Enalaprilat in acute intractable heart failure after myocardial infarction

Tohmo, H.; Karanko, Meri S.; Korpilahti, Kari; Scheinin, Mika; Viinamäki, O; Neuvonen, Pertti J.

doi:10.1097/00003246-199406000-00015

Cited by 17 publications

(3 citation statements)

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“…Lower doses of enalaprilat (Ͻ0.5 mg/hr) also may be effective, as has been shown in acute intractable heart failure after myocardial infarction (19) and in congestive heart failure with acute refractory decompensation (20). The ideal dosage for the continuous infusion of enalaprilat has not yet been clearly defined for our patient group.…”

Section: Discussionmentioning

confidence: 91%

“…Enalaprilat administered intravenously to patients with chronic heart failure (22), acute intractable heart failure after myocardial infarction (19), and acute pulmonary edema (34) has not affected plasma catecholamine concentrations. In other studies, a decrease of norepinephrine in chronic congestive heart failure has been reported (35,36).…”

Section: Discussionmentioning

confidence: 97%

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Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction*

Wagner

Yeter

Bisson

et al. 2003

Critical Care Medicine

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 97%

Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction*

Wagner

Yeter

Bisson

et al. 2003

Critical Care Medicine

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show abstract

“…Heart failure (HF) results from impaired ventricular filling and/or ejection function caused by a variety of cardiac structural or functional diseases (1). As cardiac output does not meet the requirements of body tissues for metabolism, HF behaves similarly to a series of syndromes that are characterized by having a clinical manifestation of pulmonary circulation deficiency and/or congestion of systemic circulation, and organ-tissue blood perfusion insufficiency (2). The main symptoms of HF include difficulty in breathing which limits physical activity and fluid retention.…”

Section: Introductionmentioning

confidence: 99%

Influence of androgen on myocardial apoptosis and expression of myocardial IR and IRS‑1 in chronic heart failure rat models

Wang

Zeng³

et al. 2017

Mol Med Report

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The present study aimed to investigate the effect of androgens on chronic heart failure (CHF) in a rat model. A total of 120 Sprague Dawley male rats were randomly divided into the following groups: (A) sham operation group, (B) castrated group, (C) heart failure (HF) group, (D) castrated + HF group, and (E) castrated + HF + testosterone (T) replacement therapy group. There were 20 rats in group A, and 25 rats in the other groups. Surgical castration was performed on groups B, D and E, and T replacement therapy was administered to group E. Groups C, D and E were treated with doxorubicin hydrochloride to prepare the CHF animal model. The insulin sensitivity index (ISI) was calculated from fasting blood glucose and fasting insulin levels. Echocardiography was performed. Venous blood was collected for plasma T level test. Myocardial tissue was used for apoptosis index analysis. The expression levels of myocardial insulin receptor (IR) and insulin receptor substrate‑1 (IRS‑1) were measured by reverse transcription semi‑quantitative polymerase chain reaction. Compared with group A, the T level and ISI decreased, whereas the expression level of IR and IRS‑1 were increased in the CHF group (P<0.05). Following castration, the T level and ISI were significantly decreased, and the expression of IR and IRS‑1 were increased compared with the uncastrated CHF rats (P<0.01). Following androgen administration, the ISI increased, expression of IR and IRS‑1 decreased, and the myocardial apoptosis index decreased (P<0.05). Taken together, these results demonstrated that androgen supplementation could improve insulin resistance and affect the expression of IR and IRS‑1 in CHF, thereby reducing myocardial apoptosis and improving cardiac function.

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Pathophysiological Role of Endothelin and Potential Therapeutic Targets for Receptor Antagonists

Brooks¹,

Jorkasky²,

Freed³

et al. 1998

Endothelin

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Enalaprilat in acute intractable heart failure after myocardial infarction

Cited by 17 publications

References 0 publications

Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction*

Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction*

Influence of androgen on myocardial apoptosis and expression of myocardial IR and IRS‑1 in chronic heart failure rat models

Pathophysiological Role of Endothelin and Potential Therapeutic Targets for Receptor Antagonists

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