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Biomedical subjects

G G Serneri

Publications and source records attributed to G G Serneri.

31 records · Page 2Linked to original sources
PubMed1988

Intravenous dilazep reduces blood pressure and peripheral vascular resistance in humans.

Dilazep, a coronary vasodilating drug with adenosine-mediated activity, was tested (acute double-blind study versus placebo) for its antihypertensive activity in 12 patients who had mild to moderate hypertension. Dilazep (0.2 mg/kg body weight by IV infusion for ten minutes) significantly reduced systolic and diastolic blood pressure (random-zero sphygmomanometer) on average by 13.3 and 10.6 mm Hg respectively. The antihypertensive effect started rapidly, reached its maximum 20 minutes after administration, and lasted for 90 minutes. Heart rate significantly increased between 10 and 30 minutes. The antihypertensive effect of dilazep was associated with a relevant vasodilating effect as demonstrated by the changes in upper limb blood flow (strain-gauge plethysmography, +32%; P less than .001) and vascular resistance (-29%, P less than .001). The maximal reduction of vascular resistance was directly correlated to its baseline value. For these characteristics of action, at least in acute administration, dilazep would be useful agent for the treatment of high blood pressure in mild to moderately hypertensive patients.

Adult↗
PubMed1986

Age related changes in platelet lipid composition.

Platelet lipid composition was investigated in 52 healthy subjects aged 20 to 68 years with similar dietary habits and living in a narrow geographic area in order to search possible changes referrable to aging. No significant variations were observed when platelet cholesterol, total phospholipids and different phospholipid fractions were considered, whereas cholesterol/phospholipid (C/PL) molar ratio significantly increased with aging (p less than 0.01). Moreover, a significant increase in 16:0 + 16:1 fatty acids was found in phosphatidylcholine (PC) and in sphingomyelin (SP) (r = 0.62, p less than 0.001 and r = 0.30, p less than 0.05 respectively) and a decrease in 18:2 n6 in the phospholipid fractions considered (at least p less than 0.05). These results indicate that modifications in platelet lipid composition occur with aging and that they could affect platelet functions so playing a role in the onset of atherosclerosis and in thrombotic phenomena occurring with increasing frequency in the elderly.

Adult↗
PubMed1986

Increased thromboxane A2 generation and altered membrane fatty acid composition in platelets from patients with active angina pectoris.

Lipid composition of platelet membranes and thromboxane A2 (TxA2) generation by platelets were investigated in eighty-seven anginal patients (forty-two with resting angina in active phase and forty-five with effort stable angina or rest angina in inactive phase) and in forty-five clinically healthy subjects of similar age. All subjects were on the same dietary regimen and the adherence to diet was checked by analysis of red blood cell lipids. Platelets from active angina patients produced more TxA2 than platelets from both inactive patients and controls (p less than 0.001). Moreover patients with active angina had higher arachidonic acid (AA, p less than 0.001) and lower eicosapentaenoic (EPA) and docosahexaenoic acid (DHA) levels in phosphatidylcholine (PC, p less than 0.001), than inactive patients and controls. AA and EPA changes in membrane PC significantly correlated with TxA2 production (p less than 0.001) but not with coronary pathoanatomy. Plasma lipids, content of cholesterol, total phospholipids (and their saturated and unsaturated fatty acids) and the different phospholipid fractions in platelet membrane were not different in the three groups. Present results indicate that in platelets from anginal patients phospholipid fatty acid composition is at least in part independent of plasma composition and that in active angina there are modifications leading to increased TxA2 formation and possibly contributing to the occurrence of ischemic attacks.

Adult↗
PubMed1985

Pentoxifylline treatment in patients with occlusive peripheral arterial disease. Circulatory changes and effects on prostaglandin synthesis.

Pentoxifylline has recently been reported to stimulate in vitro the synthesis of prostacyclin. However it is not known so far whether the drug is able to stimulate prostacyclin synthesis in man also in vivo. In the present study the effects of pentoxifylline on prostaglandin synthesis and several circulatory parameters were studied in 10 controls and 10 patients with occlusive arterial disease after acute i.v. and medium term oral treatment. Prostacyclin (as 6-keto-PGF1 alpha) and PGE2 plasma concentrations have been measured together with arterial blood flow, peripheral vascular resistance, platelet aggregation and red blood cell deformability. Pentoxifylline was found both in healthy subjects and patients to significantly increase prostacyclin plasma concentration after i.v. treatment. In medium term oral treatment prostacyclin concentration was found to increase only two hours after administration and not 8 hours after. No significant variations in PGE2 plasma concentration were found at any time in both groups. Pentoxifylline significantly enhanced resting and post-ischemic blood flow of the lower limbs and simultaneously decreased peripheral vascular resistance both in healthy subjects and patients. Different grades of delayed platelet aggregation and increased red blood cell deformability were also observed. In conclusion results of the present placebo controlled study show that pentoxifylline increases arterial blood flow in patients with occlusive arterial disease. Moreover pentoxifylline induces a temporary stimulation of prostacyclin synthesis which can be suggested to contribute to the clinical activity of the drug as far as an antithrombotic effect in terms of inhibition of platelet aggregation is concerned.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Efficacy of mexiletine in the medium-term treatment of ventricular arrhythmias. A randomized, double-blind, crossover trial against placebo in ambulatory patients.

A double-blind, crossover study was designed to compare the safety and efficacy of mexiletine with that of placebo in reducing premature ventricular complexes (PVC) in ambulatory patients and to find out the dose which gives a good therapeutic response with a minimal incidence of side-effects. Twenty-six patients, who had on average 427.9 PVCs/hour, were admitted to the study. The doses given were designed to reduce the frequency of PVCs by 50% or more from the baseline value. Two out of the twenty-six patients stopped treatment because of major side-effects. In the remaining twenty-four patients the 3 weeks of treatment with mexiletine significantly reduced the rate of PVCs by comparison with placebo (-63.8% versus +7.5%). In the nineteen responders (per cent reduction of PVCs over 50%) the dose of mexiletine was 600 mg daily (200 mg every 8 hours). In the non-responders plasma levels of mexiletine proved to be in the therapeutic range, not in any way different from responders. The most frequent side-effects were digestive difficulties (fifteen patients taking mexiletine and six taking placebo). These results show that mexiletine is an effective anti-arrhythmic drug in the management of ventricular arrhythmias occurring in ambulatory patients. In the majority of patients mexiletine was found to be effective even at the lowest dose studied of 600 mg/day.

Adult↗
PubMed1982

Reduced prostacyclin production in patients with different manifestations of ischemic heart disease.

Prostacyclin, a substance produced by vessel wall, has a sustained vasodilating and platelet antiaggregating activity and therefore the variations in its production in patients with ischemic heart disease are of interest. Prostacyclin production was assessed in 59 patients with ischemic heart disease and 59 control subjects matched for age, sex, body weight, smoking habits, blood pressure and serum cholesterol levels. Of the 59 patients examined, 23 had had a myocardial infarction 3 to 12 months earlier; 21 had had spontaneous angina and 15 effort angina for at least 3 months. Patients with myocardial infarction and spontaneous angina were also classified in subgroups with and without acute coronary insufficiency, according to the occurrence of ischemic attacks in the week preceding the study. Both circulating prostacyclin levels and prostacyclin produced after 3 minutes of ischemia were measured by bioassay. Circulating prostacyclin was significantly less in patients with ischemic heart disease than in matched control subjects independent of the clinical type of ischemic heart disease. Circulating prostacyclin was particularly reduced in patients with acute coronary insufficiency in comparison to patients without, both in the group with myocardial infarction (1.11 +/- 0.22 ng/ml and 2.09 +/- 1.32, respectively) and in the group with spontaneous angina (1.24 +/- 0.42 and 2.17 +/- 1.16, respectively). No differences could be found for prostacyclin produced after 3 minutes of ischemia in relation to the presence of acute coronary insufficiency. The lower level of prostacyclin production in patients with ischemic heart disease and especially in those with acute coronary insufficiency may be an important factor in the occurrence of coronary occlusion or spasm.

Adult↗
PubMed1980

Increased platelet aggregation due to plasma-aggregating activity. Identification of the responsible factors.

Platelet-poor plasmas (PPPs) from 52 out of 71 patients affected by different diseases and selected for increased amounts of circulating platelet aggregates, incubated at 37 degrees C for 30 min with control platelet-rich plasma (PRP; cross-matching test) induced the formation of platelet aggregates, stimulated the production of malondialdehyde and enhanced ADP-induced aggregation. 31 control PPPs were consistently negative at cross-matching test. Gel chromatography of plasmas on agarose 4% allowed the identification of four different fractions (A, B, C, D) provided with aggregating activity. Fraction A eluted at the void volume was to be identified with the von Willebrand factor, whereas B, C and D fractions, eluted at the same elution volumes as activated factor X were mainly composed of factor X (fraction B) and activated factor X (fractions C and D). Thrombin activity was absent in all the fractions provided with aggregating activity. Also, from control PPPs negative at cross-matching tests, the same fractions could be obtained, although of 5--10 times lower aggregating potency, thus explaining the negative cross-matching tests. These findings stress the role of some extraplatelet factors related to hypercoagulability in platelet hyperaggregability.

Adenosine Diphosphate↗
PubMed1974

Correction of the haemostatic defect in haemophiliacs without apparent correction of the coagulation defect.

The evaluation of microhaematuria may be considered as a measure of the haemostatic defect of haemophiliacs in nonhaemorrhagic periods. In order to study the relationship between coagulation disorder and haemostatic defect we have administered small amounts (1 U and 3 U/kg) of AHG and of factor IX (1U/kg) to 12 haemophiliacs (20 A and 2 B) and we have examined the effects on coagulation and microhaematuria. Microhaematuria was determined by the measurement of urinary radioactivity/24 h, after infusion of autologous RBC labelled with 51-Cr, for 11 consecutive days (4 days before and 7 after the administration). Coagulation was investigated by thromboelastography, PTT, Quick's time, PCI, factor VIII and IX activity assays, fibrinogen assay, and euglobulin lysis time. During the period of investigation, the patients remained in bed. In controls, factor VIII administration did not affect microhaematuria. On the other hand, in all haemophiliacs, factor VIII and IX administration significantly reduced microhaematuria, although the administered dose was not able to modify the coagulation defect. In all subjects the reduction of microhaematuria lasted at least 5 days. The correction of the haemostatic defect, without improvement of the clotting disorder, and its persistence for several days suggest that factor VIII is involved in the composition of the vascular wall and in its functional integrity. Moreover, on the basis of these results it is possible to carry out a rational prophylaxis of the haemorrhagic episodes using small doses of factor VIII, be determining the duration of the correction of the haemostatic defect for each subject.

Blood Coagulation↗