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Biomedical subjects

C Duilio

Publications and source records attributed to C Duilio.

18 recordsLinked to original sources
PubMed1992

Effects of ischemia and reperfusion on cardiac tolerance to oxidative stress.

Oxidative stress may affect cardiac function and metabolism. Oxidants are normally inactivated by reacting with reduced glutathione (GSH), with resulting formation and release of oxidized glutathione (GSSG). However, ischemia might affect glutathione metabolism. This might render ischemic hearts less resistant against subsequent oxidant injury during reperfusion, and it might also affect the reliability of GSSG measurements as a means to investigate oxidative stress in reperfused hearts. We compared the metabolic and functional consequences of an oxidant load in control rabbit hearts and in hearts reperfused after 30 min of normothermic total ischemia. In controls, H2O2 infusion (H2O2; 5-30 microM) induced a dose-dependent stimulation of GSSG release and a progressive impairment of cardiac function. At these doses, H2O2 challenge of postischemic hearts resulted in biochemical and functional changes identical to those observed in controls. Release of lactate dehydrogenase (LDH) and of GSH was negligible, similar in both groups. In additional experiments, infusion of H2O2 at a much higher dose (200 microM) elicited a further increase in GSSG release from both groups, although GSSG concentrations were lower in postischemic hearts. The functional effects of the 200 microM H2O2 infusion were similar in both groups, all hearts showing rapid and irreversible deterioration of function. Occurrence of irreversible cell injury was also manifested by a large release of LDH and GSH to a similar extent in both groups. These data demonstrate that cardiac tolerance toward oxidants is largely unaffected by a relatively brief episode of severe ischemia and indicate that GSSG release can be reliably used to investigate oxidative stress in reperfused hearts.

Animals↗
PubMed1992

Diastolic perfusion time and exercise posture in coronary artery disease patients: correlation with ST segment changes.

The relationship between either heart rate or diastolic time and ST segment depression has been evaluated during supine and upright exercise in 16 coronary artery disease patients. Diastolic perfusion time and ST segment depression were related by a linear regression, which was independent of exercise posture. The entity of ST segment depression was greater during supine than in upright exercise for the same heart rate. The assessment of the relationship between heart rate and diastolic perfusion time during two exercises showed that at the same heart rate, diastolic perfusion time was shorter in supine posture. In conclusion, the greater entity of ST segment depression induced by supine rather than upright exercise might be explained by the effect of supine posture on diastolic perfusion time.

Coronary Disease↗
PubMed1991

Diastolic perfusion time at ischemic threshold in patients with stress-induced ischemia.

BACKGROUND: To evaluate the relevance of diastolic perfusion time on the mechanisms underlying stress-induced ischemia, 16 patients with coronary artery disease and seven patients with syndrome X underwent five randomized stress tests (upright and supine exercise with and without therapy, transesophageal atrial pacing). METHODS AND RESULTS: Exercise duration Time to 0.1 mV ST segment depression, heart rate, rate-pressure product, and diastolic perfusion time were evaluated for each patient during stress tests. In both groups, variability coefficients of the above-mentioned parameters were not different at rest. At ischemic threshold (0.1 mV ST segment depression) in patients with coronary artery disease, the variability coefficient of exercise duration (40.1 +/- 22.2) was significantly higher (p less than 0.0001) than those of heart rate (12.8 +/- 2.9), rate-pressure product (14.8 +/- 3.3), and diastolic perfusion time (0.39 +/- 0.1). The variability coefficient of diastolic perfusion time was also significantly (p less than 0.0001) lower than those of heart rate and rate-pressure product. Similarly, the variability coefficient of diastolic perfusion time (0.44 +/- 0.1) in syndrome X patients was significantly lower (p less than 0.0001) than those of exercise duration (28.2 +/- 9.4), heart rate (12 +/- 1.4), and rate-pressure product (14.6 +/- 1.3). CONCLUSIONS: Fixed diastolic perfusion time at ischemic threshold, despite different kinds of stress tests and variability of heart rate and rate-pressure product, indicates the relevant role of diastolic perfusion time in determining myocardial ischemia.

Adult↗
PubMed1991

Oxygen radicals generated at reflow induce peroxidation of membrane lipids in reperfused hearts.

To test whether generation of oxygen radicals during postischemic reperfusion might promote peroxidation of cardiac membrane lipids, four groups of Langendorff-perfused rabbit hearts were processed at the end of (a) control perfusion, (b) 30 min of total global ischemia at 37 degrees C without reperfusion, (c) 30 min of ischemia followed by reperfusion with standard perfusate, (d) 30 min of ischemia followed by reperfusion with the oxygen radical scavenger human recombinant superoxide dismutase (h-SOD). The left ventricle was homogenized and tissue content of malonyldialdehyde (MDA), an end product of lipid peroxidation, was measured on the whole homogenate as well as on various subcellular fractions. Reperfusion was accompanied by a significant increase in MDA content of the whole homogenate and of the fraction enriched in mitochondria and lysosomes. This phenomenon was not observed in hearts subjected to ischemia but not reperfused, and was similarly absent in those hearts which received h-SOD at reflow. Reperfused hearts also had significantly greater levels of conjugated dienes (another marker of lipid peroxidation) in the mitochondrial-lysosomal fraction. Again, this phenomenon did not occur in ischemic hearts or in reperfused hearts treated with h-SOD. Unlike the effect on tissue MDA and conjugated dienes, reperfusion did not significantly stimulate release of MDA in the cardiac effluent. Treatment with h-SOD was also associated with significant improvement in the recovery of cardiac function. In conclusion, these data directly demonstrate that postischemic reperfusion results in enhanced lipid peroxidation of cardiac membranes, which can be blocked by h-SOD, and therefore is most likely secondary to oxygen radical generation at reflow.

Acetylglucosaminidase↗
PubMed1991

Diastolic time at ischemic threshold in patients with syndrome X.

The patients with so-called syndrome X experience true myocardial ischaemia in spite of their anatomically normal coronary arteries. The pathogenetic mechanism of the effort-induced ischaemia in these patients should be obviously different from that of patients with atherosclerotic coronary artery lesions. An inadequate coronary dilatory capacity in response to increased oxygen demand has been proposed as mechanism responsible of ischaemic response to effort (Canon et al., 1983; Canon et al., 1985). Since diastolic duration expressed as percentage of the cardiac cycle has implications with the myocardial oxygen demand/supply ratio (Boudoulas et al., 1982; Maseri et al., 1977), the purpose of this study has been to evaluate the behaviour of this parameter at the outcome of the ischaemic electrocardiographic changes during stress testing in the patients with syndrome X.

Adult↗
PubMed1990

Alinidine in chronic stable angina: the effect on diastolic perfusion time.

The present study has been performed to assess the effects of alinidine on diastolic duration during exercise in chronic coronary artery disease. Twelve male patients with stable effort angina and without previous myocardial infarction were studied. They received alinidine or placebo in a double-blind randomized crossover trial for 3 days after a wash-out period of 4 days. Alinidine was administered at a dosage of 30 mg 3 times a day. At the end of each treatment the patients underwent upright bicycle exercise. Left ventricular time intervals were obtained by means of carotid thermistor plethysmography. Diastolic duration was calculated by subtracting the electromechanical systole from the R-R interval and expressed as a percentage of the cardiac cycle (%D). Alinidine increased both total exercise duration from 246.7 +/- 120.7 to 346.6 +/- 114.1 s (p less than 0.05) and time to 0.1-mV ST segment depression from 98.3 +/- 53 to 187.2 +/- 105 s (p less than 0.05). Similarly the drug induced a reduction of the rate-pressure product and of the extent of ischemic ST segment depression during exercise. %D was increased by alinidine both at rest and during exercise. A direct linear regression between R-R and %D was found after both alinidine and placebo treatments either at rest or during exercise. Nevertheless, no difference was observed between both slopes and intercepts. Therefore, since the relationship between R-R interval and %D was unaffected by alinidine, it was possible to hypothesize that the changes in diastolic duration were due only to the bradycardic action of the drug.

Angina Pectoris↗
PubMed1988

Electromechanical events during spontaneous angina.

The electromechanical events occurring during acute myocardial ischemia were assessed in 10 patients who developed spontaneous angina during cardiac catheterization. Aortic pressure and electrocardiogram were recorded, and heart rate and systolic and diastolic time intervals were measured under control conditions, at the onset of angina and during the relief of chest pain. In 5 patients spontaneous angina was accompanied by an increase in heart rate and systemic arterial pressure and by ST segment changes in anterior or anterolateral precordial leads. Diastolic time, expressed as percent of cardiac cycle, shortened from 48.8 +/- 3.6% at rest to 33.6 +/- 4.8% (p less than 0.01) at the onset of angina, as a consequence of a significant increase in both electromechanical systole and heart rate, and returned to control values within 10 min after sublingual nitroglycerin. In the remaining 5 patients, spontaneous angina was accompanied by a decrease in heart rate and systemic arterial pressure and by ST segment changes in the inferior or inferolateral leads. The diastolic time increased significantly (p less than 0.05) from 39.4 +/- 6.1% at rest to 47.8 +/- 9% at the onset of angina, as a consequence of a significant decrease in heart rate and a slight decrease in electromechanical systole. Since coronary perfusion takes place mainly during diastole, our results suggest that the reflex increase in adrenergic tone may worsen myocardial ischemia by affecting diastolic perfusion time. In contrast, the increase in vagal tone may contribute to spontaneous relief of angina by prolonging diastolic perfusion time.

Adult↗
PubMed1987

Thyrotropin regulation of membrane lipid fluidity in the FRTL-5 thyroid cell line. Its relationship to cell growth and functional activity.

The mitogenic effect of thyrotropin on functional rat thyroid cells of the line FRTL-5 is correlated with membrane lipid fluidity as evaluated by fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene. Continued exposure of FRTL-5 cells to a medium lacking thyrotropin causes cessation of cell proliferation and a decrease in membrane lipid fluidity which reaches its minimum in approximately 8 days. The change in lipid fluidity is due to an absolute increase (greater than 2-fold) of membrane cholesterol, with an increased cholesterol/phospholipid ratio and an increased ratio of saturated to unsaturated fatty acids of the membrane phospholipids, contributed primarily by a nearly 4-fold increase in the ratio of saturated to unsaturated C16 fatty acids. It is also associated with a variation of the relative proportions of the major membrane phospholipids; thus, phosphatidylinositol and phosphatidylethanolamine decrease while phosphatidylcholine increases. Both membrane fluidity and lipid composition can be restored by thyrotropin to their original levels, i.e. levels measured under continuous exposure to the hormone. Complete reversal requires at least 48 h, i.e. approximately the same time required for resumption of growth when FRTL-5 cells, starved in thyrotropin, are re-exposed to the hormone. Changes in lipid composition and fluidity can be prevented or can be reversed if FRTL-5 cells are exposed to dibutyryl cAMP while being deprived of thyrotropin. Dibutyryl cAMP has only a modest direct effect on growth; however, this pretreatment eliminates the 48-h lag phase with respect to thyrotropin stimulation. It is proposed that the effects of thyrotropin on growth of FRTL-5 cells requires a modification of the molecular structure and the physical state of cell membranes, which can be mediated by cAMP, although cAMP is not sufficient by itself to promote growth.

Animals↗
PubMed1985

Alteration of erythrocyte membrane lipid fluidity in human obesity.

The lipophilic probe 1,6-diphenyl-1,3,5-hexatriene was incorporated into erythrocyte ghosts of either normal or obese humans, and the polarization of fluorescence was measured between 0 and 40 C. The membrane lipid fluidity, evaluated by fluorescence polarization, was consistently higher in the ghosts from obese subjects. A strong correlation was found between increased 1,6-diphenyl-1,3,5-hexatriene fluorescence polarization and excess body weight. Measurements of cholesterol and phospholipids indicated increased cholesterol and decreased phospholipids in erythrocyte ghosts from obese subjects. These data suggest that alterations in lipid composition in erythrocytes of obese subjects are responsible for abnormal physical properties of plasma membranes, which, in turn, may cause altered enzymatic activities.

Adolescent↗