Evidence that free radicals result in reperfusion injury in heart muscle.
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Animals↗
Biomedical subjects
G Ambrosio
Publications and source records attributed to G Ambrosio.
Can free radicals explain reperfusion damage?
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Animals↗
Pattern electroretinograms in ocular hypertension.
The authors recorded pattern electroretinograms at different spatial frequencies in 16 patients affected with ocular hypertension. In 12 of these subjects the electroretinograms dropped in amplitude around 2 cycles/degree. The authors attributed this finding to ocular hypertension, hypothesizing ischemic damage at the head of the optic nerve with consequent fiber atrophy and degeneration of ganglion cells.
Electroretinography↗
Reduction in infarct size by the prostacyclin analogue iloprost (ZK 36374) after experimental coronary artery occlusion-reperfusion.
In this study we attempted to determine whether administration of iloprost (ZK 36374), a chemically stable prostacyclin analogue, would reduce infarct size after experimental coronary artery occlusion and reperfusion. One hour of coronary artery occlusion was performed in 28 open-chest, anesthetized rabbits++, followed by 5 hours of reperfusion. Two minutes after occlusion, 99mTc-labeled albumin microspheres were injected into the left atrium for later assessment of the area at risk of infarction. Fifteen minutes after occlusion animals were randomly assigned to either the treatment group (iloprost, 1.2 micrograms/kg/min intravenously for 6 hours; n = 14) or the control group (n = 14). In vitro platelet aggregation was inhibited in rabbits receiving iloprost. In 10 rabbits (five treated and five control) regional myocardial blood flow was also measured by means of differentially labeled radioactive microspheres. Infarct size was significantly smaller in treated rabbits (53.6 +/- 4.1% of the risk zone vs 89.4 +/- 3.8% in control rabbits; p less than 0.001). Flow to the nonischemic myocardium was higher in treated animals, that is, 1.87 +/- 0.20 ml/min/gm of tissue 50 minutes after occlusion and 1.90 +/- 0.20 ml/min/gm of tissue 4 hours after reperfusion, compared with 1.54 +/- 0.20 and 1.64 +/- 0.30 ml/min/gm of tissue, respectively, in control rabbits (p less than 0.01). Collateral flow to the ischemic region was not affected by the drug. Mean arterial blood pressure, heart rate, and pressure-rate product in treated rabbits were not significantly different from values in control rabbits. In conclusion, administration of iloprost reduced myocardial infarct size in this model of myocardial ischemia and reperfusion in absence of major hemodynamic effects.
Animals↗
Increases in walking distance in patients with peripheral vascular disease treated with L-carnitine: a double-blind, cross-over study.
A double-blind, cross-over study was designed to evaluate the effects of L-carnitine in patients with peripheral vascular disease. After drug washout, 20 patients were randomly assigned to receive placebo or L-carnitine (2 g bid, orally) for a period of 3 weeks and were then crossed over to the other treatment for an additional 3 weeks. The effect on walking distance at the end of each treatment period was measured by treadmill test. Absolute walking distance rose from 174 +/- 63 m with placebo to 306 +/- 122 m (p less than .01) with carnitine. Biopsy of the ischemic muscle, carried out before and after 15 days of L-carnitine administration in four additional patients, showed that treatment significantly increased total carnitine levels. An additional goal of this study was to ascertain the effects of L-carnitine on the metabolic changes induced by exercise in the affected limb. In six patients under control conditions, arterial and popliteal venous lactate and pyruvate concentrations were determined at rest, when the maximal walking distance was reached, and 5 min after the walking test. Twenty-four hours later, L-carnitine was administered intravenously (3 g as a bolus followed by an infusion of 2 mg/kg/min for 30 min) and metabolic assessments were repeated. Five minutes after the walking test, popliteal venous lactate concentration increased by 107 +/- 16% before treatment and by only 54 +/- 32% (p less than .01) after carnitine. Furthermore, carnitine induced a more rapid recovery to the resting value of the lactate/pyruvate ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
Carnitine↗
Assessment of myocardial blood flow by real-time infrared imaging.
In order to evaluate the applicability of infrared imaging for the assessment of myocardial perfusion, 10 open-chested dogs were studied by a real-time infrared imaging system. The left anterior descending coronary artery was occluded for 90 min followed by 210 min of reperfusion. During the experiment, myocardial surface temperature was mapped by an infrared imaging system with a thermal resolution power of 0.1 degree C and correlated with regional myocardial blood flow measured using radiolabeled microspheres. Following the experiment, acute myocardial injury was evaluated using triphenyltetrazolium chloride staining. After 90 min of ischemia, there was a significant correlation between myocardial blood flow and myocardial surface temperature (R = 0.694, P less than 0.001). After reperfusion, temperature did not correlate with blood flow, but there was a significant correlation between temperature and ischemic myocardial injury (R = 0.551, P less than 0.05). Temperature changes during acute regional ischemia and reperfusion may be regulated by the changes in myocardial blood flow and myocardial metabolism. Temperature analysis using real-time infrared imaging may be a useful means for the evaluation of myocardial blood flow and myocardial injury during ischemia and reperfusion.
Animals↗
Preserved high energy phosphate metabolic reserve in globally "stunned" hearts despite reduction of basal ATP content and contractility.
Impaired energy production has been proposed as one mechanism to explain the contractile abnormality in post-ischemic "stunned" myocardium. If energy production were impaired, administration of inotropic agents should result in a deterioration of cellular energy stores because of an inability of ATP synthesis to match the rate of increased utilization. In this study we correlated changes in myocardial high energy phosphates, measured by 31P-NMR spectroscopy, with changes in left ventricular function and energy requirement in buffer perfused rabbit hearts following ischemia and reperfusion, and during stimulation with isoproterenol. Hearts were stunned by 20 min of zero flow global ischemia at room temperature. After reperfusion, isovolumic developed pressure returned to 77.8 +/- 2.2% of baseline and ATP content was reduced to 80.9 +/- 4.1% of baseline. Isoproterenol (5 x 10(-8) M for 10 min) caused increases in developed pressure and rate-pressure product (to 134.1 +/- 12.6% and 195.0 +/- 21.4% of baseline, respectively) without a decrease in ATP or phosphocreatine (PCr) content (80.0 +/- 7.1% and 103.0 +/- 3.8% of preischemia, respectively), and without functional or metabolic deterioration of the hearts after discontinuation of the drug. Control hearts not subjected to ischemia showed similar functional and metabolic responses to isoproterenol. The phosphocreatine/inorganic phosphate (PCr/Pi) ratio, an index of the balance between energy production and utilization, was higher (not lower) than baseline in stunned hearts, thus confirming that energy production was not intrinsically impaired. Together these data indicate that despite reduced myocardial ATP content, mitochondrial function in stunned hearts is capable of sustaining a large increase in function and energetic requirements.
Adenosine Diphosphate↗
Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog: comparison with myocardial stunning produced by repeated coronary occlusions.
Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
Animals↗
Evidence for a reversible oxygen radical-mediated component of reperfusion injury: reduction by recombinant human superoxide dismutase administered at the time of reflow.
It has been suggested that the beneficial effects of reperfusing ischemic myocardium might be in part reversed by the occurrence of "reperfusion injury." One possible mechanism could be the generation of oxygen free radicals. Superoxide dismutase enzymatically scavenges superoxide radicals by dismutation to hydrogen peroxide. This study tested the hypothesis that administration of recombinant human superoxide dismutase (h-SOD) at the time of reflow after a period of prolonged global ischemia would result in improved recovery of myocardial metabolism and function by preventing or reducing a potentially harmful component of reperfusion. We also sought to determine whether catalase, an enzymatic scavenger of hydrogen peroxide, was a necessary addition for optimal benefit. Langendorff perfused rabbit hearts were subjected to 30 min of normothermic (37 degrees C) total global ischemia. At the moment of reperfusion, 12 control hearts received a 10 ml bolus of normal perfusate followed by 15 min of reperfusion with normal perfusate (group I), 12 hearts received 60,000 IU of h-SOD as a bolus followed by a continuous infusion of 100 IU/ml for 15 min (group II), and 12 hearts received 60,000 IU of h-SOD and 60,000 IU of catalase as a bolus followed by 100 IU/ml of both enzymes for 15 min (group III). Myocardial ATP and phosphocreatine (PCr) content and intracellular pH during ischemia and reperfusion were continuously monitored with 31P nuclear magnetic resonance (NMR) spectroscopy. During 30 min of normothermic global ischemia intracellular pH dropped from 7.11-7.18 to 5.58-5.80 in all three groups of hearts. Likewise myocardial PCr content fell rapidly to 7% to 8% and ATP fell more slowly to 29% to 36% of preischemic control content. After 45 min of reperfusion PCr recovered to 65 +/- 5% of control in untreated (group I) hearts compared with 89 +/- 8% in h-SOD-treated (group II) hearts (p less than .01 vs group I) and with 83 +/- 6% of control in h-SOD/catalase-treated (group III) hearts (p less than .05 vs group I). Recovery of isovolumic left ventricular developed pressure was 68 +/- 5% of control in h-SOD-treated (group II) hearts and 66 +/- 6% of control in h-SOD/catalase-treated (group III) hearts after 45 min of reflow, compared with 48 +/- 6% of control in untreated (group I) hearts (p less than .005 for groups II and III vs group I). The NMR data confirmed equal depletion of ATP and PCr content in all three groups of hearts.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Improvement of postischemic myocardial function and metabolism induced by administration of deferoxamine at the time of reflow: the role of iron in the pathogenesis of reperfusion injury.
Reperfusion of ischemic myocardium has been postulated to result in a specific oxygen radical-mediated component of tissue injury. In a previous study we demonstrated improved recovery of ventricular function and metabolism when the superoxide radical scavenger superoxide dismutase was administered at the time of postischemic reflow. Studies in vitro, have suggested that superoxide toxicity might be mediated via the generation of more reactive hydroxyl radicals in an iron-catalyzed reaction. The present study was designed to test the hypothesis that myocardial reperfusion injury might be reduced by administration of the iron chelator deferoxamine at the time of reflow, most likely by preventing hydroxyl radical formation. Sixteen isolated Langendorff rabbit hearts, perfused within the bore of a superconducting magnet, were subjected to 30 min of normothermic (37 degrees C) total global ischemia followed by 45 min of reperfusion. At reflow eight treated hearts received a 10 ml bolus containing 50 mumol of deferoxamine followed by an infusion of 11 mumol/min for the first 15 min of reflow. The hearts were then perfused with standard perfusate for an additional 30 min. Eight untreated control hearts received a similar bolus of perfusate followed by 45 min of standard reperfusion. Serial 5 min 31P nuclear magnetic resonance spectra were recorded. Myocardial phosphocreatine (PCr) content fell to 5% to 7% of control during ischemia in both groups of hearts. Deferoxamine-treated hearts recovered 99 +/- 10% of control PCr content, while untreated hearts recovered 60 +/- 16% (p less than .05). Intracellular pH fell to 5.9 during ischemia in both groups, before showing more rapid and complete recovery in treated hearts (p less than .01). Recovery of developed pressure reached 70 +/- 6% of control in treated hearts compared with 35 +/- 10% in untreated hearts (p less than .05). Iron content of the perfusate was 7 microM, and by electron paramagnetic resonance spectroscopy was in the form of Fe3+-EDTA complexes. In the effluent of treated hearts iron was in the form of Fe3+-deferoxamine chelates. In summary, administration of the iron chelator deferoxamine at the time of postischemic reflow results in greater recovery of myocardial function and energy metabolism, which supports the hypothesis that iron plays an important role in the pathogenesis of reperfusion injury.
Adenosine Triphosphate↗
Inhibition of ischemia-induced phospholipase activation by quinacrine protects jeopardized myocardium in rats with coronary artery occlusion.
Phospholipase activation has been proposed as one relevant biochemical step toward irreversible myocardial injury during ischemia. Accordingly, after coronary artery occlusion, the time course of myocardial phospholipid degradation was studied in 83 control rats and 84 rats treated with quinacrine (75 mg/kg s.c. every 8 hr), a phospholipase inhibitor. Animals were sacrificed at different times ranging from 2 to 48 hr postocclusion. In controls a rapid fall in left ventricular phospholipid concentration (from 1.33 +/- 0.12 to 0.67 +/- 0.05 micrograms of P/mg of protein) and creatinkinase (CK) activity (from 9.84 +/- 0.49 to 6.93 +/- 0.60 I.U./mg of protein) was observed within 4 hr postocclusion. In quinacrine-treated animals phospholipids and CK also fell initially; however, 24 and 48 hr after occlusion they were higher than in controls (phospholipids: 0.99 +/- 0.05 vs. 0.62 +/- 0.04 micrograms of P/mg of protein, P less than .001; CK: 7.76 +/- 0.54 vs. 4.99 +/- 0.37 I.U./mg of protein, P less than .001, at 48 hr). Additional rats surviving coronary occlusion were divided randomly into a control (n = 14) and three treated groups receiving quinacrine every 8 hr at the dose of 5 (n = 13), 20 (n = 13) or 75 mg/kg (n = 15); 13 rats were sham-operated. Forty-eight hours postocclusion myocardial phospholipids were measured and infarct size calculated by CK depletion. Infarct size was significantly smaller in high dose quinacrine-treated than in control rats (16.6 +/- 5.7 vs. 42.1 +/- 4.4% of left ventricle, P less than .001). In treated animals, myocardial phospholipid concentration was also significantly higher.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A biochemical method for the quantitation of myocardial scarring after experimental coronary artery occlusion.
The histologic examination and planimetric evaluation of tissue slices has been so far the only available technique for studying the extent of experimental myocardial infarcts in long-term studies; however, this approach is rather time-consuming when the sample size is large. This study describes a new biochemical method for the quantitation of myocardial scarring, based on the determination of left ventricular hydroxyproline, and collagen content at the end of the healing process. Accordingly, several modifications were introduced into previously existing methods for the assay of hydroxyproline: our method allows a linear estimation of hydroxyproline in the range from 0.5 to 5 micrograms, with a precision of +/- 6.1% and a day-to-day variation of +/- 10.5%. The reliability of this approach for studying infarct size has been verified in rats with coronary artery occlusion divided into a control group and in a treated group receiving nitroglycerin. The animals were killed 21 days after coronary ligation and randomly assigned for infarct size evaluation either to the histologic or the collagen method. By histology infarct size averaged 30.6 +/- 4.8% (mean +/- S.E.M.) of left ventricle (LV) in control rats and 16.2 +/- 5.8% of LV in nitroglycerin-treated animals; by the proposed alternative method left ventricular collagen content was 26.8 +/- 1.0 micrograms/mg of dry weight in control rats and 19.5 +/- 1.2 micrograms/mg of dry weight in nitroglycerin-treated animals; infarct size calculated from collagen content by a simple formula, was 37.4 +/- 2.6% of LV and 22.3 +/- 2.6% of LV, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Reduction in experimental infarct size by recombinant human superoxide dismutase: insights into the pathophysiology of reperfusion injury.
To determine the importance of reperfusion injury and the ability of the free-radical scavenger recombinant human superoxide dismutase (h-SOD) to prevent it, open-chest dogs underwent 90 min of proximal circumflex coronary artery occlusion, and only at the moment of reperfusion received either h-SOD (400,000 IU bolus into the left atrium followed by a 300,000 IU iv infusion over 1 hr) or saline. After 48 hr the surviving animals were killed and measurements were made of the risk region (by postmortem angiography) and infarct size (by gross pathology). All measurements were made by investigators blinded to treatment given, and the code was broken only at the end of the study. Hemodynamic variables and collateral flow during ischemia were similar in the two groups. Infarct size in control animals (n = 8) averaged 22.4 +/- 3.1% of the left ventricle and 52.2 +/- 7.1% of the risk region, compared with 13.3 +/- 0.8% of the left ventricle and 33.6 +/- 2.1% of the risk region in h-SOD-treated dogs (n = 8) (p less than .05). Infarcts in treated animals were not only smaller, but also exhibited a distinctive "patchiness," suggesting protection along vascular distributions. Furthermore, analysis of the relationship between infarct size and collateral flow measured during ischemia in the two groups indicated that protection by h-SOD was greatest in animals with the lowest collateral flows. This study supports the concept that reperfusion of ischemic myocardium results in a separate component of cell damage, presumably linked to the generation of oxygen free radicals on reflow. Since the h-SOD preventable reperfusion component of injury was most pronounced in hearts with the most severe ischemia, scavenging of oxygen radicals at the time of reflow may offer a novel and particularly promising therapeutic approach for the protection of ischemic myocardium.
Animals↗
[Mepindolol reduction of the degradation of phospholipids and the necrosis induced by myocardial ischemia].
Mepindolol is a newly developed beta-adrenergic blocking agent, which differs from other available beta-blockers in its ability to counteract the chronotropic effect of catecholamines without depressing myocardial contractility. This study was designed to assess whether mepindolol administration is effective in reducing infarct size. Accordingly, 53 rats were randomly assigned to 3 groups: group 1 (n = 16) underwent coronary artery occlusion without receiving any treatment, and was used as control; group 2 (n = 19) was treated with mepindolol (1 mg/kg s.c.) 5 min and every 8 hours after occlusion, for 48 hours; group 3 (n = 18) underwent a sham-operation. No difference in mortality was found among groups. The animals were sacrificed 48 hours after occlusion and the left ventricle homogenized and centrifuged. Infarct size was calculated from the residual creatine phosphokinase activity, and found to average 52.4 +/- 7.8% (mean +/- SEM) of the left ventricle in control rats and 35.6 +/- 5.4% in treated rats (p less than 0.05), indicating a 32.1% reduction of infarct size. The phospholipid content of the supernatants was also measured: it averaged 0.08 microgram P/mg of protein in sham-operated rats and 0.61 + 0.04 micrograms P/mg of protein in control animals, showing that coronary ligation induced a degradation of myocardial phospholipids. Mepindolol-treated rats, however, showed a phospholipid concentration of 0.70 +/- 0.04 microgram P/mg of protein (p less than 0.05), suggesting that the drug was able to prevent ischemia-induced phospholipase activation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Antagonists↗
[Limitation of the area of necrosis induced by quinacrine after coronary occlusion in the dog].
Phospholipase activation has been suggested to represent one of the most relevant biochemical steps toward irreversible myocardial injury during ischemia. Accordingly, the time-course of myocardial phospholipid degradation was studied in 167 rats surviving coronary artery occlusion randomly divided into 83 controls and 84 treated with the phospholipase inhibitor quinacrine (75 mg/Kg s.c. every 8 h). The animals were sacrificed at different times ranging from 2 to 48 h post-occlusion and phospholipids and creatine kinase activity (CK) were measured on the supernatant of the left ventricular homogenates. In control animals a rapid fall in phospholipid concentration (from 1.33 +/- 0.12 to 0.67 +/- 0.05 microgram P/mg of protein) and CK activity (from 9.84 +/- 0.49 to 6.93 +/- 0.60 IU/mg of protein) was observed within 4 hours post-occlusion; these parameters remained almost unchanged throughout the rest of the study. In quinacrine-treated animals left ventricular phospholipids and CK also fell during the first hours post-occlusion; however, 24 and 48 h after the occlusion they were significantly higher than in controls (phospholipids: 0.99 +/- 0.05 vs 0.62 +/- 0.04 microgram P/mg of protein, p less than 0.001, and CK: 7.76 +/- 0.54 vs 4.99 +/- 0.37 IU/mg of protein, p less than 0.001, at 48 h). The effect of quinacrine on the extent of necrosis was then assessed in 13 anesthetized dogs undergoing ligation of the left anterior descending coronary artery. To measure the area at risk (RZ), 99Tc-PP labeled albumin microspheres were injected into the left atrium 5 min after coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Long-term protection of ischaemic myocardium by nitroglycerin ointment.
To assess whether the reduction in ischaemic injury during acute myocardial infarction induced by nitroglycerin (NTG) results in a decrease in tissue necrosis, 96 rats were assigned to two groups. The first group (n = 34) was sham-operated. The second group of 62 rats was randomised in a ratio of 2:1 into control (n = 43) and treated (n = 19) subgroups following coronary artery occlusion. Treated animals received an application of 2% NTG ointment every 8 h immediately post-occlusion. All rats were killed 48 h after coronary artery occlusion and total creatine kinase activity (CK) of the left ventricle (LV) was measured. Infarct size calculated by CK depletion was 65.2 +/- 14.3% (mean +/- SD) of LV in control rats, and 51.6 +/- 14.0% of LV in NTG-treated (p less than 0.02). In a further series of 46 rats with coronary occlusion, the area of infarcted myocardium 21 days post-occlusion was assessed by planimetry on histological sections. In rats with control occlusion (n = 22), the extent of infarction was 30.6 +/- 4.8% of LV, and in NTG-treated rats (n = 24) it was 16.2 +/- 5.8% of LV (p less than 0.001). The amount of scar tissue in the infarcted myocardium 21 days post-occlusion was also determined by measuring LV hydroxyproline and collagen content in an additional 32 rats randomly assigned to a control (n = 11), a NTG-treated (n = 9) and a sham-operated group (n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Inhibition of IgE-mediated histamine release from human basophils and mast cells by fenoterol.
Fenoterol, a beta 2-adrenergic agonist recently introduced to treat asthmatic disorders, inhibits antigen-induced histamine release from human basophil leukocytes and lung mast cells in a dose-dependent fashion. The dose-response inhibition curve is paralleled by a fenoterol-induced increase in the cAMP levels of human leukocyte preparations. The relationship between the effect of fenoterol and cAMP level is supported by the finding that the beta 2-adrenergic agonist only inhibits the first stage of antigen-induced histamine release and not the release caused by the Ca2+ ionophore, A23187. Propranolol, a competitive antagonist of beta 2-adrenergic receptor, blocks the inhibition of release and the cAMP accumulation caused by fenoterol. Finally, theophylline, a cAMP phosphodiesterase inhibitor, synergistically potentiates the inhibitory effect of fenoterol on histamine release and the accumulation of cAMP. These data suggest that fenoterol may modulate the in vivo release of the mediators of immediate hypersensitivity reactions via the activation of beta 2-adrenergic receptor linked to adenylate cyclase on human basophils and mast cells.
Adolescent↗
Dilazep-induced reduction of ischemic necrosis in rats with coronary artery occlusion.
To assess whether dilazep reduces myocardial necrosis we assigned 72 rats that survived coronary artery occlusion to 3 groups. The first control group (n = 26) received coronary occlusion and was untreated. The second group (n = 21) received coronary occlusion and was treated with dilazep (150 micrograms/kg s.c.) every 8 hours for 48 hours. The third group (n = 25) was sham-operated. Forty-eight hours later the creatine-kinase activity of the left ventricle was measured. The calculated left ventricular fraction that survived the occlusion was larger in dilazep-treated rats (44.5 +/- 4.1% of left ventricle) than in controls (31.2 +/- 3.2%; P less than 0.05). Twenty-six more rats also underwent coronary occlusion; 12 were controls and the remaining 14 were treated with dilazep at the same time and dose as before and killed 21 days after occlusion. Infarct size was evaluated on histological sections of the hearts by planimetry. The amount of left ventricle preserved from necrosis was larger in dilazep-treated rats, 82.1 +/- 0.9%, compared to controls 69.5 +/- 1.4% (P less than 0.05). Dilazep seems effective in preserving myocardial tissue from ischemic necrosis, and its beneficial effects are long-lasting, producing permanent reduction of infarct size.
Animals↗