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Biomedical subjects

M Pepi

Publications and source records attributed to M Pepi.

81 records · Page 5Linked to original sources
PubMed1983

Clinical use of calcium channel blockers as ventricular unloading agents.

Calcium channel blockers relax the arterial smooth vasculature and lower blood pressure when it is elevated because of excessive vasoconstriction. They may be regarded as ventricular unloading agents. Nifedipine (11 cases, Group 1) and verapamil (12 cases, Group 2) were tested in hypertensive patients with cardiac enlargement (LV diastolic diameter greater than or equal to 60 mm), ECG signs of LV strain, lung congestion and dyspnea at rest, in an acute (nifedipine 20 mg; verapamil 160 mg) and 1-month (nifedipine 20 mg q.i.d.; verapamil 160 mg t.i.d.) therapeutic evaluation. In the acute study nifedipine reduced systemic vascular resistance (SVR), mean arterial pressure (MAP), mean pulmonary wedge pressure (PWP) and LV diastolic diameter (DD) and improved cardiac index (CI) and Vcf. In Group 2 verapamil reduced SVR and MAP, improved CI and was not effective on PWP, LV DD and Vcf. Verapamil was discontinued in 2 patients who developed severe dyspnea at rest after 3-4 days of continued oral treatment. At the end of the trial Vcf, PWP and LV DD were unchanged in the remaining subjects in Group 2 despite persistent pressure reduction. In Group 1 all of the patients had relief of dyspnea and lung congestion, reduction of heart size, persistent decrease of MAP and PWP, and improvement in Vcf. The only side effect was ankle edema in 4 cases. A less potent vasodilating action of verapamil and a predominant depression in cardiac contractility may account for the different results with the two drugs, in spite of a shared antihypertensive effect. These findings prove that functional changes in the failing hypertensive heart may differ after nifedipine compared to verapamil as a result of interaction and relative preponderance of influences on afterload and contractility.

Adult↗
PubMedDate not supplied

A new formula for echo-Doppler estimation of right ventricular systolic pressure.

The Doppler formulas currently used for right ventricular systolic pressure (RVSP) evaluation include right ventricular-right atrial (RV-RA) gradient and RA pressure. The former is expressed by the velocity of the trans-tricuspid regurgitant flow; the latter is generally assumed and is different from one formula to another. In 110 patients with cardiac disease with normal or elevated pulmonary pressure, we tested a new echo-Doppler formula for the evaluation of RVSP based on the estimation of RA pressure by means of the inferior vena cava collapsibility index (IVCCI) and compared this method with two traditional formulas (methods A and B) and with cardiac catheterization values. Patients were classified into three groups on the basis of IVCCI (group 1 > 45%, group 2 between 35% and 45%, and group 3 < 35%). RVSP was evaluated by method A (RV-RA gradient + 10), method B (RV-RA gradient x 1.1 + 14), and our new method, method C, which assigns 6, 9, and 16 mmHg to RA pressure in the presence of normal (> 45%), moderately reduced (between 35% and 45%), or markedly reduced (< 35%) IVCCI, respectively. IVCCI correctly identified RA pressure in the three groups (group 1, 6.8 mmHg; group 2, 10.8 mm Hg; and group 3, 13.1 mmHg); a high correlation existed between Doppler-derived and invasively determined RV-RA gradient (r = 0.99). Method C improved noninvasive estimation of RVSP in groups 1 and 3 compared with the other methods; in group 2, Doppler estimation of RVSP by methods A and C were comparable, whereas method B significantly overestimated the actual values.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function, Right↗
PubMedDate not supplied

Molecular characterization of an n-alkane-degrading bacterial community and identification of a new species, Acinetobacter venetianus.

Twenty-five bacterial strains isolated from the Venice lagoon and implicated in the degradation of n-alkanes, n-alkanols, n-alkanals and n-alkanoates were characterized in molecular and physiological terms. The isolates were grouped by amplified ribosomal DNA restriction analysis (ARDRA) into seven clusters, corresponding to seven species, six of which were identified on the basis of 16S rDNA sequencing. Genetic variability among strains was shown by random amplified polymorphic DNA (RAPD). Only strains of the new species Acinetobacter venetianus grew with n-alkanes (C10, C14 and C20) and their respective oxidation products as sole carbon sources. Strains of the other three species identified thrived on n-alkane oxidation products (n-alkanols, n-alkanals, n-alkanoates). The other three species were not able to grow on any of the substrates tested. Analysis of plasmid content showed that only A. venetianus strains harboured plasmids. These plasmids contained sequences homologous to the Pseudomonas oleovorans alkBFGH genes.

Acinetobacter↗
PubMedDate not supplied

Oil-degrading Acinetobacter strain RAG-1 and strains described as 'Acinetobacter venetianus sp. nov.' belong to the same genomic species.

Acinetobacter strain RAG-1 (ATCC 31012) is an industrially important strain which has been extensively characterized with respect to its growth an hydrocarbons and its production of a high molecular mass bioemulsifier, emulsan. Although RAG-1 has been investigated in detail for specific biochemical characteristics, its taxonomic status is uncertain and it is usually referred to as A. lwoffii or A. calcoaceticus sensu lato. However, results obtained by restriction analysis of the amplified rDNA and subsequently substantiated by DNA-DNA hybridization, partial 16S rDNA nucleotide sequence comparison and biochemical characterization indicate that RAG-1 belongs to the genomic species recently described as 'A. venetianus'. Furthermore, these data confirm that 'A. venetianus' constitutes a new and distinct genomic species within the genus Acinetobacter.

Acinetobacter↗
PubMedDate not supplied

Acute filling pattern changes of the failing left ventricle after captopril as related to ventricular structure.

In congestive heart failure captopril modifies the left ventricular filling pattern mainly by unloading the heart. We investigated whether the structural characteristics of the left ventricle may influence the acute effects of captopril on this pattern in patients with untreated hypertensive (H group, 6 patients) or idiopathic (I group, 14 patients) cardiomyopathy. We evaluated changes of pulsed Doppler mitral flow, of systemic arterial and wedge pulmonary pressures 40 min after 25 mg captopril administered sublingually, and correlated these changes with the M-mode echocardiographic relative wall thickness index (h/r). Baseline mean arterial pressure (H = 137 +/- 20 mm Hg, mean +/- SD, I = 95 +/- 19 mm Hg; p < 0.001), and h/r (H = 0.38 +/- 0.03, I = 0.28 +/- 0.09; p < 0.05) were greater in the high blood pressure group; wedge pressure, echocardiographic biplane ejection fraction, and Doppler indexes of the left ventricular filling were similar in the two populations. After captopril, ejection fraction did not change significantly, mean arterial pressure decreased significantly in hypertensive patients (H group, baseline = 137 +/- 20, captopril = 119 +/- 10, p = 0.02; I group, baseline = 95 +/- 19, captopril = 90 +/- 24, p = nonsignificant), and the wedge pressure was reduced by the same extent in both groups (H group, baseline = 27.7 +/- 3, captopril = 21 +/- 7, p < 0.05; I group, baseline = 20 +/- 12, captopril = 15 +/- 8, p < 0.05). In the H group early mitral flow increased [(E wave integral) x (mitral annulus area)] by 38 +/- 15%, and was almost steady in the I group (-1.3 +/- 30%; group H vs. I = p < 0.01); late mitral flow [(A wave integral) x (mitral annulus area)] showed a pattern exactly opposite to this (H = +0.4 +/- 40%, I = +38 +/- 19; p < 0.01). In the whole population there was a significant correlation between the early/late flow ratio variations and baseline h/r (r = 0.6, p < 0.05). In chronic congestive heart failure, changes in left ventricular filling with captopril are related to h/r: a higher index, as recorded in the H group, is associated with "true normalization' of the filling pattern after captopril; a lower index, as recorded in the I group, is associated with "pseudonormalization' despite a similar decrease of left ventricular filling pressure.

Administration, Sublingual↗
PubMedDate not supplied

Inducible cyclooxygenase (COX-2) in glioblastoma--clinical and immunohistochemical (COX-2-VEGF) correlations.

Cyclooxygenase-2 (COX-2) is the inducible form of the enzyme responsible for the first step in the prostaglandin synthesis. COX-2 upregulation is demonstrated in different tumors. COX-2 products may modulate tumoral growth, apoptosis, metastasis, multidrug resistance and angiogenesis. Moreover, the antitumoral effect of the COX inhibitors has been documented. We studied the immunohistochemical expression and the prognostic value of COX-2 on 43 surgical specimens of glioblastoma-affected patients. Furthermore, we evaluated the correlation between the immunohistochemical expression of COX-2 and vascular endothelial growth factor (VEGF). Of the glioblastomas, 63% resulted as COX-2-positive. Median survival of the patients with COX-2-positive lesions was 10 months; median survival of the patients with COX-2 negative glioblastoma was 21 months (NS). All 4 patients who survived longer than 24 months had COX-2 negative lesions (p = 0.017). Concordance between COX-2 and VEGF was documented in 60% of the cases. Our findings show that glioblastoma can immunohistochemically express COX-2 and that its expression is unrelated with VEGF and significantly less frequent in the long survivors. Nevertheless, the absence of statistical correlation with survival time advises further studies on larger series to ascertain the concrete prognostic value of COX-2 in glioblastoma.

Aged↗