Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

68 patients with defined myocardial ischemia, undergoing aorto-coronary bypass operation were assigned either to a group supplemented with L-carnitine (n = 41) or to a control group (n = 27). When extracorporeal circulation was established, a small piece of the right atrial appendage was biopsied and prepared for analysis for ATP, lactate and carnitine fractions. The ATP concentrations were higher in the patients supplemented with carnitine. A negative correlation existed between ATP and lactate levels. The amount of total carnitine was similar in both groups. However, free carnitine was higher, and long-chain acylcarnitine was lower when L-carnitine was supplemented. Postoperatively, the patients needed less inotropic medicaments, when supplemented with L-carnitine. L-carnitine supplementation in patients needed less inotropic medicaments, when supplemented with L-carnitine. L-carnitine supplementation in patients undergoing aorto-coronary bypass operation proved to be effective and beneficial for the normalization of myocardial energy metabolism parameters.
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PMID:The effect of preoperative L-carnitine supplementation on myocardial metabolism during aorto-coronary bypass surgery. 350 44

To evaluate the protective effects of L-carnitine on the ischemic myocardium, the effects of its administration on tissue levels of high energy phosphate and phospholipids were studied in ischemic dog hearts. Myocardial ischemia was induced by the ligation of the left anterior descending coronary artery for 40 min. In the experiment, L-carnitine (300 mg/kg) was administered intravenously prior to coronary artery ligation. Mitochondrial phospholipids were extracted from nonischemic and ischemic regions of the myocardium and subsequently analyzed. In ischemic myocardial tissues, levels of adenosine 5'-triphosphate (ATP) were reduced. The decrease was significantly elevated by L-carnitine pretreatment. The mitochondrial fractions obtained from ischemic myocardia had significantly lower levels of phospholipids than those obtained from nonischemic tissues. Moreover, the amounts of phosphatidylcholine, phosphatidylinositol and phosphatidylethanolamine were significantly decreased in ischemic myocardial tissues. L-carnitine-pretreatment prevented the reduction of these phospholipids. Lysophosphatidylethanolamine and sphingomyelin did not show statistically significant decreases. This may explain why the administration of carnitine has beneficial effects on ischemic myocardium.
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PMID:Effects of L-carnitine on phospholipids in the ischemic myocardium. 359 11

Our previous studies revealed that sympathetic-nerve stimulation (SNSt) plays an important role in the precipitation and the augmentation of myocardial ischemia in dogs with coronary constriction. To clarify the underlying mechanism of the detrimental effect of free fatty acids (FFA) at a high plasma concentration and the beneficial effect of L-carnitine on myocardial ischemia, ischemic changes following SNSt were compared among three groups of dogs with mild or moderate coronary constriction: a saline control group, an intralipid [(IL) 0.1 ml/kg per min + heparin 5 mg/kg] group, and an IL + L-carnitine (200 mg/kg) group. High plasma concentration of FFA aggravated the ischemic changes induced by SNSt in dogs with coronary constriction, in which no signs of increase in myocardial oxygen consumption were seen. L-Carnitine clearly alleviated the mechanical dysfunction, acceleration of anaerobic metabolism, depletion of myocardial contents of high-energy phosphates, myocardial accumulation of lactate, and ECG ischemic changes that were augmented by high plasma FFA in the coronary-constricted dogs with SNSt. From these findings, it was suggested that an increased plasma FFA might aggravate myocardial ischemia, at least, produced by SNSt in dogs with mild or moderate coronary constriction and that L-carnitine might improve the ischemia augmented by FFA, presumably by reducing myocardial accumulation of FFA intermediates.
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PMID:Studies on experimental coronary insufficiency. Effect of L-carnitine on myocardial ischemia produced by sympathetic-nerve stimulation with high plasma fatty acids. 399 42

L-Carnitine is an essential cofactor in transfer of long-chain fatty acids across the inner mitochondrial membrane. L-Carnitine is present in living systems in free form and as short-chain and long-chain fatty acylcarnitine esters. In recent years, several clinical syndromes due to or associated with carnitine deficiency have been described. They include 2 primary types--systemic and muscle (or myopathic) carnitine deficiency--and at least 15 syndromes in which carnitine deficiency seems to be secondary to genetic defects of intermediary metabolism or to other conditions. Possible beneficial effects of exogenous carnitine in ischemic heart disease have been the focus of intensive research in recent years. Free carnitine and esterified carnitine are measured by a sensitive enzymatic-radiochemical method. In some cases, the diagnosis of carnitine deficiency can be made by assay of total (free plus esterified) carnitine in plasma or serum. Proper diagnosis, however, often depends on determination of total carnitine in skeletal muscle or liver (or both). Since the first clinical description of carnitine deficiency in 1973, considerable progress has been made in defining and classifying the carnitine deficiency syndromes. Recent efforts in basic and clinical research have provided important clues about the molecular causes of these syndromes.
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PMID:Carnitine metabolism and deficiency syndromes. 634 29

Infusions of DL-carnitine are reported to improve the tolerance to atrial pacing of patients with angina pectoris. In the present study, six patients with angina of effort and triple vessel disease received two placebo and two carnitine infusions administered in a double-blind randomized fashion. Carnitine did not affect either the double product (heart rate X systolic blood pressure) at maximal pacing (ST depression: 2.3 +/- 0.2 mm, +/- SEM) or the tolerated pacing time. Intravenous carnitine, in the dose given, is of no therapeutic benefit in myocardial ischemia precipitated by tachycardia. It could be effective when free fatty acids are elevated as during catecholamine stimulation.
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PMID:Intravenous dl-carnitine fails to increase the double-product during atrial pacing in patients with effort angina. A double-blind randomized study. 666 14

In order to evaluate the protective effects of L-carnitine on ischemic myocardium, its effects on tissue levels of free fatty acid (FFA), acyl CoA, acyl carnitine, and adenosine triphosphate (ATP) were studied in ischemic dog hearts. Myocardial ischemia was induced by the ligation of left anterior descending coronary artery for 15 min. L-Carnitine (100 mg/kg) was administered intravenously prior to coronary ligation. In ischemic myocardium, tissue levels of free carnitine and ATP decreased, whereas long-chain acyl carnitine, long-chain acyl CoA, and FFA increased. Pretreatment of L-carnitine prevented the decrease in free carnitine and ATP and the increase in long-chain acyl carnitine and long-chain acyl CoA. A positive correlation was observed between ATP and free carnitine. On the other hand, a negative correlation was observed not only between ATP and the ratio of long-chain acyl CoA to free carnitine but also between ATP and the ratio of long-chain acyl carnitine to free carnitine. These results suggest that L-carnitine has protective effects on ischemic myocardium, probably by preventing the accumulation of long-chain acyl carnitine and long chain acyl CoA.
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PMID:Effects of L-carnitine on tissue levels of free fatty acid, acyl CoA, and acylcarnitine in ischemic heart. 685 80

The effects of L-carnitine on ventricular arrhythmias were evaluated in dogs with acute myocardial ischemia and a supplement of excess free fatty acids (FFA). Acute myocardial ischemia was induced by ligation of left anterior descending coronary artery. After 80 minutes of coronary occlusion, high plasma FFA was induced by intravenous injection of heparin 200 mu/kg and Intralipid 5 ml/kg as a bolus. After additional 60 minutes, beating hearts were removed from animals and tissue levels of free carnitine, short and long chain acyl carnitine, FFA and adenosine triphosphate (ATP) were determined. L-carnitine 100 mg/kg was administered intravenously 5 minutes before coronary artery ligation. Electrocardiograms were recorded continuously by a Holter electrocardiographic recorder during the experiment and ventricular arrhythmias were quantified by an arbitrary scoring system. In ischemic and excess FFA supplemented myocardium, free carnitine and ATP decreased, whereas long chain acyl carnitine and FFA increased. And these metabolic changes tended to be reduced by L-carnitine. Pretreatment of L-carnitine also reduced the grade of ventricular arrhythmias induced both by acute myocardial ischemia and by supplemented of excess FFA. These results suggest that the administration of L-carnitine may be beneficial to prevent serious arrhythmias in ischemic heart disease, presumably by restoring the imparied FFA oxidation.
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PMID:Effects of L-carnitine on ventricular arrhythmias in dogs with acute myocardial ischemia and a supplement of excess free fatty acids. 723 May 9

Several studies have suggested that L-carnitine may limit the cellular alterations induced by myocardial hypoxia or ischemia. In the present study, rats were subjected to chronic treatment with L-carnitine (0, 25, 50 or 200 mg/kg/day i.p.) for 9 days prior to being submitted to permanent regional myocardial ischemia by left coronary artery ligation in situ. Following 48 hours of coronary occlusion, infarct size was measured using planimetry of transverse sections of the hearts, which had been stained with nitro-blue tetrazolium. Various functional and metabolic parameters have also been measured in isolated perfused hearts. Treatment with L-carnitine at 200 mg/kg/day i.p. for 9 days led to a significant reduction in infarct size and a better preservation of residual cardiac function. However, none of the metabolic parameters measured were modified. In conclusion, we suggest that the preservation of cardiac contractile function observed with L-carnitine pretreatment is secondary to carnitine-induced infarct size limitation.
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PMID:Cardioprotective effect of L-carnitine in rats submitted to permanent left coronary artery ligation. 751 37

In order to evaluate a possible antiarrhythmic action of L-carnitine (C) in ischemic heart disease, 30 patients (20 males, 10 females, average age 64 years +/- 11) with ischemic heart disease who at examination with 24-hour dynamic ECG showed extrasystolic ventricular multifocal arrhythmia with a mean hourly rate of > 300 were randomized into three groups, the first of which was given a daily oral dose of 6 g C in three divided doses; groups 2 and 3 were given propafenone (P), 900 mg daily in three divided doses. After one week, all patients were again submitted to 24-hour dynamic ECG after which treatment was continued for another week as follows: group 1 continued on C (6 g daily), group 2 continued on P (900 mg daily), group 3 continued on P (900 mg daily) plus C (6 g daily). At the end of the second week, a further 24-hour ECG was performed the results of which showed that L-carnitine can significantly reduce the antiarrhythmic activity of the ischemic myocardium. In addition, at the end of the second week, a further significant reduction of the number of premature beats compared to the first week was found in patients for whom L-carnitine had been added to propafenone treatment.
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PMID:[The evaluation of the antiarrhythmic activity of L-carnitine and propafenone in ischemic cardiopathy]. 768 88

The rationale for these experiments is that administration of L-carnitine and/or short-chain acylcarnitines attenuates myocardial dysfunction 1) in hearts from diabetic animals (in which L-carnitine levels are decreased); 2) induced by ischemia-reperfusion in hearts from nondiabetic animals; and 3) in nondiabetic humans with ischemic heart disease. The objective of these studies was to investigate whether imbalances in carnitine metabolism play a role in the pathogenesis of diabetic peripheral neuropathy. The major findings in rats with streptozotocin-induced diabetes of 4-6 weeks duration were that 24-h urinary carnitine excretion was increased approximately twofold and L-carnitine levels were decreased in plasma (46%) and sciatic nerve endoneurium (31%). These changes in carnitine levels/excretion were associated with decreased caudal nerve conduction velocity (10-15%) and sciatic nerve changes in Na(+)-K(+)-ATPase activity (decreased 50%), Mg(2+)-ATPase (decreased 65%), 1,2-diacyl-sn-glycerol (DAG) (decreased 40%), vascular albumin permeation (increased 60%), and blood flow (increased 65%). Treatment with acetyl-L-carnitine normalized plasma and endoneurial L-carnitine levels and prevented all of these metabolic and functional changes except the increased blood flow, which was unaffected, and the reduction in DAG, which decreased another 40%. In conclusion, these observations 1) demonstrate a link between imbalances in carnitine metabolism and several metabolic and functional abnormalities associated with diabetic polyneuropathy and 2) indicate that decreased sciatic nerve endoneurial ATPase activity (ouabain-sensitive and insensitive) in this model of diabetes is associated with decreased DAG.
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PMID:Neural dysfunction and metabolic imbalances in diabetic rats. Prevention by acetyl-L-carnitine. 795 1


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