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L Rochette

Publications and source records attributed to L Rochette.

At least 91 records · Page 5Linked to original sources
PubMed1997

Pattern of superoxide dismutase enzymatic activity and RNA changes in rat heart ventricles after myocardial infarction.

A multiplex reverse transcription polymerase chain reaction assay was designed to measure manganese superoxide dismutase (MnSOD) and CuZnSOD mRNAs in the left and right ventricles of rat hearts after myocardial infarction induced by occlusion of the left coronary artery. These data were compared with changes in enzymatic activities. In the left ventricle, Mn-SOD RNA increased significantly at 6 hours, peaked at 12 hours (490 +/- 38 arbitrary units), and progressively decreased (127 +/- 21 arbitrary units at 48 hours). In contrast, there was a steady accumulation of transcripts in the right ventricle up to 48 hours. In both ventricles, the changes in the MnSOD mRNA and protein content were not associated with proportional variations in enzymatic activity. There was no characteristic alteration of the CuZnSOD system in either ventricle over the 48-hour period. These results demonstrate that infarction selectively activates the MnSOD gene in the viable myocardium of both ventricles. They suggest that MnSOD may be involved in the adaptive response of myocytes to the overloading stress.

Animals↗
PubMed1996

F1F0-ATPase, early target of the radical initiator 2,2'-azobis-(2-amidinopropane) dihydrochloride in rat liver mitochondria in vitro.

This study was designed to determine which enzyme activities were first impaired in mitochondria exposed to 2,2'-azobis-(2-amidinopropane) dihydrochloride (AAPH), a known radical initiator. EPR spin-trapping revealed generation of reactive oxygen species although malondialdehyde formation remained very low. With increasing AAPH concentrations, State-3 respiration was progressively depressed with unaltered ADP/O ratios. A top-down approach demonstrated that alterations were located at the phosphorylation level. As shown by inhibitor titrations, ATP/ADP translocase activity was unaffected in the range of AAPH concentrations used. In contrast, AAPH appeared to exert a deleterious effect at the level of F1F0-ATPase, comparable with dicyclohexylcarbodi-imide, which alters Fo proton channel. A comparison of ATP hydrolase activity in uncoupled and broken mitochondria reinforced this finding. In spite of its pro-oxidant properties, AAPH was shown to act as a dose-dependent inhibitor of cyclosporin-sensitive permeability transition initiated by Ca2+, probably as a consequence of its effect on F1F0-ATPase. Resveratrol, a potent antiperoxidant, completely failed to prevent the decrease in State-3 respiration caused by AAPH. The data suggest that AAPH, when used under mild conditions, acted as a radical initiator and was capable of damaging F1F0-ATPase, thereby slowing respiratory chain activity and reducing mitochondrial antioxidant defences.

Amidines↗
PubMed1996

Alterations of lipoprotein fluidity by non-esterified fatty acids known to affect cholesteryl ester transfer protein activity. An electron spin resonance study.

The aim of the present study was to investigate the effect of saturated, monounsaturated and polyunsaturated non-esterified fatty acids (NEFA) on lipoprotein fluidity by using the electron spin resonance (ESR) method. The fluidity of the lipid phase of lipoproteins was evaluated by calculating from ESR spectra the S parameter of three different positional isomers of spin-labeled stearic acid incorporated into the lipoprotein. In non-enriched lipoproteins, S values were higher in high-density lipoprotein 3 (HDL3) than in low-density lipoprotein (LDL) indicating that the surface of HDL3 was more ordered. Prior incubation of lipoprotein particles with NEFA significantly reduced S values, indicating an increased lipoprotein fluidity as compared with non-supplemented homologous samples. In NEFA-enriched lipoproteins, the modifications in fluidity were shown to be dependent on the structure of the NEFA acyl carbon chains. Medium-chain fatty acids [lauric (12:0) and myristic (14:0) acids] appeared to be better fluidizing molecules as compared with both shorter [octanoic (8:0) and decanoic (10:0) acids] and longer [palmitic (16:0) and stearic (18:0) acids] homologues. In addition, introducing at least one double bond in the acyl carbon chain significantly increased the ability of NEFA to reduce S as compared with saturated homologues. In both LDL and HDL3, the extent of the modifications of the molecular mobility at the lipoprotein surface was dependent on the final NEFA/lipoprotein ratio. In conclusion, these results suggest that the ability of NEFA to modulate the activity of the cholesteryl ester transfer protein might relate in part to alterations in fluidity at the lipoprotein surface.

Carrier Proteins↗
PubMed1996

Effects of exhaustive exercise and vitamin B6 deficiency on free radical oxidative process in male trained rats.

There is growing evidence that oxygen free radical production and subsequent lipid peroxidation are normal sequelae to the rise in oxygen consumption concomitant with exercise. In addition, increased lipid peroxidation has also been shown in vitamin B6-deficient rat plasma, liver, and kidney. To investigate the potential for a role of vitamin B6 in exercise-induced oxidative stress, 36 male Sprague-Dawley rats received 0 (n = 12), 2 (n = 12), and 8 mg pyridoxine (PN)-HCl/kg diet (n = 12) and were trained by a 9-week swimming program. After 9-weeks of training, six rats (exhausted: E rats) of each vitamin group were exercised to exhaustion by swimming while the other six rats rested (nonexhausted: NE rats). Ascorbate, ascorbate free radical and antilipoperoxidant capability (AC) were evaluated in plasma. These parameters were higher in E rats than in NE rats. Free radical-mediated lipid peroxidation was measured in tissue and plasma by evaluation of thiobarbituric acid reactive substances (TBARS) content. This index of peroxidation was significantly increased in liver of E rats but not in plasma, heart, and gastrocnemius muscle. Concentration of TBARS in liver was the highest in vitamin B6-deficient rats (consuming 0 mg PN-HCl/kg diet) and the lowest in vitamin B6-sufficient rats (consuming 8 mg PN-HCl/kg diet). Vitamin E (alpha-tocopherol) levels in liver and heart were negatively related to vitamin B6 levels in the diet. Independently of vitamin B6, liver and muscle alpha-tocopherol levels were significantly higher in E animals than in NE animals. There is good evidence according to our results that exercise induced an oxidative stress, as indicated by a significant increase of ascorbyl radical levels in the plasma. The effects of vitamin B6 deficiency on the free radical metabolism are low in trained rats. On the contrary, exhaustive exercise induced modifications in the metabolism pathways of vitamin C and E objectivated by variations of levels of vitamin C in the plasma and vitamin E in liver.

Animals↗
PubMed1996

Comparison of the effects of nicorandil, pinacidil and nitroglycerin on hypoxic and hypercapnic pulmonary vasoconstriction in the isolated perfused lung of rat.

1. The aims of this study were to compare in the rat isolated perfused lung preparation, the dilator actions of nicorandil, pinacidil and nitroglycerin on the hypoxic pulmonary pressure response with or without hypercapnic acidosis and to investigate the possible involvement of K channels and EDRF in these effects. 2. Isolated lungs from male Wistar rats (260-320 g) were ventilated with 21%O2 + 5%CO2 + 74%N2 (normoxia) or 5%CO2 + 95%N2 (hypoxia) and perfused with a salt solution supplemented with ficoll and gassed with 40%CO2 + 60%N2 to produce hypercapnic acidosis. Glibenclamide (1 microM), charybdotoxin (0.1 microM), NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) and methylene blue (30 microM) were used to block KATP channels, KCa channels, EDRF synthesis and guanylate cyclase, respectively. 3. Hypoxic pressure response was significantly increased by hypercapnic acidosis (+115%, P < 0.001), L-NAME (+111%, P < 0.001), methylene blue (+100%, P < 0.05) but not by glibenclamide or charybdotoxin. In contrast none of these inhibitors affected the hypoxic hypercapnic acidosis response. 4. Nicorandil, pinacidil and nitroglycerin caused relaxation during the hypoxic pressure response and hypoxic hypercapnic acidosis response. Nicorandil was more potent in the latter. Glibenclamide inhibited the relaxant effects of nicorandil and pinacidil but not those of nitroglycerin during hypoxia alone. In contrast, glibenclamide inhibited the relaxant effects of the three drugs during hypoxia + hypercapnia. Charybdotoxin inhibited the relaxant effect of pinacidil during normocapnia and hypoxia but not those of nicorandil or nitroglycerin. Methylene blue inhibited partially the dilator response to pinacidil but did not modify the effects of nitroglycerin or nicorandil. 5. It is concluded that in the rat isolated lung preparation, EDRF limits hypoxic pulmonary vasoconstriction but not hypoxic vasoconstriction potentiated by hypercapnic acidosis, whereas KATP or KCa channels are not involved in either case. Nicorandil and pinacidil dilate pulmonary vessels mainly through KATP channels but the effects of pinacidil may also involve an additional mechanism of action through KCa channels. Finally it is suggested that nitroglycerin may partly exert its relaxant effects through KATP channels.

Acidosis↗
PubMed1996

Effects of cyclosporin and cremophor on working rat heart and incidence of myocardial lipid peroxidation.

Cyclosporin A (CsA) is widely used as the immunosuppressant of choice for preventing graft rejection. However, its clinical use is hampered by certain side effects, especially its nephrotoxicity and other cardiovascular side effects. CsA for intravenous infusion contains cremophor (Cre) and this vehicle has significant adverse effects on endothelial function and vascular muscle. The present study was aimed at investigating the direct effects of CsA and Cre on isolated and perfused rat hearts in the dosage that closely approximates the peak level achieved for the prevention of graft rejection in the rat. Transplantation is a clinical setting in which the myocardium may be exposed to transient ischemia. In this study, we have shown that the vehicle of CsA, namely Cre, has significant adverse effects on cardiac function. We observed a reduction in coronary flow and aortic output. Addition of CsA appeared to induce a further reduction of aortic flow. We have also shown that a significant increase of thiobarbituric acid reactive substances, considered as an index of lipid peroxidation, occurred in the reperfused heart in the presence of Cre+CsA. Our experimental study shows that Cre turned out to be toxic to myocardium by itself. In the heart, potential Cre-CsA interactions possibly potentiating CsA toxicity could not be excluded. The increase of lipid peroxidation in the heart perfused with CsA suggests that reactive oxygen species may be involved in the detrimental effects of this substance on the heart.

3,4-Methylenedioxyamphetamine↗
PubMed1996

Effects of aldosterone and spironolactone on the isolated perfused rat heart.

Aldosterone antagonists are used in the treatment of hypertension. However, the cardiac influences of aldosterone and its antagonists have not been thoroughly investigated. In the present study, we investigated the effects of aldosterone and spironolactone on an isolated rat working heart model. Aldosterone (10(-8) mol/l) decreased the coronary flow and increased aortic flow and cardiac output. Spironolactone (10(-5) mol/l) inhibited these effects. These results suggest that aldosterone directly influences the cardiac function. Spironolactone appears able to inhibit the adverse cardiac effects of aldosterone. The exact mechanisms remain to be elucidated, but the early effects of aldosterone under our experimental conditions on the functional parameters of the heart suggest a nongenomic response including activation of receptors different from those transmitting genomic steroid actions.

Aldosterone↗
PubMed1996

Changes of catalase activity after ischemia-reperfusion in rat retina.

Catalase activity was evaluated in Long Evans rat retina after ischemia and reperfusion. Ischemia was induced by ligation of the optic nerve and vessels. Rats were sacrificed after 15 and 120 min of reperfusion, respectively. Catalase activity was assessed by Claiborne's method and was expressed as U/mg of protein. In the first group, retinas of each animal were pooled. In the second group, ischemia was induced in the right eye with the left eye serving as control. In the first group, enzyme activity was 7.39 +/- 0.26 (n = 11), 7.67 +/- 0.27 (n = 9) and 9.15 +/- 0.45 (n = 7) for the sham-operated, 15- and 120-min reperfusion groups, respectively. There was a significant difference between the control and 120-min reperfusion groups (p < 0.001). In the second group, there was a significant (p < 0.01) increase in catalase activity in the ischemic eye compared to the non-ischemic eye after 15 (n = 7) and 120 min (n = 9) of reperfusion. These findings may suggest a rapid activation of catalase activity during the ischemia-reperfusion sequence.

Animals↗
PubMed1996

Creatine kinase is the main target of reactive oxygen species in cardiac myofibrils.

Reactive oxygen species (ROS) have been reported to alter cardiac myofibrillar function as well as myofibrillar enzymes such as myosin ATPase and creatine kinase (CK). To understand their precise mode and site of action in myofibrils, the effects of the xanthine/xanthine oxidase (X/XO) system or of hydrogen peroxide (H2O2) have been studied in the presence and in the absence of phosphocreatine (PCr) in Triton X-100-treated cardiac fibers. We found that xanthine oxidase (XO), with or without xanthine, induced a decrease in maximal Ca(2+)-activated tension. We attributed this effect to the high contaminating proteolytic activity in commercial XO preparations, since it could be prevented a protease inhibitor, phenylmethylsulfonyl fluoride (PMSF), and it could be mimicked by trypsin. In further experiments, XO was pre-treated with 1 mmo1/L PMSF. Superoxide anion production by the X/XO system, characterized by electron paramagnetic resonance spin-trapping technique, was not altered by PMSF. A slight increase in maximal force was then observed either with X/XO (100 mumol/L per 30 mIU/mL) or H2O2. pMgATP-rigor tension relationships have been established in the presence and in the absence of PCr to separate the effects of ROS on myosin ATPase and myofibrillar-bound CK. In the absence of PCr, pMgATP50, the pMgATP necessary to induce half-maximal rigor tension, was reduced from 5.03 +/- 0.17 (n = 21) to 4.22 +/- 0.22 (n = 4) after 25 minutes of incubation in the presence one of 30 mIU/mL. XO and 100 mumol/L xanthine or to 4.04 +/- 0.1 (n = 11) after incubation in the presence of 2.5 mmol/L H2O2. The ROS effects were partially prevented or antagonized by 1 mmol/L dithiothreitol. No effect was observed on pMgATP50 when PCr was absent. pCa-tension relationships have been evaluated to assess the effects of ROS on active tension development. Incubations with H2O2 induced on increase in Ca2+ sensitivity and resting tension when MgATP was provided through myofibrillar CK (PCr and MgADP as substrates) but not when MgATP was added directly. These results suggest that myofibrillar CK was inhibited by ROS. Active stiffness and the time constant of tension changes after quick stretches applied to the fibers were dose-dependently increased by H2O2 only in the presence of PCr. In addition, myofibrillar CK but not myosin ATPase enzymatic activity was depressed after incubation with either ROS. These results suggest that ROS mainly alters CK in myofibrils, probably by the oxidation of its essential sulfhydryl groups. Such CK inactivation results in a decrease in the intramyofibrillar ATP-to-ADP ratio. The effects of ROS on cytosolic and bound CKs may take part in the overall process of myocardial stunning after cardiac ischemia and reperfusion.

Animals↗
PubMed1996

L-NAME aggravates pulmonary oxygen toxicity in rats.

Exposure to high oxygen concentration leads to acute lung injury and death in rats after 72 h. The pathophysiology of this phenomenon relies on several mechanisms, including alteration of vascular reactivity, recruitment and activation of neutrophils and alveolar macrophages, production of cytokines and excess production of free radicals. In addition to its potent vasodilating effect, nitric oxide (NO) has also been reported to prevent free radical-mediated damage. We wanted to determine whether NG-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, might modulate oxygen toxicity. In rats exposed to continuous high oxygen concentration, we studied the effect of administration of 50 mg.kg-1 of intraperitoneal L-NAME twice a day on the first day of oxygen exposure. L-NAME resulted in earlier death, since 57% of the animals exposed to oxygen and injected with L-NAME died within 60 h as compared to 22% of the animals exposed to oxygen and treated with saline (p < 0.01). Haematocrit and bronchoalveolar lavage fluid protein were also significantly increased in animals exposed to oxygen and receiving L-NAME. The lung water content was higher in the oxygen-exposed groups (p < 0.01) and slightly decreased by L-NAME (p < 0.05). Thiobarbituaric acid reactive substances (TBARS) were elevated in plasma (p < 0.01) and decreased in lung (p < 0.001) of oxygen-exposed animals, but no significant effect of L-NAME was observed. NG-nitro-L-arginine methyl ester had a deleterious effect in rats exposed to hyperoxia, which might suggest that endogenous nitric oxide has a protective role against hyperoxia-induced pulmonary lesions.

Animals↗
PubMed1996

Crystalloid versus cold blood cardioplegia in patients operated on for myocardial revascularisation.

Post-ischemic reperfusion phenomenon has been studied in two methods of myocardial protection: a crystalloid cardioplegia (St Thomas no.2) and a cold blood cardioplegia (Buckberg) during cardiopulmonary bypass for myocardial revascularisation in patients. Myocardial protection has been assessed from the evolution of hemodynamic parameters, reperfusion arrhythmias and biochemical analysis of the coronary flow after cross-clamp removal: creatinine phosphokinase (CPK_MB) and nucleotide adenine metabolites (adenosine, inosine, hypoxanthine, xanthine and uric acid). The study was performed in two groups of 14 patients. Hemodynamic conditions were similar in both groups during reperfusion in order to avoid different coronary flow. In those conditions, myocardial protection by cold blood cardioplegia reduced reperfusion arrhythmias, and resulted in a loss of CPK-MB release. Furthermore, the reduction of metabolites release, purine bases and oxypurine bases into coronary sinus after cold blood cardioplegia suggest a better protection of myocardial high energy phosphates in this group than after crystalloid cardioplegia. Our results also show that hypoxanthine is probably the final product of ATP degradation in human myocardial tissue.

Adenosine Triphosphate↗
PubMed1996

[A study of the 30 minutes following reperfusion after crystalloid and cold blood cardioplegia by enzymatic and metabolic analysis of coronary blood flow].

Post-ischemic reperfusion phenomena were studied in two methods of myocardial protection: crystalloid cardioplegia (St Thomas n(o) 2) and cold blood cardioplegia (Buckherg) during cardiopulmonary bypass for human myocardial revascularisation. Myocardial protection was assessed on the course of hemodynamic parameters, reperfusion arrhythmias and biochemical analysis of the coronary flow after cross-clamp removal: creatine phosphokinase (CPK-MB) and nucleotide adenine metabolites (adenosine, inosine, hypoxanthine, xanthine and uric acid). The study was performed in two groups of 14 patients. Hemodynamic conditions were similar in both groups during reperfusion in order to avoid different coronary flow. Under these conditions, myocardial protection by cold blood cardioplegia reduced reperfusion arrhythmias, and resulted in a loss of CPK-MB release. Furthermore, cold blood cardioplegia provided protection of myocardial energy metabolism by reducing the loss of metabolites, purine bases and oxypurine bases into the coronary sinus. Our results also show that hypoxanthine is probably the final product of ATP degradation in human myocardial tissue.

Aged↗
PubMed1995

Enhancement of activities relative to fatty acid oxidation in the liver of rats depleted of L-carnitine by D-carnitine and a gamma-butyrobetaine hydroxylase inhibitor.

This study was designed to examine whether the depletion of L-carnitine may induce compensatory mechanisms allowing higher fatty acid oxidative activities in liver, particularly with regard to mitochondrial carnitine palmitoyltransferase I activity and peroxisomal fatty acid oxidation. Wistar rats received D-carnitine for 2 days and 3-(2,2,2,-trimethylhydrazinium)propionate (mildronate), a noncompetitive inhibitor of gamma-butyrobetaine hydroxylase, for 10 days. They were starved for 20 hr before being sacrificed. A dramatic reduction in carnitine concentration was observed in heart, skeletal muscles and kidneys, and to a lesser extent, in liver. Triacylglycerol content was found to be significantly more elevated on a gram liver and whole liver basis as well as per mL of blood (but to a lesser extent), while similar concentrations of ketone bodies were found in the blood of D-carnitine/mildronate-treated and control rats. In liver mitochondria, the specific activities of acyl-CoA synthetase and carnitine palmitoyltransferase I were enhanced by the treatment, while peroxisomal fatty acid oxidation was higher per gram of tissue. It is suggested that there may be an enhancement of cellular acyl-CoA concentration, a signal leading to increased liver fatty acid oxidation in acute carnitine deficiency.

Animals↗
PubMed1995

Influence of dietary polyunsaturated fatty acids on contractility, lusitropy and compliance of isolated rat myocardium.

Two groups of 15 rats were fed for 4 weeks with diets containing 15% by weight of fat varying in polyunsaturated fatty acids (PUFA) content and type. Diet C18:2 (n-6) contained 20% of total fatty acids as linoleic acid and small amount of (n-3) PUFA (0.4% of the total fatty acids). Diet LC (n-3) contained the same amount of 18:2 (n-6) and of long chain (n-3) C20 and C22 PUFA (10% of the total fatty acids). Contents of both saturated fatty acids and amount of total PUFA were kept constant in the two diets. Left ventricular papillary muscle mechanics were studied blind at Lmax and over the entire load-continuum, in terms of inotropy, characteristics of the force-velocity relationship, relaxation and compliance. Inotropy, force-velocity relationships and muscle compliance were similar in both groups. There was a trend towards a lower peak lengthening velocity at preload in the LC (n-3) group (P = 0.10) together with an unchanged peak rate of isometric force decline. This resulted in a significant impairment of the two mechanical indexes testing the load dependence of myocardial relaxation (P = 0.019 and P = 0.002). In conclusion, short-term differences in PUFA regimen were associated with an unchanged myocardial contractility and economy of force generation. The decreased load dependence of relaxation together with unchanged myocardial compliance strongly favored a physiological relevance of the previously reported modifications of sarcoplasmic reticulum phospholipid composition and calcium transport under (n-3) PUFA regimen.

Animals↗
PubMed1995

Increase in antilipoperoxidant activity of plasma as a consequence of an inflammatory reaction induced by subcutaneous turpentine in the rabbit.

In the rabbit, an acute inflammatory reaction triggered by the subcutaneous administration of turpentine induces in hepatic tissues an oxidative stress, as well as a decrease in activity of enzymatic scavengers of reactive oxygen species (ROS). The objective of this study was to investigate, the repercussions of a local inflammatory reaction on the antioxidant capacity and markers of systemic oxidative stress in plasma. To this purpose, rabbits received a.s.c. injection of turpentine (5 mL/kg) or NaCl 0.9% (w/v). Blood samples were collected at different times during the 48 hours of the experiment to evaluate: firstly, the antilipoperoxidant activity of plasma by measuring the inhibition of autoxidation of brain homogenate, and the concentrations of tocopherol and ascorbic acid; secondly, the severity of oxidative stress in plasma by assaying the concentration of thiobarbituric acid reactive substances (TBARS), and the concentration of ascorbyl radical. The results show that the antilipoperoxidant capacity of plasma gradually increased to be 167% higher than baseline values (p < 0.05) after 48 hours of experiment. alpha-Tocopherol and ascorbic acid levels increased by 49% and 80%, respectively (p < 0.05) during the first 24 hours. Lipid peroxidation continuously increased to be 98% higher than baseline values (p < 0.05) at 48 hours, while ascorbyl radical levels were not modified (p < 0.05). In summary, an acute local inflammatory reaction causes a steady progression of oxidative stress, while it stimulates the antilipoperoxidant activity of plasma, to which alpha-tocopherol and ascorbic acid appear to contribute, essentially early in the inflammation.

Animals↗
PubMed1995

Effect of in vivo heart irradiation on the development of antioxidant defenses and cardiac functions in the rat.

During radiotherapy of thoracic tumors, the heart is often included in the primary treatment volume, and chronic impairment of myocardial function occurs. The cellular biomolecules are altered directly by radiation or damaged indirectly by free radical production. The purpose of this investigation was to evaluate the biochemical and functional responses of the rat heart to a single high dose of radiation. The effect of 20 Gy local X irradiation was determined in the heart of Wistar rats under general anesthesia. Mechanical performances were measured in vitro using an isolated perfused working heart model, and cardiac antioxidant defenses were also evaluated. Hearts were studied at 1 and 4 months after irradiation. This single dose of radiation induced a marked drop in the mechanical activity of the rat heart: aortic output was significantly reduced (18% less than control values) at 1 month postirradiation and remained depressed for the rest of the experimental period (21% less than control 4 months after treatment). This suggests the development of myocardial failure after irradiation. The decline of functional parameters was associated with changes in antioxidant defenses. The decrease in cardiac levels of vitamin E (-30%) was associated with an increase in the levels of Mn-SOD and glutathione peroxidase (+45.5% and +32%, respectively, at 4 months postirradiation). However, cardiac vitamin C and catalase levels remained constant. Since these antioxidant defenses were activated relatively long after irradiation, it is suggested that this was probably due to the production of free radical species associated with the development of inflammation.

Aging↗
PubMed1995

Magnetic resonance relaxation times in ventricular hypertrophy induced by myocardial infarction in the rat.

The purpose of this study was to evaluate changes in the proton nuclear magnetic resonance relaxation times (T1 and T2) after chronic infarction in the rat. Ligation of the left coronary artery was followed by various degrees of reduction in myocardial blood flow. The ligation induced infarction in the left ventricle and compensatory hypertrophy in the right ventricle, as evaluated by the ratio of right ventricle to body weight. The interventricular septum and the right ventricle did not become ischemic in this model and served as control areas. In the infarcted left ventricle our results showed an increase in the T1 and T2 relaxation times after 15 and 30 days of ligation and a slight decrease after 60 days. A similar change in the T1 values was observed in the right ventricle. In contrast, a persistent increase in the T2 relaxation times was observed in the right ventricle and correlated with the ratio of right ventricle to body weight (r = 0.54, p < 0.01). The observation that the magnetic resonance relaxation times in vitro are modified in the hypertrophic right ventricle after myocardial infarction could be important in interpreting magnetic resonance imaging in vivo. There was no relation between the changes in the relaxation times and the degree of myocardial ischemia.

Animals↗