PubMed Health⌕ Search

Biomedical subjects

M Pistolese

Publications and source records attributed to M Pistolese.

At least 19 recordsLinked to original sources
PubMed2006

Protective effect of melatonin against mitochondrial dysfunction associated with cardiac ischemia- reperfusion: role of cardiolipin.

Reactive oxygen species (ROS) are considered an important factor in ischemia/reperfusion injury to cardiac myocytes. Mitochondrial respiration, mainly at the level of complex I and III, is an important source of ROS generation and hence a potential contributor of cardiac reperfusion injury. Appropriate antioxidant strategies could be particularly useful to limit this ROS generation and associated mitochondrial dysfunction. Melatonin has been shown to effectively protect against ischemic-reperfusion myocardial damage. The mechanism by which melatonin exerts this cardioprotective effect is not well established. In the present study we examined the effects of melatonin on various parameters of mitochondrial bioenergetics in a Langerdoff isolated perfused rat heart model. After isolation of mitochondria from control, ischemic-reperfused and melatonin-treated ischemic-reperfused rat heart, various bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, complex I and complex III activity, H2O2 production as well as the degree of lipid peroxidation, cardiolipin content, and cardiolipin oxidation. We found that reperfusion significantly altered all these mitochondrial parameters, while melatonin treatment had strong protective effect attenuating these alterations. This effect appears to be due, at least in part, to the preservation, by ROS attack, of the content and integrity of cardiolipin molecules which play a pivotal role in mitochondrial bioenergetics. Protection of mitochondrial dysfunction was associated with an improvement of post-ischemic hemodynamic function of the heart. Melatonin had also strong protective effect against oxidative alterations to complex I and III as well as to cardiolipin in isolated mitochondria.

Animals↗
PubMed2005

Mitochondrial dysfunction associated with cardiac ischemia/reperfusion can be attenuated by oxygen tension control. Role of oxygen-free radicals and cardiolipin.

Reactive oxygen species (ROS) are considered an important factor in ischemia/reperfusion injury to cardiac myocites. Mitochondrial respiration is an important source of ROS generation and hence a potential contributor to cardiac reperfusion injury. Appropriate treatment strategy could be particularly useful to limit this ROS generation and associated mitochondrial dysfunction. In the present study, we examined the effect of lowering the oxygen tension, at the onset of the reperfusion, on various parameters of mitochondrial bioenergetics in rat heart tissue. After isolation of mitochondria from control, ischemic, normoxic and hypoxic reperfused rat heart, various bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, complex I and complex III activity, H2O2 production and in addition, the degree of lipid peroxidation, cardiolipin content and cardiolipin oxidation. We found that normoxic reperfusion significantly altered all these mitochondrial parameters, while hypoxic reperfusion had a protective effect attenuating these alterations. This effect appears to be due, at least in part, to a reduction of mitochondrial ROS generation with subsequent preservation of cardiolipin integrity, protection of mitochondrial function and improvement of post-ischemic hemodynamic function of the heart.

Animals↗
PubMed2001

Reactive oxygen species generated from the mitochondrial electron transport chain induce cytochrome c dissociation from beef-heart submitochondrial particles via cardiolipin peroxidation. Possible role in the apoptosis.

Cytochrome c release from mitochondria is a critical event in the apoptosis induction. Dissociation of cytochrome c from the mitochondrial inner membrane (IMM) is a necessary first step for cytochrome c release. In the present study, the effect of reactive oxygen species (ROS) on the dissociation of cytochrome c from beef-heart submitochondrial particles (SMP) and on the cardiolipin content was investigated. Exposure of SMP to mitochondrial-mediated ROS generation resulted in a large dissociation of cytochrome c from SMP and in a parallel loss of cardiolipin. Both these effects were directly and significantly correlated and also abolished by superoxide dismutase+catalase. These results demonstrate that ROS generation induces the dissociation of cytochrome c from IMM via cardiolipin peroxidation. The data may prove useful in clarifying the molecular mechanism underlying the release of cytochrome c from the mitochondria to the cytosol.

Animals↗
PubMed2001

Reactive oxygen species generated by the mitochondrial respiratory chain affect the complex III activity via cardiolipin peroxidation in beef-heart submitochondrial particles.

The aim of this study was to investigate the effect of reactive oxygen species (ROS), produced by the mitochondrial respiratory chain, on the activity of complex III and on the cardiolipin content in bovine-heart submitochondrial particles (SMP). ROS were produced by treatment of nicotinamide adenine dinucleotide (NADH) respiring SMP with rotenone. This treatment resulted in a production of superoxide anion, detected by the epinephrine method, which was blocked by superoxide dismutase (SOD). Exposure of SMP to mitochondrial-mediated ROS generation resulted in a marked loss of complex III activity and in a parallel loss of mitochondrial cardiolipin content. Both these effects were completely abolished by SOD + catalase. Exogenous added cardiolipin was able to almost completely prevent the ROS-mediated loss of complex III activity. No effect was obtained with other major phospholipid components of the mitochondrial membrane such as phosphatidylcholine and phosphatidylethanolamine, or with peroxidized cardiolipin. The results demonstrate that mitochondrial-mediated ROS generation affects the activity of complex III via peroxidation of cardiolipin, which is required for the functioning of this multisubunit enzyme complex. These results may prove useful in probing molecular mechanisms of ROS-induced peroxidative damage to mitochondria, which have been proposed to contribute to those physiopathological conditions characterized by an increase in the basal production of ROS such as aging, ischemia/reperfusion and chronic degenerative diseases.

Journal Article↗
PubMed2000

The effect of reactive oxygen species generated from the mitochondrial electron transport chain on the cytochrome c oxidase activity and on the cardiolipin content in bovine heart submitochondrial particles.

The effect of reactive oxygen species (ROS), produced by the mitochondrial respiratory chain, on the activity of cytochrome c oxidase and on the cardiolipin content in bovine heart submitochondrial particles (SMP) was studied. ROS were produced by treatment of succinate-respiring SMP with antimycin A. This treatment resulted in a large production of superoxide anion, measured by epinephrine method, which was blocked by superoxide dismutase (SOD). Exposure of SMP to mitochondrial mediated ROS generation, led to a marked loss of cytochrome c oxidase activity and to a parallel loss of cardiolipin content. Both these effects were completely abolished by SOD+catalase. Added cardiolipin was able to almost completely restore the ROS-induced loss of cytochrome c oxidase activity. No restoration was obtained with peroxidized cardiolipin. These results demonstrate that mitochondrial mediated ROS generation affects the activity of cytochrome c oxidase via peroxidation of cardiolipin which is needed for the optimal functioning of this enzyme complex. These results may prove useful in probing molecular mechanism of ROS-induced peroxidative damage to mitochondria which have been proposed to contribute to aging, ischemia/reperfusion and chronic degenerative diseases.

Animals↗
PubMed1999

Lipid peroxidation and alterations to oxidative metabolism in mitochondria isolated from rat heart subjected to ischemia and reperfusion.

Ischemia-reperfusion injury to cardiac myocytes involves membrane damage mediated by oxygen free radicals. Lipid peroxidation is considered a major mechanism of oxygen free radical toxicity in reperfused heart. Mitochondrial respiration is an important source of these reactive oxygen species and hence a potential contributor to reperfusion injury. We have examined the effects of ischemia (30 min) and ischemia followed by reperfusion (15 min) of rat hearts, on the kinetic parameters of cytochrome c oxidase, on the respiratory activities and on the phospholipid composition in isolated mitochondria. Mitochondrial content of malonyldialdheyde (MDA), an index of lipid peroxidation, was also measured. Reperfusion was accompanied by a significant increase in MDA production. Mitochondrial preparations from control, ischemic and reperfused rat heart had equivalent Km values for cytochrome c, although the maximal activity of the oxidase was 25 and 51% less in ischemic and reperfused mitochondria than that of controls. These changes in the cytochrome c oxidase activity were associated to parallel changes in state 3 mitochondrial respiration. The cytochrome aa3 content was practically the same in these three types of mitochondria. Alterations were found in the mitochondrial content of the major phospholipid classes, the most pronounced change occurring in the cardiolipin, the level that decreased by 28 and by 50% as function of ischemia and reperfusion, respectively. The lower cytochrome c oxidase activity in mitochondria from reperfused rat hearts could be almost completely restored to the level of control hearts by exogenously added cardiolipin, but not by other phospholipids nor by peroxidized cardiolipin. It is proposed that the reperfusion-induced decline in the mitochondrial cytochrome c oxidase activity can be ascribed, at least in part, to a loss of cardiolipin content, due to peroxidative attack of its unsaturated fatty acids by oxygen free radicals. These findings may provide an explanation for some of the factors that lead to myocardial reperfusion injury.

Animals↗
PubMed1990

Transcutaneous cardiac pacing: evaluation of cardiac activation.

The effects of transcutaneous cardiac pacing (TCP) on cardiac activation were evaluated by endocavitary recording (HRA, RVA) in eight patients, in order to test the possibility to obtain a simultaneous atrial and ventricular stimulation. The transcutaneous pacemaker used was the Pace Aid 52 (pacing rate 50-160 ppm, current output 10-150 mA, pulse width 20 sec). The two skin electrodes (surface area 50 cm2) were placed on the chest in anteroposterior position. Ventricular capture was observed in all patients (threshold = 74 +/- 14 mA), simultaneous atrial capture was obtained in only four cases (threshold = 138 +/- 25 mA). In conclusion, our data show that four-chamber simultaneous stimulation by TCP is possible, but only with pacing energies much higher than those usually required to capture the ventricle. The ability of TCP to simultaneously pace the atria and ventricles, though not relevant in the emergency cardiac stimulation for symptomatic severe bradyarrhythmias, could be useful in the treatment of reentrant supraventricular tachycardias.

Adult↗
PubMed1990

Transcutaneous cardiac pacing for termination of tachyarrhythmias.

Transcutaneous cardiac pacing (TCP) was used for interruption of tachyarrhythmias in 31 patients: 20 with ventricular tachycardia (VT); eight with atrioventricular reentrant tachycardia (AVRT) and three had atrioventricular nodal tachycardia (AVNT). The stimulators used (Pace Aid 50/52) allow pacing at programmable rates (50-160 ppm) and output (10-200 mA at 20-msec pulse duration), when possible overdrive pacing was used. Short bursts of stimuli were delivered with increasing current intensity until interruption of the arrhythmia or to the maximum energy tolerated by the patient. VTs were interrupted in eight of the 20 patients: four of the six (67%) treated by overdrive pacing and four of the 14 (29%) were treated by underdrive pacing. Supraventricular tachycardias (SVT) were terminated in eight of the 11 patients: seven out of eight (88%) AVT, and one out of three AVNT (33%). We observed two cases of arrhythmia worsening: a VT acceleration and induction of ventricular fibrillation in a patient with AVNT. TCP was well tolerated by the majority of the patients. We conclude that TCP is an effective method for interruption of ventricular and supraventricular reentrant tachycardias, but the risk of arrhythmia worsening must be considered.

Cardiac Pacing, Artificial↗
PubMed1990

Emergency cardiac pacing for severe bradycardia.

UNLABELLED: Our study included the treatment of transcutaneous cardiac pacing (TCP) in 32 patients: (A) 19 patients were treated in the emergency area for complete symptomatic AV block before endocavitary pacing; (B) five patients were in asystole following DC shock or out-of-hospital cardiac arrest; and (C) eight patients were affected by bifascicular block undergoing emergency surgery and were treated in order to prevent complete AV block. Two transcutaneous stimulators were used. PaceAid-CRC model 50/52 with 20-msec pulse width; the electrodes were positioned on the V3 ECG position and on the back. RESULTS: in all but two patients, it was possible to obtain stable cardiac capture; in one patient arrived in hospital in asystole after prolonged cardiac arrest and in the other one was affected by complete AV block, TCP was ineffective. In groups A and B, TCP was maintained for a mean time of 15 minutes; in group C, TCP was tested in all patients, but performed in only one patient during surgery. Mean threshold was 81 mA. Stimulation was well tolerated in all but five patients. TCP is a reliable, noninvasive method that offers the possibility to initiate pacing within seconds and can be used by medical staff. In our opinion, it should be considered as the first choice emergency treatment of severe symptomatic bradycardia. In asystole, beneficial effects can be obtained only if TCP is performed early enough after the onset of arrhythmia.

Adult↗
PubMed1989

Effectiveness of intravenous propafenone for conversion of atrial fibrillation and flutter of recent onset.

The efficacy of intravenous propafenone (2 mg/kg) was assessed in 83 consecutive patients: 68 with atrial fibrillation (AF) and 15 with atrial flutter lasting less than 15 days. Conversion to sinus rhythm occurred in 47 patients (57%), including 42 (62%) of those with AF and 5 (33%) of those with atrial flutter (p less than 0.05). The mean time to conversion was 29 +/- 24 minutes. The success rate was strongly affected by arrhythmia duration. Thus, conversion occurred in 40 patients (71%) among the 56 with arrhythmia lasting less than 48 hours but in 7 patients (26%) among the 27 with a longer lasting arrhythmia (p less than 0.0005). Left atrial size (determined echocardiographically in 56 patients) was significantly larger in nonconverters (49 +/- 12 vs 39 +/- 7 mm, p less than 0.0005). In nonconverters the mean ventricular rate decreased from 141 +/- 26 to 104 +/- 22 beats/min (p less than 0.0005). Except for reversible low output state in 3 patients already hemodynamically compromised, no significant side effects were observed. In conclusion, (1) intravenous propafenone allows a quick restoration of sinus rhythm in the majority of patients with AF of recent onset, whereas it seems less effective in atrial flutter; (2) its efficacy is influenced by the duration of the arrhythmia and by left atrial dimensions; (3) the drug allows control of ventricular rate; and (4) its use seems to be safe except in patients with severe cardiac failure.

Adult↗
PubMed1989

Treatment of ventricular and supraventricular tachyarrhythmias by transcutaneous cardiac pacing.

The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.

Cardiac Pacing, Artificial↗
PubMed1987

[Fibrillation and atrial flutter. Immediate control and conversion to sinus rhythm with intravenous propafenone].

The safety and efficacy of intravenous Propafenone, in the treatment of atrial fibrillation (a.f.) or flutter (A.F.) of recent onset (15 days), were assessed. Propafenone (2 mg/kg) was administered to 36 consecutive patients (mean age 60.8 years), 28 with a.f. and 8 with A.F. Nineteen patients (52.7%) reverted to sinus rhythm within 85 min (mean 27.2 min): 17 of 28 (60.7%) with a.f. and 2 of 8 (25%) with A.F. The efficacy of the drug was significantly influenced by the time elapsed from the onset of the arrhythmia: 14/21 (66.6%) patients with the arrhythmia lasting less then 48 hours and only 5/15 (33.3%) of those with the arrhythmia lasting more than 48 hours or of unknown onset, were converted (p less than 0.05). 18 patients underwent echocardiographic control: mean left atrial dimensions were 41.4 +/- 11.4 mm in converters and 47.4 +/- 11.2 mm in non converters (p = NS). Mean QRS lengthening observed was 16% (from 89 +/- 35.1 to 103.5 +/- 48.8 msec) (p = NS); QTc interval increased from 390 +/- 64.3 to 403 +/- 36.2 msec (p = NS). Arterial blood pressure showed significant changes only in two patients in whom a serious hypotension developed, needing infusion of adrenergic drugs. Non converters showed a reduction of the ventricular rate from 141.8 +/- 29.4/min to 101.8 +/- 18/min (p less than 0.01) meanwhile the shortest RR interval increased from 359.5 +/- 60.8 to 450 +/- 81.5 msec (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Transvenous cardioversion in the treatment of sustained ventricular tachycardia. Preliminary results in 3 patients with implantable cardioverter].

The efficacy of intracardiac cardioversion was verified in 11 pts suffering from coronary heart disease and recurrent sustained VT. All pts were receiving anti-arrhythmic drugs. Tachycardia cycle length was between 280 and 400 msec. 65 episodes of VT (21 spontaneous and 44 induced) were treated with synchronized shocks of low energy between 0.27 and 2 J using the external cardioverter. Cardioversion was successful in 83% of VT episodes. VT acceleration occurred in one case; transient atrial fibrillation was induced six times. All pts tolerated shocks from 0.27 to 1 J with moderate discomfort; shocks exceeding 1.0 J were less well tolerated. CK levels were not increased. In three pts (VT cycle length of 320, 380 and 400 msec) a permanent Cardioverter (Medtronic Model 7210) was implanted and programmed to operate in non-automatic mode. Every month the pts underwent a follow-up visit to verify the electrophysiological features of VT in non invasively induced VT episodes and the efficacy of transvenous cardioversion. In a mean follow-up period of 9 months, respectively 5, 4 and 3 spontaneous VT episodes occurred. In two pts cardioversion resulted constantly effective, whereas in the third one provoked VT acceleration requiring DC-shock in the last spontaneous episode of VT.

Aged↗
PubMed1983

[Malignant ventricular hyperkinetic arrhythmia: role of permanent electric treatment].

While the technics of cardiac pacing have shown to have a precise role in the diagnosis and treatment of ventricular arrhythmias on a temporary basis, the role of permanent antiarrhythmic devices (PAD) in the treatment of these arrhythmias is still ill defined mainly because of the technological limits concerning the pacemakers and the frequent complications observed during the attempts to interrupt such tachycardias. On the basis of the available data and of theoretical considerations, three groups of pts susceptible of treatment with PAD can be selected: a) pts with brady-dependent arrhythmias where PAD is used as a prophylactic mean; b) pts with recurrent sustained ventricular tachycardia refractory to medical treatment, in whom PAD can be used to interrupt tachycardia; c) pts affected by ventricular fibrillation or rapidly deteriorating ventricular tachycardia (sudden death pts), refractory to conventional treatment, in whom the implantable defibrillator represents the only therapeutic possibility. Even if scanty, the data available seem to confirm that PAD does have a role in the treatment of malignant arrhythmias, although in selected cases and almost always together with drug treatment.

Arrhythmias, Cardiac↗
PubMed1981

[Physiopathologic mechanism of ventricular fibrillation induced by atropine. Report of two cases (author's transl)].

The authors report on two cases of ventricular fibrillation induced by bolus of atropine injected for diagnostic purpose. The electrophysiologic effect of adrenergic stimulation following the parasympathetic blockade, is probably the responsible mechanism rather than myocardial ischemia in the first patient, affected by complete a-v block with narrow QRS. The second patient, affected by coronary heart disease and suspected sick sinus syndrome, had more probably a ventricular fibrillation because of a worsening of the underlying myocardial ischemia due to the increase of the cardiac rate. the reported observations, together with those of other Authors, suggest that atropine, at least when used for diagnostic purpose, should be employed cautiously and preferably having available all the equipment for emergency treatment of cardiorespiratory arrest.

Aged↗