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Biomedical subjects

R Ferrari

Publications and source records attributed to R Ferrari.

At least 109 records · Page 6Linked to original sources
PubMed1999

Whiplash.

Explore the source record for details and available documents.

Culture↗
PubMed1998

Metabolic derangement in ischemic heart disease and its therapeutic control.

The term myocardial ischemia describes a condition that exists when fractional uptake of oxygen in the heart is not sufficient to maintain the rate of cellular oxidation. This leads to extremely complex situations that have been extensively studied in recent years. Experimental research has been directed toward establishing the precise sequence of biochemical events leading to myocyte necrosis, as such knowledge could lead to rational treatments designed to delay myocardial cell death. At the present time, there is no simple answer to the question of what determines cell death and the failure to recover cell function after reperfusion. Problems arise because: (1) ischemic damage is not homogeneous and many factors may combine to cause cell death; (2) severity of biochemical changes and development of necrosis are usually linked (both the processes being dependent on the duration of ischemia) and it is impossible to establish a causal relation; and (3) the inevitability of necrosis can only be assessed by reperfusion of the ischemic myocardium. Restoration of flow, however, might result in numerous other negative consequences, thus directly influencing the degree of recovery. From the clinical point of view, we have recently learned that there are several potential manifestations and outcomes associated with myocardial ischemia and reperfusion. Without a doubt, ventricular dysfunction (either systolic or diastolic) of the ischemic zone is the most reliable clinical sign of ischemia, since electrocardiographic changes and symptoms are often absent. The ischemia-induced ventricular dysfunction, at least initially, is reversible, as early reperfusion of the myocardium results in restoration of normal metabolism and contraction. In the ischemic zone, recovery of contraction may occur instantaneously or, more frequently, with a considerable delay, thus yielding the condition recently recognized as the "stunned" myocardium. On the other hand, when ischemia is severe and prolonged, cell death may occur. Reperfusion at this stage is associated with the release of intracellular enzymes, damage of cell membranes, influx of calcium, persistent reduction of contractility, and eventual necrosis of at least a portion of the tissue. This entity has been called "reperfusion damage" by those who believe that much of the injury is the consequence of events occurring at the moment of reperfusion rather than a result of changes occurring during the period of ischemia. The existence of reperfusion damage, however, has been questioned, and it has been argued that, with the exception of induction of arrhythmias, it is difficult to be certain that reperfusion causes further injury. The existence of such an entity has clinical relevance, as it would imply the possibility of improving recovery with specific interventions applied at the time of reperfusion. In 1985, Rahimtoola described another possible outcome of myocardial ischemia. He demonstrated that late reperfusion (after months or even years) of an ischemic area showing ventricular wall-motion abnormalities might restore normal metabolism and function. He was the first to introduce the term "hibernating myocardium," referring to ischemic myocardium wherein the myocytes remain viable but in which contraction is chronically depressed. In this article we review our data on metabolic changes occurring during ischemia followed by reperfusion, obtained either in the isolated and perfused rabbit hearts or in ischemic heart disease patients undergoing intracoronary thrombolysis or aortocoronary bypass grafting.

Animals↗
PubMed1998

Different outcomes of the reperfused myocardium: insights into the comments of stunning and hibernation.

There are several potential outcomes of myocardial ischaemia. When ischaemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. Interventions aimed at reducing mechanical activity and oxygen demand either before ischaemia or during reperfusion have been shown to delay the onset of ischaemic damage and to improve recovery during reperfusion. When myocardial ischaemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischaemia leading to a reversible, chronic left ventricular dysfunction has been termed 'hibernating myocardium'. It is important clinically recognize hibernation as reperfusion of hibernating myocardium by angioplasty or heart surgery restores contraction and this correlates with long term survival. A third possible outcome after a short period of myocardial ischaemia is a transient post-ischaemic ventricular dysfunction, a situation termed 'stunned myocardium'.

Chronic Disease↗
PubMed1998

Inter-laboratory validation of solid-phase microextraction for the determination of triazine herbicides and their degradation products at ng/l level in water samples.

The accuracy and precision of solid-phase microextraction (SPME) were validated in an inter-laboratory study including ten laboratories for the analysis of triazine herbicides and their metabolites at ng/l level in aqueous samples. The SPME conditions were optimised in order to obtain maximum sensitivity. Especially, salt addition and choice of the SPME fibre coated with Carbowax-divinylbenzene increased the sensitivity. The average detection limits were in the range from 4 to 24 ng/l for the triazine herbicides, and 20 and 40 ng/l for desisopropylatrazine and desethylatrazine, respectively. The average r2 values of the calibration curves were above 0.99 for all of the analytes. The statistical data treatment was performed in accordance with the International Standardisation Organisation (ISO) standard 5725. Relative repeatability standard deviations between 6 and 14% and relative reproducibility standard deviations between 10 and 17% were found. The determined concentrations of the reference sample compared well to the "true" values, thus proving the good accuracy of the method. It is concluded that SPME is a reliable technique for the quantitative analysis of water samples containing triazine herbicides in concentrations around the European limit of 100 ng/l for individual pesticides in drinking water.

Calibration↗
PubMed1998

Effects of chronic noradrenaline on the nitric oxide pathway in human endothelial cells.

Altered endothelium-dependent vasodilation has been observed in congestive heart failure (CHF), a disease characterized by a sustained adrenergic activation. The purpose of our study was to test the hypothesis that chronically elevated catecholamines influence the nitric oxide (NO) pathway in the human endothelium. Human umbilical vein endothelial cells (HUVEC) were exposed for 7 days to a concentration of noradrenaline (NA, 1 ng/mL) similar to that found in the blood of patients with CHF. Kinetics of endothelial constitutive NO synthase (ecNOS) and inducible NO synthase (iNOS) activity, measured by [3H]L-arginine to [3H]L-citrulline conversion, and protein expression of ecNOS and iNOS, assessed by Western blot analysis, were unaffected by chronic NA treatment. Furthermore, no changes in subcellular fraction-associated ecNOS were found; this indirectly shows that chronic NA did not cause phosphorylation of the enzyme. Moreover, [3H]L-arginine transport through the plasma membrane was conserved in chronically NA-treated cells. The data demonstrate that prolonged in vitro exposure to pathologic CHF-like NA does not affect the L-arginine: NO pathway in human endothelial cells.

Arginine↗
PubMed1998

Skeletal muscle myosin heavy chain expression in rats with monocrotaline-induced cardiac hypertrophy and failure. Relation to blood flow and degree of muscle atrophy.

BACKGROUND: In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy characterised by atrophy and shift from the slow to the fast type fibres. The mechanisms responsible for these changes are not clear yet. OBJECTIVES: We investigated the influence of blood flow and degree of muscle atrophy on the myosin heavy chains (MHC) composition of the soleus and extensor digitorum longus (EDL) of rats with right ventricle hypertrophy and failure. METHODS: CHF was induced in 16 rats by injecting 30 mg/kg monocrotaline. Eight animals had the same dose of monocrotaline but resulting in compensated right ventricle hypertrophy. Two age- and diet-matched groups of control animals (nine and five respectively) were also studied. The relative percentage of MHC1 (slow isoform), MHC2a (fast oxidative) and MHC2b (fast glycolytic) was determined by densitometric scan after electrophoretic separation. The relative weights of soleus and EDL (muscle weight/body weight) were taken as an index of muscle atrophy. Skeletal muscle blood flow was measured by injecting fluorescent micropheres. RESULTS: CHF and Control (Con) rats showed similar degree of atrophy both in soleus (0.40 +/- 0.06 vs. 0.44 +/- 0.06 p = NS), and EDL (0.47 +/- 0.04 vs. 0.45 +/- 0.02, p = 0.09). In CHF rats these two muscles showed a statistically significant MHCs redistribution toward the fast type isozymes. In fact in EDL of CHF rats MHC2a was 30.5 +/- 6.1% vs. 35.8 +/- 8.6% of the Con (p < 0.05). MHC2b was however higher (68.5 +/- 6.6% vs. 61.0 +/- 9.6%, p = 0.017). In the soleus of CHF rats MHC1 was decreased (87.6 +/- 3.4% vs. 91.9 +/- 5.2%, p = 0.02), while MHC2a was increased (12.04 +/- 3.5% vs. 7.9 +/- 5.2%; p = 0.028). Similar changes were not found in the muscles of the compensated hypertrophy animals. No correlation was found between MHC pattern and the relative muscle weight in the CHF animals. Soleus blood flow in CHF rats was significantly lower than that of Con (0.11 +/- 0.03 ml/min/g vs. 0.22 +/- 0.03 p < 0.05), while no differences were found in EDL (0.06 +/- 0.02 ml/min/g vs. 0.08 +/- 0.02, p = NS). CONCLUSIONS: In rats with CHF a skeletal muscle myopathy characterised by a shift of the MHCs toward the fast type isoforms occurs. The magnitude of the shift correlates neither with the degree of atrophy, nor with the skeletal muscle blood flow, suggesting that these two factors do not play a pivotal role in the pathogenesis of the myopathy.

Animals↗
PubMed1998

The emergence of the volume transmission concept.

Interneuronal communication in the central nervous system (CNS) have always been of basic importance for theories on the cerebral morphofunctional architecture. Our group has proposed that intercellular communication in the brain can be grouped into 2 broad classes based on some general features of the transmission: wiring (WT) and volume (VT) transmission. WT occurs via a relatively constrained cellular chain (wire), while VT consists of 3-dimensional diffusion of signals in the extracellular fluid (ECF) for distances larger than the synaptic cleft. Both morphological and functional evidence indicates that dopamine (DA) synapses in striatum are 'open' synapses, i.e., synapses which favor diffusion of the transmitter into the surrounding ECF and observations are compatible with the view that DA varicosities can synthesize, store and release DA for VT. The DAergic mesostriatal transmission has, therefore, been examined by several groups to give experimental support to VT. Moreover, due to its minor structural requirements, VT may become prevalent under some pathological conditions, e. g. Parkinson's disease. In animal models of DAergic pathway degeneration, it has been shown that a compensatory activation of surviving DA terminals may lead to a preferential potentiation of VT. WT and VT favor different and complementary types of computation. VT is markedly slower and less safe than WT, but has minor spatial constraints and allows the reach of a large number of targets. Models of neuronal systems integrating classical neuronal circuits and diffusible signals begin to show how WT and VT may interact in the neural tissue.

Animals↗
PubMed1998

Quantification of apolipoprotein AI-containing lipoprotein particles in non-insulin-dependent diabetes mellitus.

Quantification of LpAI (lipoprotein particles containing apolipoprotein AI not associated with apolipoprotein AII) was performed through an electroimmunoassay on serum from 49 non-insulin-dependent diabetic patients (mean age 60 +/- 9 years) and 53 age-matched control subjects of both sexes not affected by coronary heart disease. Serum lipid and lipoprotein levels were not significantly different between the two groups. Serum levels of LpAI determined for diabetic patients did not differ from those of control subjects, while concentrations of LpAI in men were significantly lower than in women, both among diabetics (P < 0.05) and controls (P < 0.005). Serum levels of apolipoprotein AI and high density lipoprotein cholesterol were significantly correlated with those of LpAI (P < 0.005, for both variables). On the contrary, levels of LpAI/AII (lipoprotein particles containing both apolipoprotein AI and AII) were significantly increased in diabetic patients (P < 0.005).

Apolipoprotein A-I↗
PubMed1998

Acute and chronic effects of propionyl-L-carnitine on the hemodynamics, exercise capacity, and hormones in patients with congestive heart failure.

Carnitine is an important cofactor in the intermediary metabolism of the heart, and carnitine deficiency is associated with congestive heart failure. We therefore studied the effects of acute (IV bolus, 30 mg/kg body weight) and chronic administration (1.5 mg/d for 1 month) of propionyl-L-carnitine on hemodynamics, hormone levels, ventricular function, exercise capacity, and peak oxygen consumption in 30 patients with chronic congestive heart failure (NYHA II-III, mean EF 29.5 +/- 7%) in a phase II, parallel, single-blind, randomized, and placebo-controlled study. Acute administration of propionyl-L-carnitine caused a significant reduction in pulmonary artery and pulmonary wedge pressures at both day 1 (P < 0.001) and day 30 (P < 0.05) of the study but no other hemodynamics changes. Hormone levels did not change following acute administration of the drug. Chronic administration of propionyl-L-carnitine increased peak oxygen consumption by 45% (from 16.0 +/- 3 to 23.5 +/- 2 mL/kg/min, P +/- 0.001), exercise time by 21% (from 8.1 +/- 0.5 to 9.8 +/- 0.4 minutes, P < 0.01), and peak exercise heart rate by 12% (P < 0.01). These changes were concomitant with a reduction of pulmonary artery pressure. In the treated group, there was a slight, but significant (P < 0.01), reduction in left ventricular dimensions. Hemodynamics and hormones measured after 1 month of oral therapy remained unchanged, except for a fall in pulmonary artery pressures, with a nonsignificant trend towards a fall in filling pressures and plasma norepinephrine. The chronic changes in the propionyl-L-carnitine group were seen at 15 days of treatment, and no further changes in these parameters were seen at 1 month. We conclude that propionyl-L-carnitine increases exercise capacity and reduces ventricular size in patients with congestive heart failure. The drug has no significant effects on hemodynamics or neurohormone levels. The use of a single-blind design reduces the impact of the positive finding on exercise capacity.

Adult↗