulmonary vasomotion with calcium blockade during arithmetic. It would seem that after verapamil the sympathetic system was still activated during cold to such an extent as to maintain the same vasoconstrictor potency. NE pc suggests that the sympathetic discharge was not reduced by nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Assessment of the systolic function and contractility of the hypertensive left ventricle.

Sustained hypertension is a stimulus for development of cardiac hypertrophy, which may be either concentric or eccentric. For a given rise of aortic pressure, left ventricle (LV) wall stress (afterload) may remain normal or reduced in the former and become enhanced in the latter condition, and the LV systolic function may vary in a direction opposite to that of wall stress. It is unknown whether there are also differences in contractile properties that may have a role in the shift from normal systolic function. To clarify this we evaluated the velocity of LV fiber shortening and the fractional fiber shortening in normotensive and hypertensive subjects with normal heart size (group 1), or concentric LV (group 2) or eccentric LV (group 3) hypertrophy during baseline and after an acute hemodynamic overload induced by a cold pressor test (CPT). We found that the functional pattern in the two conditions was similar to normal in group 1, significantly enhanced during baseline and CPT in group 2, and was depressed during baseline and more so during CPT in group 3. These findings suggest that the contractile properties of the two types of hypertrophy are different, supported by the slope of the force-length line defined by the end systolic stress-end systolic volume relation in the baseline and during the hemodynamic overload imposed by the CPT. This line was steeper than normal in group 2 and less steep than normal in group 3. It remains to be defined whether the two types of hypertrophy are a separate disorder or represent a different stage of the same disease.

Blood Pressure↗