Vascular and Myocardial Protective Effects of Converting Enzyme Inhibition in Experimental Heart Failure

Mulder, Paul; Devaux, Bruno; Fertak, Lahcen El; Compagnon, Patricia; Henry, Jean‐Paul; Scalbert, Elizabeth; Desché, P.; Macé, Bertrand; Thuillez, Christian

doi:10.1016/s0002-9149(99)80500-1

Cited by 14 publications

(7 citation statements)

References 22 publications

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“…This tematically been reported to be active, at least vs fibrosis again underlines the major contribution of the renindevelopment [8][9][10]14]. Finally, that irbesartan opposed angiotensin system interruption to these effects and, alcardiac hypertrophy but not fibrosis development in our though not excluding it, minimizes the possible role of study supports the hypothesis of independent mechanisms bradykinin in their determinism.…”

Section: Infarct Sizesupporting

confidence: 59%

“…These include improvement of Angiotensin I-converting enzyme (ACE) inhibition is the hemodynamic status [8][9][10][11][12] with reduced afterload and now an established therapy for patients with chronic heart preload, decreased sympathetic activity [13] and limitation failure (CHF) and systolic left ventricular (LV) dysfuncor prevention of cardiac and vascular remodeling [8-tion and for patients who have had a myocardial infarction 10,14]. These effects have mostly been attributed to [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

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Effects of long-term angiotensin II AT1 receptor blockade on survival, hemodynamics and cardiac remodeling in chronic heart failure in rats

Richer¹,

Fornès²,

Cazaubon

et al. 1999

Cardiovascular Research

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Section: Infarct Sizesupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Effects of long-term angiotensin II AT1 receptor blockade on survival, hemodynamics and cardiac remodeling in chronic heart failure in rats

Richer¹,

Fornès²,

Cazaubon

et al. 1999

Cardiovascular Research

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“…The basal release of NO is unchanged.52 This is confirmed in treatments for 12 months with, in addition, a reduction of media cross-sectional area and collagen density. 53 In patients, these observations in the animal are confirmed by chronic treatment with inhibitors of converting enzyme, which reverse the inability of peripheral vessels to dilate. This delayed improvement can be attributed to an interaction with the NO pathway (Fig.…”

Section: Congestive Heart Failurementioning

confidence: 89%

Endothelium‐dependent Responses and Inhibition of Angiotensin‐converting Enzyme

Vanhoutte

1996

Clin Exp Pharma Physio

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1. Experimental and clinical studies have demonstrated the efficacy of inhibitors of angiotensin-converting enzyme (ACE) in a variety of cardiovascular diseases. Both structural and functional improvements have been reported. 2. Hypertension, atherosclerosis, congestive heart failure or ageing are accompanied by endothelial dysfunctions. The vasoactive endothelium-derived relaxing factors, nitric oxide, endothelium-derived hyperpolarizing factor and prostacyclin, could be involved, depending on the pathology. 3. Some of the beneficial effects of ACE inhibitors may be due to the augmented release of these endothelial factors resulting from the protection of locally produced bradykinin, particularly at the endothelial level.

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“…This indicates substantial myocardial hypertrophy, as the fraction area of fibrosis was only 12%. 4. Coronary small arteries preconstricted with 30mmol/l KCI showed a normal contractile response to acetylcholine and 5-hydroxytryptamine.…”

mentioning

confidence: 93%

“…An imbalance between these opposing factors would change coronary blood flow. Both clinical [3] and experimental studies [4] point to an endothelial dysfunction in heart failure. It is shown in a number of studies that the relaxation of small arteries to the endothelium-dependent vasodilator acetylcholine is attenuated in heart failure [4-61. This decreased stimulated release of EDRF is in contrast to the enhanced decrease in flow induced by administration of blockers of the basal N O production [7, 81.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Characterization of Coronary Small Arteries from Pigs with Chronic Ischaemic Myocardial Remodelling

et al. 1998

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1. The effect of chronic ischaemic myocardial remodelling on small coronary artery reactivity in vitro was studied in a newly developed pig model. 2. Pigs were subjected to selective intracoronary embolizations with microspheres in the left anterior descending artery and circumflex artery causing scattered myocardial fibrosis. After an observation period of 130 days, heart dimensions and ejection fraction were determined with magnetic resonance imaging. Small arteries were isolated from the left ventricle and mounted as ring preparations in a myograph. Control arteries were taken from matched non-embolized pigs. 3. Compared with control pigs, end-systolic and diastolic volumes increased and left ventricular mass nearly doubled in embolized pigs. This indicates substantial myocardial hypertrophy, as the fraction area of fibrosis was only 12%. 4. Coronary small arteries preconstricted with 30 mmol/l KCI showed a normal contractile response to acetylcholine and 5-hydroxytryptamine. Sensitivity of the relaxation to bradykinin was nearly 3-fold increased and also slightly enhanced to isoprenaline in arteries from embolized pigs compared with controls, whereas relaxation to 5-hydroxytryptamine in the presence of ketanserin was similar. After inhibition of nitric oxide synthase with NG-nitro-L-arginine the sensitivity to acetylcholine increased to a similar extent in arteries from embolized pigs and controls. NG-Nitro-L-arginine abolished the relaxing effects of bradykinin and of 5-hydroxytryptamine in the presence of ketanserin. 5. We conclude that both the contractile function of the smooth muscle cells and the endothelial production or action of nitric oxide is preserved or slightly enhanced in coronary small arteries from pigs with chronic myocardial remodelling.

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Vascular and Myocardial Protective Effects of Converting Enzyme Inhibition in Experimental Heart Failure

Cited by 14 publications

References 22 publications

Effects of long-term angiotensin II AT1 receptor blockade on survival, hemodynamics and cardiac remodeling in chronic heart failure in rats

Effects of long-term angiotensin II AT1 receptor blockade on survival, hemodynamics and cardiac remodeling in chronic heart failure in rats

Endothelium‐dependent Responses and Inhibition of Angiotensin‐converting Enzyme

Pharmacological Characterization of Coronary Small Arteries from Pigs with Chronic Ischaemic Myocardial Remodelling

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