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Biomedical subjects

M Romano

Publications and source records attributed to M Romano.

At least 271 records · Page 15Linked to original sources
PubMed1993

[The practical aspects of treatment in heart failure].

Congestive heart failure (CHF) has been treated for several years on empiric basis, until the results of the major clinical trials have made possible a pathophysiological approach to the treatment of patients with CHF. Studies from our laboratories have demonstrated that hemodynamic and neurohormonal responses to acute volume expansion are markedly impaired in patients with dilated cardiomyopathy and mild heart failure (NYHA Class I) and that pretreatment with ACE-inhibitors is able to prevent these abnormal responses. New insights into a more pathophysiological approach to CHF treatment are now possible by the development of new noninvasive techniques for the study of cardiac function. In particular, through radionuclide techniques we were able to demonstrate that patients with CHF show an exercise induced hemodynamic response different from that of normal subjects. Both ACE-inhibitors and digitalis were able to restore a normal response to exercise in patients with CHF.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

[Contribution of new technologies to the management of acute complications of coronary angioplasty].

This retrospective study of 4,000 coronary angioplasty procedures performed between 1/1/87 and 31/1/92 was undertaken to assess the benefits of new therapeutic options (perfusion balloon catheter, temporary and permanent stenting, laser balloon angioplasty, cardiopulmonary bypass) in the management of major complications of angioplasty and to evaluate the results of emergency coronary bypass surgery. Angioplasty was performed before (1,000 angioplasties: Group 1) and after (3,000 angioplasties: Group 2) the introduction of these new techniques at the Centre cardiologique du Nord. Despite the increasing complexity of the clinical and angiographic features of the patients, the global results show a significant decrease in the rates of emergency bypass surgery (2.1% in Group 1 versus 0.7% in Group 2; p < 0.0015) and of periprocedural acute myocardial infarctions (1.8% in Group 1 versus 0.7% in Group 2; p < 0.015). The use of these new techniques in cases of acute complications of coronary angioplasty decreases the signs of ischaemia before surgery (61.9% in Group 1 versus 68.1% in Group 2; p < 0.05). Coronary bypass surgery was performed under haemodynamically stable conditions in all patients requiring the procedure in Group 2, enabling the surgeon to perform more complete revascularisation with implantation of the mammary artery in 50% of cases (9.5% of cases in Group 1; p < 0.001). The interval to emergency bypass surgery depends mainly on the rapidity of the operative decision in cases of failure of these new techniques.

Angioplasty, Balloon↗
PubMed1993

[Echo-color Doppler in thyroid disease].

One-hundred and sixty-six patients affected with thyroid diseases were examined, together with 41 healthy volunteers, by means of color-Doppler US. Four main reference patterns were identified: no appreciable glandular flow (I); presence of signal in perinodular location (II); peri- and intranodular flow (III); increased vascularization (IV). In 72 cases, parenchymal and nodular goiters, with no signs of thyroid hyperfunction, were characterized as belonging to pattern III, while pattern II was observed in 57 nodular lesions; only in 7 patients was pattern III detected. Hyperfunctioning autonomous nodules exhibited pattern III in 10/11 cases and the same pattern was followed by the six carcinomas. Pattern IV resulted peculiar to Basedow disease and to glandular hyperplasia related to high values of circulating thyroid hormone (6 cases). When color-Doppler specificity in typifying the major thyreopathies can be confirmed, the possibility is actually in sight of reducing, in the near future, the number of thyroid scintigraphies and of US-guided needle biopsies.

Adolescent↗
PubMed1993

Decision-making model for a non-invasive diagnosis of compensated liver cirrhosis.

Liver biopsy is used as a gold standard in the diagnosis of chronic liver disease. However, this procedure is not without risk to the patients. This study was aimed to evaluate whether clinical, ultrasonographic, and biochemical variables may discriminate between well-compensated liver cirrhosis and non-cirrhotic chronic liver disease. Logistic regression analysis was used to assess the independent predictive value of each variable. Moreover, the post-test probability of the diagnostic variables was converted into "weights" which positively correlated with the likelihood of diagnosis of liver cirrhosis. We applied a decisional rule based on the diagnostic "weight" of each variable to 412 patients, 278 with well-compensated liver cirrhosis and 134 with non-cirrhotic chronic liver disease, diagnosed by liver biopsy with/without laparoscopy. By adding the diagnostic "weights" of each variable, liver cirrhosis and non-cirrhotic chronic liver disease were correctly diagnosed in 67% and 75% of cases, respectively. This result was validated in a split sample of 100 patients (50 with compensated liver cirrhosis and 50 with non-cirrhotic chronic liver disease) randomly selected from the acquisition sample. Based on this data, diagnosis of well-compensated liver cirrhosis can be reached in over 67% of cases without using invasive procedures. However, a prospective study is needed to confirm the clinical reliability of this method.

Adult↗
PubMed1992

Lipoxin generation by permeabilized human platelets.

Human platelets convert leukocyte-derived leukotriene (LT) A4 to lipoxins during transcellular lipoxin biosynthesis. Here, we examined lipoxin generation in intact human platelets and compared it with that elicited from permeabilized platelets. Conversion of LTA4 to lipoxins by permeabilized cells exceeded (10-15 times) that to peptidoleukotrienes, while intact cells exposed to thrombin generated similar amounts of these two series (LT/LX). Permeabilized platelets also generated 3-5 times more lipoxins than intact cells. Lipoxin A4 (LXA4), lipoxin B4 (LXB4), and their respective all-trans isomers were identified by physical methods including HPLC and GC-MS. Chiral analysis of platelet-derived all-trans-containing LXs revealed that greater than 69.5 +/- 0.5% carried alcohol groups in the R configuration at carbons 6 and 14 (e.g., 11-trans-LXA4 and 8-trans-LXB4), respectively. More than 50% of these all-trans LX were formed by isomerization of native LXA4 and LXB4 during isolation. Lipoxin formation with permeabilized platelets gave an apparent Km of 8.9 microM and Vmax of 83.3 ng/(min-10(9) platelets) with maximal conversion in pH range 7-9. In addition, permeabilized platelets converted 14,15-LTA4 and LTA5, but not LTA3, to lipoxins. Consecutive exposure to LTA4 did not alter LXA4 generation but inhibited LXB4 by 40-50%, suggesting that LXB4 formation can be regulated by suicide inactivation. Unlike platelets, human endothelial cells did not convert LTA4 to lipoxins. These results indicate that lipoxin formation is a major route of LTA4 metabolism in thrombin-activated platelets and those that have undergone a loss of membrane barriers.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1992

Lipoxin generation by human megakaryocyte-induced 12-lipoxygenase.

Eicosanoid biosynthesis was examined with a human megakaryocytic cell line (Dami). Megakaryocytes incubated with [1-14C]arachidonic acid and either ionophore A23187 or thrombin generated both thromboxane and 12-hydroxyheptadecatrienoic acid (HHTrE). Exposure to phorbol myristate acetate (PMA) for 1 through 9 days induced differentiation and revealed an increase in the conversion of [1-14C]arachidonate to cyclooxygenase- and lipoxygenase (LO)-derived products. The LO-derived product was identified as 12S-HETE by its physical characteristics including GC/MS and chiral column SP-HPLC. PMA-treated Dami cells did not generate 5-HETE, leukotrienes or lipoxins from exogenous arachidonic acid while they did convert leukotriene A4 (LTA4) to lipoxin A4, lipoxin B4 and their respective all-trans isomers. In addition, COS-M6 cells transfected with a human 12-lipoxygenase cDNA and incubated with either arachidonic acid or LTA4 generated 12-HETE and lipoxins, respectively. The lipoxin profile generated by transfected COS-M6 cells incubated with LTA4 was similar to that generated by the PMA-treated Dami cells. Results indicate that human megakaryocytes can transform arachidonate and LTA4 to bioactive eicosanoids and that the 12-lipoxygenase appears upon further differentiation of these cells. In addition, they indicate that the 12-LO of human megakaryocytes and the 12-LO expressed by transfected COS cells can generate both lipoxins A4 and B4. Together they suggest that the human 12-LO can serve as a model of LX-synthetase activity with LTA4.

Arachidonate 12-Lipoxygenase↗
PubMed1992

Influence of atenolol on the relationship between heart rate and QT interval in patients with exercise-induced myocardial ischemia.

The aim of this study was to analyze the relationship between heart rate and QT interval (HR-QT) during exercise in control subjects (Group A) and in patients with coronary artery disease (CAD) with effort angina and without previous myocardial infarction (MI) (Group B). The diagnosis of CAD was confirmed by coronarographic examination. The correlation HR-QT was significant (p < 0.001) in both groups on effort and at recovery. The analysis of the regression HR-QT was carried out separately, both on effort in upright position and at rest in supine position, to avoid the influence of posture on QT length. During effort, the regression line showed lower slope and intercept values in Group B (p < 0.001) than those for Group A. A similar behavior was also observed at rest. Thus, at the highest heart rate, where ECG signs of ischemia (ST depression > 1 mm) frequently occurred, a longer QT interval was present in Group B. Moreover, in Group B, the QT interval in the presence of ECG signs of ischemia was significantly longer (p < 0.01) than in Group A at comparable heart rates both on effort and at rest, thereby confirming the result obtained by comparing both regression lines. The same effort protocol was repeated in Group B patients after acute administration of atenolol 100 mg per os. After atenolol administration, the analysis of the regression HR-QT in Group B clearly showed a shorter QT interval than that obtained in washout period during the baseline test at the highest heart rates where the ECG frequently showed signs of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Beyond cold cardioplegia.

One hundred fifteen consecutive patients were operated on for myocardial revascularization or valvular disease or both with continuous antegrade and retrograde aerobic warm (37 degrees C) blood cardioplegia. Mean cross-clamp time was 56.3 +/- 21 minutes (+/- standard deviation). Mean reperfusion time was 18.4 +/- 11.8 minutes (range, 5 to 81 minutes). Five patients (4.3%) died, and 15 (13%) needed inotropic support. Two (1.7%) required intraaortic balloon support. Two patients (1.7%) had evidence of perioperative myocardial infarction, and 98 (85%) returned spontaneously to normal sinus rhythm. Sixteen patients had a cross-clamp time greater than 80 minutes. All 16 of them had an uneventful postoperative course except for 1 patient who required inotropic drugs. This method of myocardial protection is now used for all open heart procedures in our institution.

Adult↗
PubMed1992

A novel pharmacological approach for paraquat poisoning in rat and A549 cell line using ambroxol, a lung surfactant synthesis inducer.

Paraquat (PQ) is a widely used herbicide that causes acute adult respiratory distress syndrome (ARDS) and chronic lung damage (diffuse fibrosis). One of the earliest biochemical effects induced by PQ is damage to type II pneumocytes with consequent depletion of surfactant. With the aim of counteracting the toxic effects of PQ, a series of investigations were performed into the possible protective effect of the drug ambroxol, which induces the synthesis of surfactant in lung alveolar type II cells. The number of survivors and survival time of rats treated ip with 35 mg PQ/kg was significantly increased by 3 days of ambroxol pretreatment and by ambroxol treatment 30 min or 2 hr after PQ. Total phospholipid content in lung and bronchoalveolar lavage fluid (BALF) was significantly reduced 30 hr after treatment with PQ alone. The association of ambroxol with PQ significantly antagonized this reduction. In BALF the ratio between palmitic acid and stearic acid concentrations was significantly lower in animals treated with PQ alone but was returned to normal by the association with ambroxol. The cell line A549, exposed in vitro to PQ concentrations from 0.5 x 10(-4) to 2 x 10(-3) M, showed a significant dose-dependent loss of viability. Cells pretreated with ambroxol (10 mg/ml) were more resistant to PQ and their viability started to decrease significantly only from a PQ concentration of 0.8 x 10(-3) M. Membrane microviscosity was measured on the same cells. Cells treated with PQ alone showed a reduction of membrane microviscosity, which was significantly counteracted by ambroxol pretreatment. The curves of modification of membrane microviscosity of cells treated with PQ and with ambroxol plus PQ paralleled those of cell viability, indicating that the stimulation of surfactant synthesis in vitro may be a prerequisite for counteracting some of the early effects of PQ.

Adenocarcinoma↗
PubMed1992

Cysteamine protects gastric epithelial cell monolayers against drug induced damage: evidence for direct cellular protection by sulphydryl compounds.

The sulphydryl containing drug cysteamine protects gastric mucosa in vivo against acute injury. It is not known whether this protection includes a direct effect on gastric cells. Using gastric epithelial cell monolayers derived from a well differentiated human cell line, we evaluated whether cysteamine protects against taurocholate or indomethacin induced damage in conditions which completely exclude the influence of vascular, hormonal, and neural factors. The effect of cysteamine on prostaglandin production by monolayer cells in vitro was also assessed. Cysteamine decreased damage brought about by sodium taurocholate and indomethacin by 40% (p less than 0.01) and 50% (p less than 0.01) respectively. The sulphydryl blocker iodoacetamide prevented the protective effect of cysteamine. Pretreatment with indomethacin, which inhibited prostaglandin E2 output by 60%, did not prevent protection by cysteamine; incubation with cysteamine decreased prostaglandin E2 production by cultured cells. We conclude that (i) cysteamine directly protected gastric epithelial cells in vitro (ii) this protection occurred with indomethacin, which interferes with cellular metabolism of prostaglandins, and taurocholate, whose damaging action at neutral pH is unrelated to interference with prostanoid metabolism, (iii) cysteamine protection in vitro is unrelated to endogenous prostaglandins and is probably mediated by endogenous sulphydryl compounds.

Cell Line↗
PubMed1992

Angiotensin converting enzyme inhibition restores cardiac and hormonal responses to volume overload in patients with dilated cardiomyopathy and mild heart failure.

BACKGROUND: Angiotensin converting enzyme (ACE) inhibition exerts a favorable effect on the response to exercise in heart failure. This study was planned to define the influence of ACE inhibition on the adaptation to volume overload. METHODS AND RESULTS: We studied the hemodynamic, hormonal, and renal responses to acute volume expansion (sodium chloride, 0.9%, 0.25 ml.kg-1.min-1 for 2 hours) in patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (New York Heart Association class I or II, ejection fraction < or = 50%). The patients were studied without any pretreatment (n = 14) or after 1 week of treatment with the oral ACE inhibitor quinapril at a dosage of 10 mg/day (n = 11). Seven patients were studied during constant intravenous infusion with nitroglycerin (0.1 micrograms.kg-1.min-1). The study groups had similar hemodynamic and clinical characteristics and hormonal profile at baseline evaluation. In the untreated patients, volume expansion did not increase left ventricular end-diastolic volume measured by echocardiography and was associated with a reduction in ejection fraction (p < 0.05) and with a paradoxical increase in forearm vascular resistance (p < 0.05) estimated by plethysmography. In addition, plasma atrial natriuretic factor did not change, and plasma norepinephrine was increased by saline loading. In contrast, in the patients treated with quinapril, volume expansion induced an increase of both left ventricular volumes (p < 0.001) without changing ejection fraction and reduced forearm vascular resistance (p < 0.05). In addition, in this group, plasma atrial natriuretic factor levels increased (p < 0.05) and plasma norepinephrine did not change during volume overload. During nitroglycerin infusion, volume expansion was associated with peripheral vasodilatation, increases of left ventricular volumes, and no change in ejection fraction. In this group, however, plasma atrial natriuretic factor levels did not change in response to volume overload. CONCLUSIONS: We conclude that pretreatment with the ACE inhibitor quinapril significantly improves compromised responses to acute isotonic volume overload in patients with dilated cardiomyopathy and mild heart failure. The favorable influence of ACE inhibition on cardiovascular and hormonal responses to volume expansion seems to be related to the cardiac unloading produced by this treatment.

Adult↗
PubMed1992

Transforming growth factor alpha protection against drug-induced injury to the rat gastric mucosa in vivo.

This study was designed to determine whether transforming growth factor alpha (TGF alpha) protects rat gastric mucosa against ethanol- and aspirin-induced injury. Systemic administration of TGF alpha dose-dependently decreased 100% ethanol-induced gastric mucosal injury; a dose of 50 micrograms/kg delivered intraperitoneally 15 min before ethanol decreased macroscopic mucosal injury by > 90%. At the microscopic level, TGF alpha prevented deep gastric necrotic lesions and reduced disruption of surface epithelium. Pretreatment with orogastric TGF alpha (200 micrograms/kg) only partially (40%) decreased macroscopic ethanol damage. Intraperitoneal administration of TGF alpha at a dose of 10 micrograms/kg, which does not significantly inhibit gastric acid secretion, decreased aspirin-induced macroscopic damage by > 80%. TGF alpha protection does not seem to be mediated by prostaglandin, glutathione, or ornithine decarboxylase-related events, as evidenced by lack of influence of the inhibition of their production. Pretreatment with the sulfhydryl blocking agent N-ethylmaleimide partially abolished (40%) the protective effect of TGF alpha. In addition, systemic administration of TGF alpha resulted in a two-fold increase in tyrosine phosphorylation of phospholipase C-gamma 1 and in a time- and dose-dependent increase in levels of immunoreactive insoluble gastric mucin; these events occurred in a time frame consistent with their participation in the protective effect of TGF alpha.

Animals↗
PubMed1992

[Heart surgery in normothermia and aerobiosis: apropos of 530 patients].

Between February and October 1991, 530 consecutive patients underwent myocardial revascularization or valvular surgery with warm continuous antegrade and retrograde cardioplegia (37 degrees C). Three hundred and thirty three patients had isolated myocardial revascularization, 159 valvular surgery alone and 25 had combined valvular and coronary bypass. The global mortality was 5.1%, 3.7% for coronary bypass, 7.5% for valvular surgery and 8% for combined valvular and coronary surgery. A multivariate analysis identified the "reperfusion time" as the only predictive factor of hospital mortality (p < 0.001). Intraortic balloon counterpulsation was required postoperatively in 3.2% of cases, 5.2% of coronary bypass and 0.8% of the valvular patients. Inotropic drugs were used to come off cardiopulmonary bypass in 16.5% of coronary and 37.5% of valvular patients. There were 0.9% perioperative infarctions: 1.2% in the coronary bypass cases and 0.6% in the valvular cases. Spontaneous return to sinus rythm was observed in 87.9% of cases. The average "reperfusion time" was 20.48 +/- 0.7 mn. Analysis of the influence of aortic cross clamp time on cardiac morbidity in two groups of coronary patients (Group I: short cross clamp time less than 60 mn; Group II: long cross clamp time, 60 to 33 mn) showed that the hospital mortality, the prevalence of the use of inotropic drugs and balloon counterpulsation the postoperative cardiac index, the rate of spontaneous de fibrillation and the reperfusion time did not depend on the aortic cross clamp time. Cardiac morbidity.

Adolescent↗
PubMed1992

[Current role of reconstructive surgery in the treatment of acute mediastinitis after cardiac surgery].

Infected median sternotomy often requires wide debridement. A large thoracic defect usually results with subsequent exposition of heart, great vessels, aortocoronary bypass grafting, vascular prosthesis. Coverage with muscles transplantation was the standard procedure carried out in this series of 150 cases observed between 1983 and 1991. Details of technique are presented as well as a review of our reconstructive options. Rewarding results were observed even in the most challenging circumstances, suggesting that pursuing this aggressive approach was warranted.

Acute Disease↗
PubMed1991

Endotoxic lipid A induces intracellular Ca2+ increase in human platelets.

The activation of protein kinase C by endotoxic lipid A was observed with both intact platelets and in a cell-free system [Romano & Hawiger (1990) J. Biol. Chem. 265, 1765-1770]. We have now studied the action of lipid A on intracellular Ca2+ concentration ([Ca2+]i). Lipid A induced a concentration-dependent rise in [Ca2+]i in human platelets loaded with fura-2, which reached a maximum at 37.1 +/- 3.8 s (tmax). Maximum [Ca2+]i levels, observed at 30 microM lipid A, were 432 +/- 60 nM. EGTA (2 mM) or NiCl2 (1 mM) each decreased the lipid A-dependent elevation of [Ca2+]i by 50-60% without significant modification of tmax, but shortening the time for 50% recovery (t50) from greater than 400 s to 113.1 +/- 29.1 s and 54 +/- 2.1 s, respectively. Quenching of the fura-2 signal was also observed in lipid A-stimulated platelets resuspended with MnCl2 (1 mM), suggesting that both mobilization and external influx of Ca2+ occur. Intracellular Ca2+ mobilization depended on release from Ins(1,4,5)P3-sensitive stores, since Ins(1,4,5)P3 accumulation was detected in lipid A-activated platelets. Staurosporine, an inhibitor of protein kinase C, blocked the [Ca2+]i rise generated by lipid A in platelets [concn. giving 50% inhibition (IC50) = 0.1 microM], prolonging the tmax. to 54.7 +/- 5.1 s, but decreasing the t50 to 157.5 +/- 31.8 s. Staurosporine also suppressed InsP3 accumulation (IC50 = 0.15 microM). These results suggest that platelet activation by lipid A involves an interaction between [Ca2+]i elevation and protein kinase C activation.

Blood Platelets↗