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Clin Cardiol. 1993 Mar;16(3):235-8.
Hemodynamic response to intravenous enalaprilat in patients with severe congestive heart failure and mitral regurgitation.

Varriale P, David W, Chryssos BE.

Cardiology Division, Cabrini Medical Center, New York, NY 10003.

The hemodynamic response 1 hour after 1.25 mg of intravenous (IV) enalaprilat was examined in 20 patients (mean age 75 years) with severe congestive heart failure (CHF) and mitral regurgitation (MR), secondary to ischemic heart disease (NYHA Class IV). Patients were classified into two groups based upon the magnitude of MR as derived from Doppler color flow imaging: Group I (n = 13) had severe MR and Group II (n = 7) had moderate MR. Acute therapy significantly reduced systemic vascular resistance index in both groups and provided effective afterload reduction. Although cardiac and stroke volume indices increased in both groups, an improved forward flow was significant only for Group I (cardiac index 2.2 +/- 0.5 to 2.7 +/- 0.5 l/min/m2, p < 0.02). The magnitude of MR, acutely reduced in all patients, was similarly significant only for Group I (56 +/- 10% to 31 +/- 12%, p < 0.01). The reduction of both pulmonary capillary wedge pressure and mean arterial pressure was significant for both groups. This study supports the use of IV enalaprilat, a parenteral angiotensin-converting enzyme (ACE) inhibitor, as an effective and rapidly acting vasodilator in the management of selected patients with chronic heart failure and MR who require immediate hemodynamic improvement.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8383028&dopt=Abstract




Cor Vasa. 1990;32(3):225-30.
Acute effect of intrapulmonary enalaprilat in ten patients with severe pulmonary hypertension due to toxic oil syndrome.

Gomez Pajuelo C, Gomez Sanchez MA, Alonso Gutierrez M, Lombera Romero F, Gabriel Sanchez R, Fernandez Cruz A, Saenz de la Calzada C.

Cardiology Service, Hospital 12 de Octubre, Madrid, Spain.

Ten patients with severe pulmonary hypertension due to Toxic Oil Syndrome underwent cardiac catheterization to analyse the acute effect of intrapulmonary injection of 1.25 mg of enalaprilat. Haemodynamic parameters were obtained at basal state, 15, 30, 45 and 60 minutes after administration of the drug. Enalaprillat did not produce any statistically significant changes in pulmonary pressures and resistances or cardiac output. This lack of response is unknown but may be related to the presence of endothelial damage and fixed pulmonary vascular lesions observed at autopsy in three patients.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2209025&dopt=Abstract




Br J Clin Pharmacol. 1994 Jul;38(1):53-6.
The effect of angiotensin-converting enzyme inhibitors on human neutrophil chemotaxis in vitro.

Clapperton M, McMurray J, Fisher AC, Dargie HJ.

Department of Cardiology, Western Infirmary, Glasgow.

1. Myocardial 'reperfusion injury' has been partly attributed to the production of free radicals which are cytotoxic towards cells. Neutrophils are recruited by ischaemic tissue and are one source of free radicals. Angiotensin-converting enzyme (ACE) inhibitors can reduce 'reperfusion injury' and we decided to determine if ACE inhibitors might contribute to this effect by inhibiting neutrophil chemotaxis. 2. The effects of captopril (a thiol containing ACE inhibitor) and enalaprilat (a nonthiol ACE inhibitor) and N-mercaptopropionyl glycine (MPG) (a simple thiol) on neutrophil chemotaxis were tested in an in vitro Boyden chamber assay. 3. The chemotactic response of human neutrophils to fMLP was reduced by 27.6% with MPG (n = 8; P < 0.05), by 13.2% with enalaprilat (n = 8; P = 0.075) and by 5.2% with captopril (n = 8; P = 0.66) at 5 microM (therapeutic concentration.) 4. Neutrophil chemotaxis was significantly decreased with 50 microM and 500 microM MPG and enalaprilat and 500 microM captopril. 5. Supratherapeutic concentrations of ACE inhibitors can reduce neutrophil chemotaxis at high concentrations and this effect does not appear to be -SH dependent.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7946937&dopt=Abstract












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