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Biomedical subjects

A Lechi

Publications and source records attributed to A Lechi.

At least 55 records · Page 3Linked to original sources
PubMed1995

[Multicenter comparative study of meropenem, a new carbapenemic preparation, administered intramuscularly. Treatment of respiratory and urinary infections in hospitalized patients]l.

263 hospitalized patients were enrolled in a multicentre study to assess efficacy and safety of i. m. meropenem, compared to ceftazidime, in the treatment of lower respiratory tract infections and urinary infections as well. Meropenem, administered at a dose of 500 mg tid, was therapeutically equivalent to the reference agent (1000 mg tid in RTI's and 500 mg tid in UTI's) in both indications. The two treatments were well tolerated, without any serious local or systemic side effect.

Adult↗
PubMed1995

Oxidized LDL and reduction of the antiaggregating activity of nitric oxide derived from endothelial cells.

Oxidized LDL has been observed to induce abnormalities in endothelial function which may be relevant for the progression of atherosclerotic lesions. We studied in vitro the possible effects of oxidized LDL on the antiaggregating activity of endothelial cells, which is dependent on release of prostacyclin and nitric oxide. We used an experimental model in which cultured human endothelial cells were placed in the aggregometer in contact with human platelets, after blockade of cyclo-oxygenase by adding acetylsalicylic acid. In this way the antiaggregant effect of endothelial cells was dependent on the release of nitric oxide alone; prevention of antiaggregant activity by preincubation of endothelial cells with 300 microM L-NG-mono-methylarginine confirmed this. When this system was used, endothelial cells (2-7.5 x 10(5)/ml) almost completely inhibited thrombin-induced (0.02-0.08 U/ml) platelet aggregation (2 x 10(8) platelets/ml), measured according to Born (11.1% +/- 8.5 vs 68.6% +/- 12.6, M +/- SD). This antiaggregating activity was reduced when slightly oxidized LDL 100 micrograms/ml (35.2% +/- 14.9, p < 0.001), but not native LDL 100 micrograms/ml (7.5% +/- 7.6), was added immediately before aggregation was induced. Incubation of endothelial cells with oxidized LDL 100 micrograms/ml for 1 h did not affect the antiaggregating capacity, unless oxidized LDL was present during aggregation (18.3% +/- 10.2 vs 35.8% +/- 9.6, p < 0.02). No significant direct effect of either oxidized or native LDL on stimulated platelet aggregation was observed. Our results indicate that slightly oxidized LDL can reduce the antiaggregating properties of the endothelium, probably by interaction with NO rather than through inhibition of its synthesis.

Aspirin↗
PubMed1994

Early agonist-induced intracellular acidification is increased in platelets from patients with essential hypertension.

Enhanced Na+/H+ exchange has been reported to be increased in patients with essential hypertension. However, early variations of intracellular pH, although influenced by the antiport, are only partially dependent on the exchange. In this study, we measured the initial platelet pH response to agonists in a group of untreated subjects with essential hypertension (EH, n = 24) and in a group of age- and sex-matched normotensive control subjects (CS, n = 24). Intracellular pH was measured with the specific fluorescence indicator 2'7'bis(carboxyethyl)-5,6-carboxyfluorescein. Measurements were performed on platelets in the presence or absence of extracellular calcium, in a carbonate-free medium. Intracellular calcium was measured by the Fura 2 method. Mean pH values were slightly higher in the platelets of EH (7.469 +/- 0.017 U) compared with CS (7.423 +/- 0.012 U, P < .05), although there was a substantial overlap. When stimulated with physiologic agonists ADP and thrombin and with the calcium ionophore ionomycin, a biphasic response consisting of early acidification followed by alkalinization was observed, the second phase not being detectable with ADP. The initial acidification was greater in EH, particularly with ADP (EH, -0.046 +/- 0.002 U; CS, -0.036 +/- 0.002 U, P < .001) and with ionomycin (EH, -0.074 +/- 0.007 U; CS, -0.051 +/- 0.005 U, P < .05). This acidification proved in some way calcium dependent, as it was reduced in the absence of extracellular calcium (EGTA) in both EH and CS. After incubation with amiloride a further decrease in intracellular pH, more marked in EH, was observed. Alkalinization induced by thrombin was increased in EH (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1994

Erythrocyte Na(+)-H+ exchanger and Na(+)-Li+ countertransport activity in primary aldosteronism.

Several authors have described increased Na-H exchanger activity in essential hypertension but no data are available in secondary forms of hypertension such as primary aldosteronism. We measured Na-H exchanger kinetics together with Na-Li countertransport Vmax in the erythrocytes of eight patients with primary aldosteronism and in 15 normotensive control subjects. Plasma aldosterone, plasma renin and plasma potassium were also evaluated. Na-H exchanger Vmax appear to be increased in patients with primary aldosteronism and Hill's n, an index of co-operativity amongst intracellular proton binding sites, was significantly lower in patients than in controls. No statistically significant differences were found between affinity for intracellular protons (K50%) and for Na-Li countertransport Vmax between the two groups studied. We were unable to find any correlations between Na-H exchanger Vmax and Na-Li countertransport Vmax in the two groups considered as a whole. From the present data Na-H exchanger overactivity would not appear to be a specific feature of essential hypertension but seems to be characteristic in patients with primary aldosteronism.

Adult↗
PubMed1994

Changes induced by nicardipine slow release in forearm and myocardial hemodynamics of subjects with essential hypertension.

OBJECTIVE: To evaluate the modifications induced by chronic treatment with a new formulation of nicardipine (slow release) on the hemodynamic parameters in peripheral artery and left ventricle diastolic function. MATERIALS AND METHODS: Ten mild to moderate essential hypertensive male patients (mean age 42 years, range 32-54 years) received nicardipine slow release (40 mg b.i.d.) for six months. Peripheral hemodynamic and cardiac parameters were evaluated by duplex scanner, coupled with a plethysmographic method, basally (T0) and after 1 (T1) and 6 months' treatment (T2). RESULTS: Blood pressure showed a significant reduction after 1 month (mean blood pressure 109 +/- 2 vs 124 +/- 3 mmHg, M +/- SE, p < 0.001), which was maintained after 6 months (mean blood pressure 112 +/- 3 mmHg, p < 0.001), while heart rate showed only a slight, non-significant increase. There were highly significant changes in distensibility (0.29 +/- 0.02 vs 0.16 +/- 0.01 s2.cm-2, T2 vs T0, p < 0.001), characteristic impedance (55 +/- 3 vs 78 +/- 3 dyn.s.cm-5.10(2), T2 vs T0, p < 0.001) and local resistances (71 +/- 5 vs 118 +/- 4 mmHg.ml-1. s, T2 vs T0, p < 0.001) in the brachial artery, and also in left ventricle posterior wall diastolic thickness (10.2 +/- 0.4 vs 11.5 +/- 0.3 mm, T2 vs T0, p < 0.05), end diastolic volume (127 +/- 3 vs 109 +/- 3 ml, T2 vs T0, p < 0.01) and mass/volume index (1.21 +/- 0.03 vs 1.35 +/- 0.03, p < 0.05). CONCLUSIONS: The antihypertensive efficacy of nicardipine slow release, with only two daily administrations, allows the restoration of the dumping function of the large arteries, and the regression of the functional modifications affecting the left ventricular diastole.

Adult↗
PubMed1993

Erythrocyte Na(+)-H+ exchange activity in essential hypertensive and obese patients: role of excess body weight.

INTRODUCTION: Several authors have described increased Na(+)-H+ exchanger activity in essential hypertension, and an increase in activity of this transport system has also been postulated in situations of hyperinsulinism, such as obesity and essential hypertension. METHODS: We measured Na(+)-H+ exchanger activity in a group of 37 subjects with essential hypertension (18 obese, 19 non-obese), in a group of nine normotensive obese subjects and in a control group of 16 healthy volunteers. Plasma insulin and glucose values during an oral glucose tolerance test were evaluated, together with other variables such as plasma aldosterone, plasma renin activity and plasma potassium. RESULTS: Na(+)-H+ exchanger system activity did not appear to be abnormally raised in the hypertensive subjects, but was significantly increased in the normotensive obese group. Upon dividing the hypertensive subjects into two subgroups on the basis of body mass index, it was noted that, whereas the non-obese hypertensives showed Na(+)-H+ exchanger activity patterns similar to those in controls, the obese hypertensive subjects exhibited increased activity of the transport system. Na(+)-H+ activity correlates with body mass index and shows a significant inverse correlation with plasma potassium. No correlations were found between Na(+)-H+ exchanger activity and the sum of plasma insulin values during the oral glucose tolerance test. CONCLUSION: Na(+)-H+ exchanger overactivity appears to be characteristic in overweight subjects, but would not appear to be a specific feature of essential hypertension. The increased Na(+)-H+ exchanger activity observed in obese subjects may be postulated to be related to the hypermineralocorticoidism characteristic of this condition.

Adult↗
PubMed1993

Unilateral trismus caused by vertebrobasilar dolichoectasia.

Vertebrobasilar dolichoectasia is a relatively uncommon pathological entity and generally asymptomatic. We report a quite unusual case of unilateral motor trigeminal involvement with trismus, due to VD. Apart from tetanus or local morbid conditions of the mouth, trismus is often attributed to disturbed programming and co-ordination of the masticatory muscles within the mesencephalic nucleus. The possibility of truncal compression of the trigeminal motor root by vertebrobasilar dolichoectasia being responsible for masseter muscle spasm, in analogy with the pathogenetic mechanisms proposed in hemifacial spasm, is proposed as an alternative explanation in the present case.

Aged↗
PubMed1993

Acute esotropia from small thalamic hemorrhage.

A 74 year-old patient developed transient acute esotropia, upward gaze palsy and imbalance of standing and gait. Computed Tomography (CT) demonstrated a small left thalamic hemorrhage in the absence of midbrain lesions. The role of thalamic lesion in the genesis of monocular supranuclear palsy is discussed.

Acute Disease↗
PubMed1993

Hemodynamic changes induced by cilazapril and atenolol during isometric stress in hypertensive patients.

We studied 16 mild to moderate essential hypertensive patients (14 male, 2 female; mean age 45 years, range 34-55 years) in order to investigate the effects of an ACE inhibitor, cilazapril (5 mg o.d.) and a selective beta-blocker, atenolol (100 mg o.d.) on the hemodynamics of the brachial and carotid arteries after an isometric stress test with a handgrip. Both drugs caused a statistically significant decrease in blood pressure after three months' treatment, but only cilazapril reduced it after the first dose. Heart rate was reduced only by atenolol (61 +/- 3 vs 71 +/- 3 bpm; p < 0.01). Changes in forearm compliance and characteristic impedance showed a difference statistically significant both for acute test and after three months of treatment. The increase in blood pressure during handgrip did not differ appreciably between the two treatment groups. On the contrary, after handgrip only cilazapril caused a significant increase of the reactive hyperemia.

Adult↗
PubMed1993

Platelet intracellular pH and glucose metabolism in hypertensive patients.

Intracellular platelet pH was studied by the BCECF fluorescent pH-sensitive intracellular indicator method in 52 patients with essential hypertension and 42 control subjects of similar age and sex. In 40 hypertensive patients studied by oral glucose tolerance test (standard OGTT) 23 presented with pathological blood glucose and plasma insulin values. Intracellular pH was on average higher in hypertensives (7.415 +/- 0.114, mean +/- SD) than in controls (7.348 +/- 0.109, P < 0.05), although there was a considerable overlap in values. In the group of hypertensive patients, no difference was observed between those with normal and those with pathological OGTT. There was also no significant correlation between intracellular pH and blood glucose, plasma insulin after OGTT, plasma cholesterol and triglycerides, age, BP or body mass index. These data are consistent with an anomaly of intraplatelet pH, perhaps owing to alteration of Na+/H+ exchange in essential hypertension, but do not indicate that this is related to a condition of hyper-insulinaemia or insulin resistance.

Adolescent↗
PubMed1992

Changes in the haemodynamics of large arteries induced by single doses of nicardipine, enalapril, atenolol and urapidil.

Haemodynamic changes in the carotid and brachial arteries produced by single doses of four anti-hypertensive drugs (nicardipine, enalapril, atenolol, and urapidil) have been studied in 12 patients with essential hypertension. Measurements were performed noninvasively using a mechanographic method and B-mode pulsed Doppler ultrasonography. Within 7 h all of the drugs had caused a significant reduction in blood pressure, whereas heart rate showed a significant change only after atenolol. All the drugs produced a marked reduction in brachial pulse-wave velocity. Only nicardipine caused a significant reduction in vessel wall tension both in the carotid and brachial arteries, while brachial peripheral resistance was significantly reduced by all the drugs except atenolol. Neither atenolol nor enalapril caused any significant reduction in carotid peripheral resistance. The results show that all four antihypertensive drugs led to a beneficial increase in arterial compliance despite their different effects on peripheral resistance.

Adult↗
PubMed1992

Left ventricular diastolic function and responses to adrenergic stimuli in borderline arterial hypertension.

OBJECTIVE: To detect the existence of a possible relationship between arterial hypertension and adrenergic reactivity to pressure stimuli, and changes in left ventricular diastolic function (LVDF). PATIENTS: Fifty-nine young subjects with borderline arterial hypertension and ten sex- and age-matched controls were investigated. After three medical examinations, the subjects were divided into hypertensive and borderline groups on the basis of the blood pressure reading at visit 3. A complete echocardiographic study was performed in 25 of the 59 subjects. DESIGN: Blood pressure was measured in baseline conditions and during pressure stimuli (mental stress, handgrip and cold pressor tests). LVDF was evaluated primarily by means of filling velocities during diastolic phases taken from the left ventricular volume curve (obtained from a complete echocardiographic study). RESULTS: No significant changes in blood pressure responses were observed for the borderline or hypertensive groups during the adrenergic test. The echocardiographic indices of diastolic function were statistically different for the two groups when compared with the control group. The LVDF parameters correlated significantly with systolic blood pressure and diastolic blood pressure measured at the time of the echocardiogram, but not with blood pressure measured occasionally. CONCLUSIONS: Blood pressure increases similarly during adrenergic stimuli in both the hypertensive and borderline groups. The correlation between systolic blood pressure, diastolic blood pressure and LVDF parameters may indicate a very early onset of reduced compliance of the left ventricle, even in a preclinical phase of hypertension.

Adolescent↗
PubMed1992

Wernicke's encephalopathy: occurrence and pathological aspects in a series of 400 AIDS patients.

BACKGROUND: Wernicke encephalopathy (WE), acute (microhaemorrhages) and chronic (proliferation of capillaries) is actually considered as a not uncommon, and curable, condition in several diseases, and not only in alcoholic patients. Why serotoninergic nuclei, and whether blood brain barrier (BB) are involved were our questions. METHODS: In a dramatic series of AIDS cases we selected 380 brains, all belonging to drug addicted subjects. In all Thiamine administration had been under 20 mg pro die and by oral way. In the cases considered, opportunistic infections were present in the 40%, and/or HIV specificity in the 35%. RESULTS: "Acute" WE was found in nearly the 10%. All patients presented with CNS lesions, other than those of WE, but HIV specificity was found only in 5. They all showed changes in Choroid Plexus, namely alterations of various type of the cuboid epithelium, such as swelling, disruption, hyperplasia. DISCUSSION: WE is set in connection with pyruvate accumulation at capillary level, likely bound to the Thiamine deficiency and to the lack of energy thus induced. Apart from obvious haemorrhagic aspects, CFS studies in WE are lacking. Choroid structure is not merely a permeable membrane (CSF is not a filtrate). Our findings would suggest that Thiamine plays a role in the energy supply to BB. Moreover, the existence of free nerve endings through the ependyma for the release and uptake of monoamines, allows to consider the elective involvement of serotoninergic neurons as somehow connected to the choroid plexus changes described.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Effect of picotamide on platelet aggregation and on thromboxane A2 production in vivo.

Effects of picotamide (900 mg in 3 oral administrations for 7 days) on ex vivo and in vivo platelet TxA2 production and on platelet aggregation were evaluated in 8 patients with peripheral arteriopathy and in 8 normal subjects. Picotamide significantly reduced ADP-induced platelet aggregation, but had no effect on that induced by arachidonic acid or the thromboxane analogue U46619. Though ex vivo platelet TxA2 production (TxB2 concentration after arachidonic-acid-induced aggregation) was reduced from 946 +/- 141 (mean +/- SD) to 285 +/- 91 ng/ml in controls and from 1515 +/- 673 to 732 +/- 420 ng/ml in patients with arteriopathy, there was no effect on urinary excretion of 2,3-dinor-TXB2 (in vivo indicator of platelet TxA2 production), or on in vivo PGI2 production (urinary excretion of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha). In the same subjects, single-dose aspirin reduced ex vivo TxB2 production by at least 98% and 2,3-dinor-TxB2 excretion from 116.7 +/- 61.4 to 32.6 +/- 17.0 ng/g creatinine in control subjects, and from 156.3 +/- 66.1 to 59.1 +/- 19.2 ng/g creatinine in patients with peripheral arteriopathy. Our data suggest that inhibition of platelet TxA2 production in vivo may not be picotamide's main mechanism of action.

Aged↗