Plasma endothelin determination as a prognostic indicator of 1-year mortality after acute myocardial infarction.

Omland, T; Lie, Rolv Terje; Aakvaag, A.; Aarsland, T; Dickstein, Kenneth

doi:10.1161/01.cir.89.4.1573

Cited by 362 publications

(187 citation statements)

References 39 publications

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“…Increased ET-1 activity is not only a causative factor to intestinal I/R injury, 17,36 but most importantly, elevated plasma ET-1 levels might be related to the size and extent of myocardial infarction and the mortality after myocardial infarction in patients, 37 a situation that is often accompanied with gastrointestinal complications. 38,39 Propofol attenuation of ET-1 production in the injured intestinal mucosa (Table) could potentially reduce its release to the circulation. It may also represent a mechanism whereby propofol attenuates MDA formation (Table), since ET-1 has been shown to stimulate superoxide production.…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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Purpose:We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury. Methods:Rats were randomly allocated into one of five groups (n = 10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg·kg -1 was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu's scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined. Results:Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu's scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity. Conclusion:These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol's antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels. CAN J ANESTH 2007 / 54: 5 / pp 366-374 Objectif : Nous avons cherché à savoir si le propofol, en dose sédative, pouvait empêcher les lésions d'ischémie/reperfusion (I/R) de la muqueuse intestinale, et s'il pouvait atténuer le stress oxydatif et les augmentations dans la libération d'oxyde nitrique (NO) et d'endothéline-1 (ET-1) pouvant survenir lors de lésions I/R intestinales. Méthode : Des rats ont été randomisés en cinq groupes (n = 10 chacun) : (i) faux témoin (sham control) ; (ii) lésion (occlusion de

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Section: Discussionmentioning

confidence: 99%

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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“…In addition, ET-1 actively participates in the infarction size evolution of the ischemic heart (36), and plasma ET levels are an independent predictor of 1-yr mortality after acute myocardial infarction (24).…”

Section: Effects Of Type 2 Diabetes Mellitus On Myocardial Insulin Rementioning

confidence: 99%

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Monti¹,

Landoni²,

Setola³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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dial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients. Am J Physiol Heart Circ Physiol 287: H1225-H1231, 2004. First published May 6, 2004; 10.1152/ajpheart.00629.2003.-We evaluated the influence of chronic hypertriglyceridemia and endothelial dysfunction on myocardial glucose uptake (MGU) in Type 2 diabetic patients without coronary heart disease. Patients were divided into two groups according to fasting triglyceride (TG) levels: 5.4 Ϯ 1.1 and 1.5 Ϯ 0.3 mmol/l for high-and normal-TG groups, respectively. Five subjects were assigned to the high-TG group and 11 to the normal-TG group. Age, gender, body mass index, systolic and diastolic blood pressure, glucose, insulin, HbA1c, cholesterol, and HDL cholesterol were similar in the two groups, whereas free fatty acid (FFA) levels were higher in the high-TG group basally and at the end of the clamp. Furthermore, five healthy subjects were subjected to the same protocol and used as the control group. MGU was assessed by using 18 F-labeled 2-fluoro-2-deoxy-D-glucose under hyperglycemic-hyperinsulinemic conditions. Basal endothelin-1 and nitric oxide levels were significantly higher in the high-TG group than in the normal-TG and control groups, and cGMP and maximal postischemic vasodilation were significantly decreased in the high-TG group compared with the normal-TG and control groups. However, significant alterations were found in the same parameters in the normal-TG group compared with the control group. By the end of the hyperglycemic clamp, in the high-TG group, MGU was ϳ40 and 65% of that in the normal-TG and control groups. MGU negatively correlated with TG, FFA, and endothelin-1, whereas a positive correlation was found with cGMP and maximal postischemic vasodilation. In conclusion, increased TG and FFA levels are risks, in addition to Type 2 diabetes mellitus, for myocardial insulin resistance, endothelial dysfunction, and alteration of nitric oxide/cGMP levels. triglycerides; myocardial glucose uptake; positron emission tomography study; endothelium; free fatty acid FOR MANY YEARS, hypertriglyceridemia was considered a marker of cardiovascular disease only in certain subjects, such as women (5, 12) and patients with Type 2 diabetes (10). The association between triglycerides (TGs), independently of HDL cholesterol levels, and definite cardiovascular disease, such as myocardial infarction or angina, was found in some studies (5) and denied in others, in which the simultaneous association of high TG and low HDL cholesterol was necessary to predict cardiovascular risk (8). This apparent discrepancy is probably related to the fact that it is quite difficult to match for duration and degree of cardiovascular disease in different populations, and, when cardiovascular disease is established, some factors might have lost their primary pathogenic significance. Hypertriglyceridemia occurs frequently in patients with coronary heart disease (CHD) and in survivors of myocardial infarction (5), and, durin...

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“…bosentan; heart; extracellular matrix; cardiac function DISCOVERED ONLY 16 years ago, the neurohormone endothelin-1 (ET-1) has been intensely investigated due to its potent cardiovascular effects and strong association with the pathophysiological worsening of cardiac function in congestive heart failure (7,13,16,29,35). ET-1 is a 21 amino acid peptide predominantly synthesized and secreted by endothelial cells.…”

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confidence: 99%

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

Murray

Gardner²,

Brower³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Murray DB, Gardner JD, Brower GL, Janicki JS. Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cellmediated ventricular remodeling in rats. Am J Physiol Heart Circ Physiol 294: H1251-H1257, 2008. First published January 4, 2008 doi:10.1152/ajpheart.00622.2007.-The objective of this study was to investigate the effect a nonselective endothelin-1 (ET-1) receptor antagonist (bosentan) had on the acute myocardial remodeling process including left ventricular (LV) mast cells and matrix metalloproteinase (MMP) activity secondary to volume overload. Additionally, we investigated the overall functional outcome of preventative endothelin receptor antagonism during 14 days of chronic volume overload. LV tissue from sham-operated (Sham), untreated-fistula (Fist), and bosentan (100 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 )-treated animals (Fist ϩ Bos) was analyzed for mast cell density, MMP activity, and myocardial collagen volume fraction at 1 and 5 days after the creation of an aortocaval fistula. When compared with untreated fistulas, bosentan treatment prevented the marked increase in LV mast cell density at 1 day postfistula (3.1 Ϯ 0.3 vs. 1.3 Ϯ 0.3 LV mast cells/mm 2 , Fist vs. Fist ϩ Bos, P Յ 0.01). Additionally, the substantial increase in MMP-2 activation in the untreated fistula at 1 day was prevented following bosentan treatment (1.6 Ϯ 0.3 vs. 0.9 Ϯ 0.1 arbitrary activity units, Fist vs. Fist ϩ Bos, P Յ 0.01). The marked decrease in collagen volume fraction seen in the Fist group (1.4 Ϯ 0.1 vs. 0.8 Ϯ 0.1% myocardial tissue, Sham vs. Fist, P Յ 0.01) was significantly attenuated following bosentan treatment at both the 1-and 5-day time points. Lastly, a 2-wk preventative treatment with bosentan resulted in significant attenuation of the increase in LV end-systolic and -diastolic volumes compared with those in untreated fistula hearts. In summary, nonselective ET-1 antagonism prevents the acute increases in cardiac mast cell density and MMP activation induced secondary to chronic volume overload. By preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits in the first 2 wk of chronic volume overload. Accordingly, these results are the first to demonstrate that cardiac mast cells are responsive to the endogenous endothelin system in vivo. Another novel finding from this study is that chronic nonspecific endothelin antagonism may inadvertently potentiate ET-1-mediated signaling.bosentan; heart; extracellular matrix; cardiac function DISCOVERED ONLY 16 years ago, the neurohormone endothelin-1 (ET-1) has been intensely investigated due to its potent cardiovascular effects and strong association with the pathophysiological worsening of cardiac function in congestive heart failure (7,13,16,29,35). ET-1 is a 21 amino acid peptide predominantly synthesized and secreted by endothelial cells. The effects of ET-1 are dictated by binding to one of two G protein-linked receptor subtypes A or B (ET A or ET B ) (16). In th...

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Plasma endothelin determination as a prognostic indicator of 1-year mortality after acute myocardial infarction.

Abstract: Plasma endothelin concentrations are strongly related to outcome after myocardial infarction and provide prognostic information independent of clinical and biochemical variables previously associated with a poor prognosis.

Cited by 362 publications

References 39 publications

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

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