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M Ovize

Publications and source records attributed to M Ovize.

At least 37 records · Page 2Linked to original sources
PubMed2000

Brief preconditioning ischemia alters diacylglycerol content and composition in rabbit heart.

In order to give further insight into the potential role of PKC in the beneficial effects of ischemic preconditioning, we have characterized the production of diacylglycerol, the endogenous activator of PKC, and its molecular species composition in ischemic control and preconditioned hearts. Preconditioning was induced by 1 cycle of 5 min of ischemia followed by 5 min of reperfusion. In control and preconditioned groups, hearts were harvested under deep anesthesia at baseline (preischemia) and at 2, 5 and 10 min into the sustained coronary artery occlusion, i.e., preceding myocyte death. Diacylglycerol content and fatty acid composition were analyzed by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC), respectively. Myocardial diacylglycerol content was increased at 2 min into the sustained ischemia in the control group (481 +/- 34 vs 292 +/- 64 ng x mg(-1) at baseline; p < 0.05), but was comparable to the baseline value at 5 and 10 min. In the preconditioned group, diacylglycerol production remained unchanged throughout the 10-min test ischemia (317 +/- 17 at 2 min vs 312 +/- 38 ng x mg(-1) at baseline; p = NS). A detailed analysis of the molecular species composition at the time of 2 min revealed a reduced contribution of phosphatidylinositol to diacylglycerol production in preconditioned myocardium (global correlation coefficient 0.57 vs 0.66 in control myocardium) with a trend toward an enrichment of diacylglycerol composition with some species originating from phosphatidylcholine. Thus, our study revealed that brief preconditioning ischemia: (1) prevents the increase of diacylglycerol content in the early minutes of the sustained ischemia, and (2) emphasizes the contribution of phosphatidylcholine in diacylglycerol formation to the detriment of that of phosphatidylinositol.

Animals↗
PubMed2000

Biphasic response after brain death induction: prominent part of catecholamines release in this phenomenon.

BACKGROUND: The physiopathology of hemodynamic instability that occurs after brain death remains unknown. The aim of this study was to examine the initial response to brain death induction. METHODS: After anesthesia and monitoring, 16 pigs were randomized into a control group (C, n = 8) and a brain death group (BD, n = 8). We inflated a subdural catheter balloon to induce brain death. We analyzed hemodynamic and plasmatic biochemical data for 180 minutes after brain death induction. Energetic compounds were measured. We expressed the results in comparison with the C group. RESULTS: The C group remained stable. One minute after brain death, the Cushing reflex appeared, with a hyperdynamic response to plasma catecholamines levels increasing (norepinephrine and epinephrine, 3.1-fold, p = 0. 02, and 3.8-fold, p = 0.07, respectively). After a return to baseline, we recorded a second hyperdynamic profile 120 minutes later. At this time, a second peak of catecholamines appeared (6. 3-fold, p = 0.04, and 9.1-fold, p = 0.02, concerning norepinephrine and epinephrine). At the same time, we observed brief myocardial lactate production (+175%, p < 0.01), with a rise of troponine I (+64%, p = 0.03). The energetic index was similar in both groups: 0. 85 (+/-0.02) in the C group vs 0.87 (+/-0.02) in the BD group. CONCLUSIONS: In this model, biphasic plasmatic catecholamine release appears to primarily explain the physiopathology of the hemodynamic response to brain death induction.

Animals↗
PubMed2000

Prevention of isoflurane-induced preconditioning by 5-hydroxydecanoate and gadolinium: possible involvement of mitochondrial adenosine triphosphate-sensitive potassium and stretch-activated channels.

BACKGROUND: Both mitochondrial adenosine triphosphate-sensitive potassium (MKATP) channels (selectively blocked by 5-hydroxydecanoate) and stretch-activated channels (blocked by gadolinium) have been involved in the mechanism of ischemic preconditioning. Isoflurane can reproduce the protection afforded by ischemic preconditioning. We sought to determine whether isoflurane-induced preconditioning may involve MKATP and stretch-activated channels. METHODS: Anesthetized open-chest rabbits underwent 30 min of coronary occlusion followed by 3 h of reperfusion. Before this, rabbits were randomized into one of six groups and underwent a treatment period consisting of either no intervention for 40 min (control group; n = 9) or 15 min of isoflurane inhalation (1.1% end tidal) followed by a 15-min washout period (isoflurane group; n = 9). The two groups received an intravenous bolus dose of either 5-hydroxydecanoate (5 mg/kg) or gadolinium (40 micromol/kg) before coronary occlusion and reperfusion (5-hydroxydecanoate, n = 9; gadolinium, n = 7). Two additional groups received 5-hydroxydecanoate or gadolinium before isoflurane exposure (isoflurane-5-hydroxydecanoate, n = 10; isoflurane-gadolinium, n = 8). Area at risk and infarct size were assessed by blue dye injection and tetrazolium chloride staining. RESULTS: Area at risk was comparable among the six groups (29 +/- 7, 30 +/- 5, 27 +/- 6, 35 +/- 7, 31 +/- 7, and 27 +/- 4% of the left ventricle in the control, isoflurane, isoflurane-5-hydroxydecanoate, 5-hydroxydecanoate, isoflurane-gadolinium, and gadolinium groups, respectively). Infarct size averaged 60 +/- 20% (SD) in untreated controls versus 54 +/- 27 and 65 +/- 15% of the risk zone in 5-hydroxydecanoate- and gadolinium-treated controls (P = nonsignificant). In contrast, infarct size in the isoflurane group was significantly reduced to 26 +/- 11% of the risk zone (P < 0.05 vs.control). Both 5-hydroxydecanoate and gadolinium prevented this attenuation: infarct size averaged 68 +/- 23 and 56 +/- 21% of risk zone in the isoflurane-5-hydroxydecanoate and isoflurane-gadolinium groups, respectively (P = nonsignificant vs.control). CONCLUSION: 5-Hydroxydecanoate and gadolinium inhibited pharmacologic preconditioning by isoflurane. This result suggests that MKATP channels and mechanogated channels are probably involved in this protective mechanism.

Adenosine Triphosphate↗
PubMed2000

Severity and extent of perfusion defects provoked by transient coronary occlusion compared with myocardial damage observed after infarction.

A peripheral perfusion tracer injection at the time of coronary occlusion during percutaneous transluminal coronary angioplasty (PTCA) may delineate the myocardial 'area at risk' related to a given artery. To evaluate the location, size and severity of the corresponding scintigraphic defects, we conducted a prospective study of 36 patients who received a 99Tcm-sestamibi injection during single-vessel coronary angioplasty (PTCA = 18 LAD, 16 RCA and 2 LCX) followed by SPET. For comparison, a reference group of 36 successive patients examined during the early phase of myocardial infarction (MI), matched for the same vascular territories (18 anterior, 16 inferior and 2 lateral), were analysed in the same way after standard stress/reinjection 201Tl SPET. The imaging characteristics of both groups showed excellent agreement as well degree of uptake defects, in terms of topography and extent. A defect index, taking into account both size and severity, was in the same range for PTCA and MI patients (mean +/- standard deviation): for LAD vs anterior = 28.4 +/- 13.5% (PTCA), 27.1 +/- 12.2% (MI-stress) and 24.2 +/- 10.0% (MI-reinjection); for RCA vs inferior = 15.5 +/- 10.2% (PTCA), 14.7 +/- 9.7% (MI-stress) and 13.2 +/- 8.2% (MI-reinjection). Sectoral correlations between PTCA and MI groups were also highly significant.

Adult↗
PubMed2000

[Transluminal coronary angioplasty performed in patients with single vessel disease of the right coronary artery disease. Long-term results].

The patients who have only single vessel disease of the right coronary artery have an excellent prognosis, unaffected by surgery. The object of this study was to evaluate the long-term prognosis of these patients after transluminal coronary angioplasty. The criteria of analysis were survival, anginal symptoms, quality of life and ergometric parameters. Two hundred and forty eight patients with an isolated lesion of the right coronary artery who underwent angioplasty were reassessed 39.6 +/- 22 months after angioplasty. The primary success rate was 89.9% with 5.2% of severe complications during the hospital period (myocardial infarction, bypass surgery, coronary angiography +/- angioplasty). The actuarial global and cardiac survival rates at 7 years were 88.4 and 96.2% respectively with no difference between the success and failure groups. The eight cardiovascular deaths and thirteen myocardial infarctions which were observed in the long-term were all in the successful angioplasty group. From the symptomatic viewpoint, 76% of the population became asymptomatic. The same results were observed in terms of quality of life with 58% of patients estimating it to be good in correlation with anginal status. The comparison of ergometric tests showed a significant gain in performance in 67% of patients. The authors conclude that the results suggest that angioplasty in single vessel disease of the right coronary artery provides a significant symptomatic and ergometric benefit but that it is impossible to assess the eventual benefits in terms of survival which would have needed a group of similar patients assessed under anti-ischaemic treatment and taking into consideration the recent innovations (stents, statins).

Adult↗
PubMed2000

[Myocardial metabolism abnormalities during ischemia and reperfusion].

Normal cardiac function requires adequate oxygen and substrate (fatty acids, glucose lactate) supply for the energetic requirements of the myocardium. Ischaemia induces abnormalities in the production and excretion of products of myocardial metabolism. During ischaemia, the equilibrium which exists during aerobic respiration between the beta-oxidation of fatty acids and carbohydrates and which generates ATP is disturbed. Pyruvate oxidation and beta-oxidation of fatty acids decrease, and ATP is mainly produced by anaerobic glycolysis. Under these conditions, intracellular glycogen is mobilised, the lactate and protons accumulate in the cardiomyocyte. If reperfusion occurs before irreversible lesions are produced, then functional recovery is possible and is mostly dependant on the type of energetic substrate available. Circulating fatty acids are produced in large quantities after ischaemia: their beta-oxidation, which is then the principal source of ATP, may contribute to the aggravation of contractile dysfunction during reperfusion and accentuate or generate arrhythmias. The decoupling between acceleration of anaerobic glycolysis and the defect of pyruvirate oxidation (inhibition of pyruvirate dehydrogenase) participate in a significant fashion to the accumulation of protons. Rapid correction of intracellular acidosis during reperfusion by activation of the Na+/H+ exchanger, coupled with the accumulation of intracellular Na+ induces a deleterious calcium overload via the Na+/Ca++ exchanger. These different aspects of intracellular metabolism constitute pharmacological targets for the development of future cardio-protective agents.

Acidosis↗
PubMed1998

Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion.

BACKGROUND: Quantification of regional myocardial function is a major unresolved issue in cardiology. We evaluated the accuracy of pulsed Doppler tissue imaging (DTI), a new echocardiographic technique, to quantify regional myocardial dysfunction induced by acute ischemia and reperfusion. METHODS AND RESULTS: In nine open-chest anesthetized pigs, various degrees of regional wall motion abnormalities were induced by graded reduction of left anterior descending coronary artery (LAD) blood flow. Pulsed Doppler tissue imaging was performed from an epicardial apical four-chamber view with the sample placed within the middle part of the septal wall. Peak septal velocities were calculated during systole, isovolumic relaxation, and early and late diastole. Regional myocardial blood flow and systolic and diastolic dysfunctions were assessed by radioactive microspheres and ultrasonic crystals, respectively. Ischemia resulted in a significant rapid reduction of systolic velocities and an early decrease in the ratio of early to late diastolic velocities. Both changes were detected by pulsed DTI within 5 seconds of coronary artery occlusion. The decrease in systolic velocity significantly correlated with both systolic shortening (r=.90, P<.0001) and regional myocardial blood flow (r=.96, P<.0001) during reduction of LAD blood flow. CONCLUSIONS: These results suggest that DTI may be a promising new tool for the quantification of ischemia-induced regional myocardial dysfunction.

Animals↗
PubMed1998

Stretch-induced protection shares a common mechanism with ischemic preconditioning in rabbit heart.

We sought to determine whether stretch-induced preconditioning may be related to activation of adenosine receptors, ATP-sensitive K+ (K+ATP) channels, and/or protein kinase C (PKC) in the rabbit heart. Anesthetized rabbits underwent 30 min of coronary artery occlusion followed by 3 h of reperfusion. Ischemic preconditioning was induced by one episode of 5 min of ischemia followed by 5 min of reperfusion, and stretch preconditioning was induced by a transient volume overload. The abilities of gadolinium (Gd3+), a blocker of stretch-activated channels, glibenclamide (Glib), a blocker of K+ATP channels, 8-(p-sulfophenyl)-theophylline (8-SPT), a blocker of adenosine receptors, and polymyxin B (PMXB), an antagonist of PKC, to prevent the infarct size-limiting effect of stretch-induced preconditioning were evaluated. Because the infarct size-reducing effect of stretch occurred in the absence of ischemia and was prevented by previous administration of Gd3+, Glib, 8-SPT, and PMXB, we propose that activation of mechanosensitive ion channels protects the rabbit heart from subsequent sustained ischemic insult, likely through a mechanism that involves downstream activation of PKC, adenosine receptors, and/or K+ATP channels.

Animals↗
PubMed1997

Beneficial actions of preconditioning and stretch on postischemic contractile function of isolated working rat heart: effects of staurosporine.

Preconditioning is commonly induced by a brief ischemic insult; myocardial stretch can trigger this protection by an unknown mechanism. Myocardial stretch preconditions the in vivo canine heart; however, the existence of a stretch-induced protection in the rat heart remains unknown. The purpose of this study was to test this myocardial protection induced, in isolated working rat heart, by global ischemia and stretch initiated by a transient increase in the left ventricle (LV). Isolated rat hearts underwent 30 min of global ischemia followed by 30 min of reperfusion. Before this, hearts received a 15-min period of either no intervention (control; C), 5 min of global ischemia + 10 min of reperfusion (preconditioning; PC) or 5 min of stretch + 10 min with no intervention (stretch; S). Stretch was induced by a transient increase in LV preload from 5 to 20 cm H2O. LV work started under a afterload of 80 cm H2O. Control, PC, and S hearts received either no drug (untreated) or staurosporine (50 nM), a protein kinase C inhibitor, before the "preconditioning" period. Creatine kinase (CK) release, ventricular fibrillation during reperfusion, and postischemic recovery of contractile function (aortic flow) were the end points of the study. In the S group, the abrupt increase in preload resulted in a significant increase of aortic flow (42 +/- 2 to 47 +/- 2 ml/min; p < 0.05). During the 30-min reperfusion period, control hearts displayed a poor recovery of contractile functions (8 +/- 3 ml/min, 30 min after reflow, versus 40 +/- 2 ml/min at baseline; p < 0.05). Both untreated PC and S groups exhibited a significant reduction in CK release, incidence of ventricular fibrillation (55% of control hearts developed persistent VF vs. 6% in both the PC and S groups), and postischemic dysfunction during reperfusion (p < 0.05 vs. control). Staurosporine prevented these beneficial effects in PC and S groups. Our study suggests that myocardial protection can be induced by stretch in the isolated working rat heart, likely through activation of protein kinase C. In conclusion, our results show that ischemic preconditioning and stretch had comparable favorable effect on functional recovery after a sustained ischemic insult in the isolated rat heart.

Animals↗
PubMed1997

Ventricular fibrillation in preconditioned pig hearts: role of K+ATP channels.

ATP-dependent potassium (K+ATP) channels play a role in the infarct size-limiting effect of preconditioning in pigs. We previously demonstrated that preconditioning shortens monophasic action potential duration (MAPD) and accelerates the time to ventricular fibrillation (VF) during a prolonged ischemia in pigs. We sought to determine whether the mechanism of the reduced time to VF in preconditioned pigs is a consequence of K+ATP, channel activation. Pigs underwent 40 min of coronary occlusion and 2 h of reperfusion. Before this, animals received either no intervention (control), 10 min of ischemia and 10 min of reperfusion (preconditioned), or an intravenous infusion of nicorandil, a K+ATP channel opener. Additional control, preconditioned, and nicorandil-treated pigs were pretreated by glibenclamide, an antagonist of K+ATP channels. Because 1) the K+ATP channel activator nicorandil did not produce shorter time to VF, 2) the K+ATP channel inhibitor glibenclamide did not block the acceleration of VF by preconditioning, and 3) there was no relationship between time to VF and infarct size or MAPD, the major conclusion is that reduced time to VF in preconditioned animals is not a consequence of K+ATP channel activation.

Action Potentials↗
PubMed1997

[Analysis of the diagnostic value of endovascular ultrasound with roc curves. Practical implications].

Intravascular ultrasound enables detection of the components of atherosclerotic plaques. The diagnostic value was assessed by ROC (receiver operating characteristic) curves on images acquired in vitro and correlated with the histological findings in 61 arteries. Five questions were asked of each operator; the reply was represented by a continuous variable in order to express all nuances of judgement. The area under the ROC curve, Az, was the criterion of performance (0.5 : chance response : 1.0 : all replies were accurate). Detection of plaque was satisfactory (Az = 0.89). The three layer appearance of muscular arteries was well recognised (Az = 0.94). The fibrous composition of a plaque was only just satisfactory (Az = 0.88) with 38.7% interindividual variability. The lipid composition of the plaque was poorly recognised (Az = 0.76) with large interindividual variability (52.8%) : hypoechogenicity was too ambiguous a sign from the acoustic point of view. A hypoechogenic zone must not be synonymous with a lipid plaque but a cellular zone. Calcium can almost always be detected (Az = 0.98) with a very low interindividual variability (10.7%), fibrohyaline progression of some plaques can be confusing. The authors present a more objective description of endovascular ultrasonographic images. They conclude that the diagnostic performance of 30 MHz intravascular ultrasound is satisfactory but several limitations are apparent in the interpretation of images, especially hypoechogenic zone and hyper-reflective zones with high attenuation.

Arteries↗
PubMed1997

[Preconditioning and preservation of myocardial viability].

Preservation of myocardial viability is a major objective of modern cardiology. Many patients develop large infarcts with major functional consequences in the short and long term. Too many still develop progressive left ventricular dysfunction for which cardiac transplantation, with all its limitations, is the only therapeutic possibility. It is therefore essential to prevent or delay the extension of necrosis. Preconditioning is a natural form of protection which delays the development of myocardial necrosis. A great deal of research is under way to understand this complex process of cardiac protection with the objective to develop pharmacological agents able of simulate or to reproduce its effects in the clinical setting.

Animals↗
PubMed1995

Gender does not influence acute myocardial infarction in adult dogs.

Mechanisms responsible for the well-documented "protection" against myocardial ischemia and infarction in young women and subsequent loss of protection after menopause remain speculative. One possibility is that gender-related variables (such as endogenous hormone levels or regular loss of stored iron) alter the susceptibility of the heart to ischemia: if so, then premenopausal women when compared with men may manifest endogenous protection against acute myocardial ischemic injury. Using the canine model we therefore sought to determine whether gender influences acute myocardial ischemia and infarction. Retrospective analysis was performed on data compiled from 60 mature adult dogs subjected to 1 hour of coronary artery occlusion and > or = 4 hours of reperfusion. We first compared the incidence of lethal ventricular fibrillation in the male and female cohorts and then for survivors compared collateral blood flow during coronary occlusion (by injection of radioactive microspheres), infarct size (assessed by tetrazolium staining and expressed as a percentage of the myocardium at risk), and regional wall motion (by somomicrometry) in the infarct-related area. The incidence of lethal ventricular fibrillation was 23% in the male dogs and 19% in the female dogs (p = 0.70, difference not significant). For survivors, the area at risk of infarction was comparable in males and females (23 +/- 2% and 22% +/- 1% of the total left ventricular weight), and the groups were equally ischemic during coronary occlusion, with collateral blood flow to the ischemic subendocardium averaging 0.05 +/- 0.02 and 0.07 +/- 0.01 ml/min/g tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗