Hemodynamic effects of diuresis by ethacrynic acid in normal subjects and in patients with congestive heart failure

We carried out studies to determine whether the neutrophil-activation peptide-2 (NAP-2) plays a role in the recruitment and/or degranulation of neutrophils into the lungs of patients with the adult respiratory distress syndrome (ARDS) or congestive heart failure (CHF). NAP-2 precursors plus NAP-2 (beta-thromboglobulin-like antigen) were measured in lung fluids and plasmas with a radioimmunoassay, and NAP-2 was separated from its precursors by high-performance liquid chromatography. Pulmonary edema fluids (PEFs) from patients with CHF contained higher concentrations of the beta-thromboglobulin-like antigen than PEFs from patients with ARDS, and bronchoalveolar lavage fluids (BALs) from patients with ARDS contained higher concentrations of beta-thromboglobulin-like antigen than BALs from normal subjects. beta-Thromboglobulin-like antigen concentration was 4.1-fold greater in PEFs from patients with CHF than in their plasmas. Chemotactically active NAP-2 was also demonstrated in PEFs but not in plasmas from patients with CHF and ARDS. These data suggest that significant platelet degranulation occurred into the lungs of the patients with CHF and that NAP-2 and other platelet constituents may contribute to fluid formation in patients with CHF.

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Neurohumoral and hemodynamic effects of lower body negative pressure in patients with congestive heart failure

American Heart Journal ◽

10.1016/0002-8703(89)90075-6 ◽

1989 ◽

Vol 118 (1) ◽

pp. 78-85 ◽

Cited By ~ 51

Author(s):

Pramod K. Mohanty ◽

James A. Arrowood ◽

Kenneth A. Ellenbogen ◽

Marc D. Thames

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Hemodynamic Effects

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Hemodynamic effects of PN 200-110 (isradipine) in congestive heart failure

The American Journal of Cardiology ◽

10.1016/0002-9149(87)90085-3 ◽

1987 ◽

Vol 59 (3) ◽

pp. B70-B74 ◽

Cited By ~ 27

Author(s):

Barry Greenberg ◽

Deirdre Siemienczuk ◽

David Broudy

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Hemodynamic Effects

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Marked early attenuation of hemodynamic effects of oral prazosin therapy in chronic congestive heart failure

The American Journal of Cardiology ◽

10.1016/0002-9149(79)90409-0 ◽

1979 ◽

Vol 44 (3) ◽

pp. 540-545 ◽

Cited By ~ 84

Author(s):

Uri Elkayam ◽

Thierry H. Lejemtel ◽

Mitlesh Mathur ◽

Hillel S. Ribner ◽

William H. Frishman ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Chronic Congestive Heart Failure ◽

Hemodynamic Effects

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Increasing Transforming Growth Factor Beta-1 and its Receptor Expression in Human Myocardium with End-Stage Congestive Heart Failure.

Microscopy and Microanalysis ◽

10.1017/s1431927600035558 ◽

2000 ◽

Vol 6 (S2) ◽

pp. 612-613

Author(s):

S. Ren ◽

C. Wei

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Normal Subjects ◽

Human Myocardium ◽

Receptor Expression ◽

Growth Factor Beta ◽

End Stage

Transforming growth factor-beta (TGF-β) is a growth-regulating peptide that has been shown to enhance collagen production both in vivo and in vitro. The previous studies demonstrated that TGF-β 1 is present in the normal animal myocardium. However, the expression and localization of TGF-β 1 and TGF-P receptor in human myocardium remain unclear. Therefore, the present study was designed to determine the TGF-β 1 and its receptor in human myocardium in normal subjects and in patients with end-stage congestive heart failure (CHF).Human ventricular tissues were obtained from five normal subjects and five patients with end-stage CHF during cardiac transplantation. TGF-β 1 and TGF-beta type I receptor (TGF-βRI) were determined by immunohistochemical staining (IHCS). The results of IHCS was evaluated by staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining). The positive staining area (+%) in entire section was also determined.

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Decrease Tyrosine Phosphorylation of Stat3 in Human Myocardium with End-Stage Congestive Heart Failure

Microscopy and Microanalysis ◽

10.1017/s1431927600035479 ◽

2000 ◽

Vol 6 (S2) ◽

pp. 596-597

Author(s):

C. Wei ◽

J. S. McLaughlin

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Protein Expression ◽

Cardiac Tissue ◽

Normal Subjects ◽

Human Myocardium ◽

Stat3 Phosphorylation ◽

Normal Human ◽

Human Cardiac Tissue ◽

End Stage

Recent study demonstrated that decrease signal transducer and activator of transcription-3 (STAT3) phosphorylation and increase apoptosis might be a critical point in the transition between compensatory cardiac hypertrophy and heart failure. To date, the protein expression of STAT3 in normal and failing human heart remains unclear. Therefore, the current study was designed to investigate the protein expression of STAT3 in human myocardium with end-stage congestive heart failure (CHF) and compared with that in normal human cardiac tissue.Human cardiac atrial tissue was obtained from normal subjects (n=5) and end-stage CHF patients (n=5) during cardiac transplantation. To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) was performed. An average of 1000 nuclei was analyzed for TUNEL study. STAT3 protein expression and phosphorylation of STAT3 were determined by immunohistochemical staining (IHCS) with total STAT3 and phospho-specific STAT3 antibodies.

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