scholarly journals Studies of Circulation Time During the Valsalva Test in Normal Subjects and in Patients with Congestive Heart Failure

Circulation ◽  
1955 ◽  
Vol 11 (6) ◽  
pp. 900-908 ◽  
Author(s):  
PAUL STUCKI ◽  
J. D. HATCHER ◽  
WALTER E. JUDSON ◽  
ROBERT W. WILKINS
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Normal Subjects ◽  
Circulation Time ◽  
Valsalva Test

Neutrophil-activating peptide-2 in patients with pulmonary edema from congestive heart failure or ARDS

1993 ◽  
Vol 264 (5) ◽  
pp. L490-L495 ◽  
Author(s):  
A. B. Cohen ◽  
M. D. Stevens ◽  
E. J. Miller ◽  
M. A. Atkinson ◽  
G. Mullenbach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Pulmonary Edema ◽  
High Performance ◽  
Distress Syndrome ◽  
Normal Subjects ◽  
Antigen Concentration ◽  
Fluid Formation

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.

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

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.

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

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.

The Influence of Acenocumarole on the Fibrinogen-turnover in Normal Subjects, Venous Thrombosis and Congestive Heart Failure

1972 ◽  
Vol 28 (03) ◽  
pp. 496-508
Author(s):  
A. P. C. van der Maas ◽  
F. A. G Teulings ◽  
W Schopman ◽  
G. J. H. den Ottolander
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Normal Subjects ◽  
Time Interval ◽  
Normal Range ◽  
The Mean ◽  
The Moment ◽  
Continuous Deposition

SummaryUsing 131Iodine-tagged fibrinogen the influence of acenocumarole on the biological half-life of fibrinogen was investigated in healthy patients, patients with venous thrombosis and patients with congestive heart failure.In 16 healthy patients the mean t½ was 3.8 days. In two of them after administration of acenocumarole the t½ was lengthened. This supports the opinion of a continuous deposition of fibrin on the vascular endothelium in the hemostatic balance.In 13 patients with venous thrombosis the mean t½ was 2.45 days, lengthening to the normal range after acenocumarole therapy. The time interval between the start of acenocumarole therapy and the moment of normalization of the t½ was approximately 4 days. The prothrombin time-index at this moment was 2.3 (thrombotest 5%), which argues in favour of a vigorous anticoagulant therapy.In our 10 patients with congestive heart failure probably venous thrombosis occurred in 40%. Prophylactic anticoagulant therapy as in surgical patients therefore has to be considered.

Enhancement of Endothelin Converting Enzyme and Endothelin Receptor Subtypes in Human Myocardium with Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 608-609
Author(s):  
J. Lin ◽  
C Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Tissue ◽  
Vascular Endothelial Cells ◽  
Normal Subjects ◽  
Human Myocardium ◽  
Endothelin Receptors ◽  
Receptor Subtypes ◽  
Converting Enzyme ◽  
Endothelin Converting Enzyme

Endothelin-1 (ET-1) is a potent endothelial cell-drived vasoconstrictive peptide which is increased in congestive heart failure (CHF). ET-1 is converted from its precursor big ET-1 by activation of endothelin converting enzyme (ECE). ET-1 binding to ET-A receptor in vascular smooth muscle cells stimulates vasoconstriction and binding to ET-B receptor in vascular endothelial cells mediates vasodilation. In previous studies, we and others demonstrated that plasma ET-1 was significantly increased in congestive heart failure. However, the presentation and localization of endothelin converting enzyme and endothelin receptors (ET-A and ET-B) in human cardiac tissue with and without heart failure remain unclear. Therefore, the current study was designed to investigate the expression and localization of endothelin receptors and endothelin converting enzyme in human myocardium in the absence or presence of congestive heart failure.Human atrial tissues (n=6) were obtained from normal subjects and end-stage CHF patients during cardiac transplantation. The expression of ECE, ET-A and ET-B were determined by immunohistochemical staining (IHCS).

Paradoxical forearm vasodilatation and haemodynamic improvement during cardiopulmonary baroreceptor unloading in patients with congestive heart failure

1993 ◽  
Vol 84 (3) ◽  
pp. 271-280 ◽  
Author(s):  
Katsuhiko Nishian ◽  
Seinosuke Kawashima ◽  
Tadaaki Iwasaki
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Plasma Level ◽  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Normal Subjects ◽  
Lower Body ◽  
Vascular Response

1. To examine the contribution of paradoxical reflex forearm vasodilatation during unloading of cardiopulmonary baroreceptors to systemic haemodynamics, the responses of central and peripheral haemodynamics during lower-body negative pressure were measured in 24 patients with chronic congestive heart failure (New York Heart Association functional class II-IV) and were compared with those of 10 normal subjects. 2. Lower-body negative pressure of less than −20 mmHg caused a significant forearm vasoconstriction in normal subjects but not in patients with congestive heart failure. In the individual cases, however, eight patients (subgroup A) had a significant forearm vasoconstriction, whereas 10 patients (subgroup B) had a paradoxical forearm vasodilatation. The remaining six patients had a blunted forearm vascular response. Baseline pulmonary capillary wedge pressure (26 ± 3 versus 20 ± 1 mmHg, means ± SEM) and left ventricular wall stress in end-diastole (57 ± 6 versus 37 ± 4 g/cm2) were significantly (P <0.05) higher in subgroup B than in subgroup A. 3. During lower-body negative pressure of −20 mmHg, the plasma level of noradrenaline, systemic vascular resistance and cardiac index did not change significantly in subgroup A. In subgroup B, however, during this orthostatic stimulus systemic vascular resistance fell significantly from a baseline value of 2023 ± 109 to 1740 ± 110 dyns−1 cm−5 (P <0.01) and cardiac index increased significantly from a baseline value of 2.0 ± 0.1 to 2.5 ± 0.21 min−1 m−2 (P <0.01) despite there being no significant change in the plasma level of noradrenaline. 4. After treatment, a second bout of lower-body negative pressure was applied to seven patients in subgroup B. The forearm vascular response to the second bout of lower-body negative pressure was normalized. 5. These data suggest that the patients with more severe heart failure show a paradoxical forearm vasodilatation during mild lower-body negative pressure and that this altered cardiopulmonary baroreflex control of the circulation serves to improve the depressed cardiac performance.

Use of Radioisotopes in the Study of Shoulder to Thigh Circulation Time

1971 ◽  
Vol 10 (04) ◽  
pp. 316-324
Author(s):  
Vernon Ficken ◽  
Carl Smith ◽  
Samuel Halpern
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Femoral Artery ◽  
Subclavian Vein ◽  
Circulation Time ◽  
Inguinal Ligament ◽  
Comatose Patient ◽  
Clinical Chart ◽  
Hyperthyroid Patients

SummaryA method is described for the measurement of shoulder to thigh circulation times using isotopic methodology. Following the positioning of scintillation probes over the subclavian vein at the shoulder and the femoral artery at the level of the inguinal ligament, one millicurie of 99mTcO4 – is injected as a bolus into the arm distal to the shoulder probe. The time between arrival of the radionuclide at the shoulder and femoral artery is the circulation time. The method is accurate and reproducible. Normal circulation times averaged 13.7 ± 2.8 seconds. Patients with congestive heart failure averaged 32 seconds with a range of 19.6—15.6. Hyperthyroid patients averaged 9.1 seconds with a range of 6.2— 13.8. Following treatment the hyperthyroid patients who became euthyroid generally developed normal circulation times while those that remained hyperthyroid continued to have shortened circulation times. The method for doing the circulation time described is useful since it is completely objective, non toxic, may be used in studying the comatose patient, and gives a written record for incorporation into the patient’s clinical chart.

scholarly journals Effects of supplemental oxygen on forearm vasodilation in humans

1997 ◽  
Vol 82 (5) ◽  
pp. 1601-1606 ◽  
Author(s):  
Paul Crawford ◽  
Peter A. Good ◽  
Eric Gutierrez ◽  
Joshua H. Feinberg ◽  
John P. Boehmer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vascular Resistance ◽  
Peak Flow ◽  
Lower Body Negative Pressure ◽  
Normal Subjects ◽  
Supplemental Oxygen ◽  
Lower Body ◽  
Minimal Resistance ◽  
Minimum Resistance

Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway.Effects of supplemental oxygen on forearm vasodilation in humans. J. Appl. Physiol. 82(5): 1601–1606, 1997.—Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml ⋅ min−1 ⋅ 100 ml−1; P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg ⋅ min ⋅ 100 ml ⋅ ml−1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; −30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC, P < 0.04). When O2 alone ( experiment 1) was compared with O2+LBNP+VC ( experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

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