Heart failure depresses endothelium-dependent responses in canine femoral artery

1989 ◽  
Vol 256 (4) ◽  
pp. H962-H967 ◽  
Author(s):  
L. Kaiser ◽  
R. C. Spickard ◽  
N. B. Olivier
Keyword(s):  
Heart Failure ◽  
Femoral Artery ◽  
Peripheral Resistance ◽  
Vascular Control ◽  
Experimental Heart Failure ◽  
Low Concentrations ◽  
Local Mechanism ◽  
Before And After ◽  
Significant Depression ◽  
Response To Exercise

Vascular responses to many physiological stresses are abnormal in heart failure. Increased peripheral resistance and a reduction in the vasodilator response to exercise and ischemia are examples of this abnormal vascular control. Such abnormal vascular control in heart failure is a result of interplay between neural, hormonal, and local vascular factors. This study was designed to test the hypothesis that a specific local mechanism, endothelium-dependent relaxation to acetylcholine (ACh), is depressed in experimental heart failure. Experiments were performed on 11 purebred beagles. Experimental heart failure was induced by rapid ventricular pacing for approximately 30 days. Femoral artery diameter was measured by sonomicrometry, and dose-response relationships to ACh, norepinephrine (NE), and nitroglycerin (NTG) were done before and after inhibition of cyclooxygenase by indomethacin. Heart failure resulted in a significant depression of ACh relaxation at all concentrations. In dogs with heart failure, indomethacin enhanced the dilation response to low concentrations of ACh. Constriction to NE and dilation to NTG were unchanged by heart failure. These data demonstrate that in the canine femoral artery endothelium-dependent dilation to ACh is depressed in experimental heart failure. Depression of endothelium-dependent vasodilation represents one local mechanism for abnormal control of the vasculature in congestive heart failure.

Hemodynamic effects of normovolemic polycythemia in dogs at rest and during exercise

1964 ◽  
Vol 207 (6) ◽  
pp. 1361-1366 ◽  
Author(s):  
Allen B. Weisse ◽  
Farrell M. Calton ◽  
Hiroshi Kuida ◽  
Hans H. Hecht
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Oxygen Transport ◽  
Peripheral Resistance ◽  
Relative Increase ◽  
Red Cells ◽  
Hemodynamic Effects ◽  
Venous Oxygen Saturation ◽  
Before And After ◽  
Response To Exercise

The hemodynamic effects of acutely induced normovolemic polycythemia were studied in four anesthetized and seven unanesthetized dogs at rest and, in three of the latter, during treadmill exercise. Control observations were made in four other animals. Volume of packed red cells values of 60–79% were produced by exchange transfusion with washed centrifuged red cells. Normovolemic polycythemia in both anesthetized and unanesthetized resting animals was associated with a decrease in cardiac output and oxygen transport; little change in pulmonary artery, carotid artery, right atrium, and pulmonary artery wedge pressures; and increases in calculated total systemic and pulmonary vascular resistances. Mixed venous oxygen saturation was not necessarily reduced. The relative increase in cardiac output and oxygen transport in response to exercise was similar before and after normovolemic polycythemia, but the absolute increments were significantly less after normovolemic polycythemia. Results obtained are consistent with the concept that cardiac output reduction with normovolemic polycythemia is mediated by increased peripheral resistance.

Factors involved in delaying the rise in peripheral resistance in developing heart failure

1994 ◽  
Vol 267 (1) ◽  
pp. H211-H216 ◽  
Author(s):  
K. Kiuchi ◽  
R. P. Shannon ◽  
N. Sato ◽  
M. Bigaud ◽  
C. Lajoie ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Peripheral Vascular ◽  
Vascular Control ◽  
Developing Heart

The development of heart failure (HF) on peripheral vascular control was studied in 10 conscious dogs with measurements of cardiac output (CO) and left ventricular (LV), arterial, and right atrial pressures. At 3 wk after pacing-induced HF, CO was not decreased from 2.5 +/- 0.2 l/min, whereas LV dP/dt fell (from 2,858 +/- 71 to 1,409 +/- 69 mmHg/s) and LV end-diastolic pressure increased (from 4.8 +/- 0.4 to 27.3 +/- 1.1 mmHg) (P < 0.05). At 4–7 wk after pacing, CO was significantly decreased (to 1.6 +/- 0.1 l/min; P < 0.05), but total peripheral resistance (TPR) did not rise, despite increases in plasma norepinephrine and renin activity (P < 0.05). In the presence of ganglionic blockade, TPR was still not increased in HF. In vitro studies in isolated femoral artery segments demonstrated reduced intrinsic tone (0.028 +/- 0.007 g/mg; P < 0.05) as compared with vessels from sham-operated controls (0.124 +/- 0.023 g/mg), whereas the intracellular calcium level was not altered in HF. Thus, during the development of HF, severe contractile dysfunction precedes the fall in CO, which, in turn, precedes the rise in TPR. The delayed rise in TPR appears to involve a reduction in intrinsic peripheral vascular tone, despite neurohumoral activation.

scholarly journals Effects of postural changes and removal of vestibular inputs on blood flow to and from the hindlimb of conscious felines

2009 ◽  
Vol 297 (6) ◽  
pp. R1777-R1784 ◽  
Author(s):  
K. J. Yavorcik ◽  
D. A. Reighard ◽  
S. P. Misra ◽  
L. A. Cotter ◽  
S. P. Cass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Femoral Artery ◽  
Venous Return ◽  
Peripheral Resistance ◽  
Postural Changes ◽  
Femoral Artery Blood Flow ◽  
Before And After ◽  
Arterial Inflow ◽  
Regulation Of Blood Pressure

Considerable data show that the vestibular system contributes to blood pressure regulation. Prior studies reported that lesions that eliminate inputs from the inner ears attenuate the vasoconstriction that ordinarily occurs in the hindlimbs of conscious cats during head-up rotations. These data led to the hypothesis that labyrinthine-deficient animals would experience considerable lower body blood pooling during head-up postural alterations. The present study tested this hypothesis by comparing blood flow though the femoral artery and vein of conscious cats during 20–60° head-up tilts from the prone position before and after removal of vestibular inputs. In vestibular-intact animals, venous return from the hindlimb dropped considerably at the onset of head-up tilts and, at 5 s after the initiation of 60° rotations, was 66% lower than when the animals were prone. However, after the animals were maintained in the head-up position for another 15 s, venous return was just 33% lower than before the tilt commenced. At the same time point, arterial inflow to the limb had decreased 32% from baseline, such that the decrease in blood flow out of the limb due to the force of gravity was precisely matched by a reduction in blood reaching the limb. After vestibular lesions, the decline in femoral artery blood flow that ordinarily occurs during head-up tilts was attenuated, such that more blood flowed into the leg. Contrary to expectations, in most animals, venous return was facilitated, such that no more blood accumulated in the hindlimb than when labyrinthine signals were present. These data show that peripheral blood pooling is unlikely to account for the fluctuations in blood pressure that can occur during postural changes of animals lacking inputs from the inner ear. Instead, alterations in total peripheral resistance following vestibular dysfunction could affect the regulation of blood pressure.

Effect of adrenomedullin on load and myocardial function before and after experimental heart failure

1999 ◽  
Vol 5 (3) ◽  
pp. 12
Author(s):  
John G. Lainchbury ◽  
Michihisa Jougasaki ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Heart Failure ◽  
Myocardial Function ◽  
Experimental Heart Failure ◽  
Before And After

Comparative Arterial Antithrombotic Activity of Clopidogrel and Acetyl Salicylic Acid in the Pig

1992 ◽  
Vol 68 (05) ◽  
pp. 500-505 ◽  
Author(s):  
Ch M Samama ◽  
Ph Bonnin ◽  
M Bonneau ◽  
G Pignaud ◽  
E Mazoyer ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Femoral Artery ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Flow Reduction ◽  
Cyclic Flow ◽  
Left Femoral Artery ◽  
Before And After ◽  
The Right ◽  
Induced Aggregation

SummaryWe investigated the comparative antithrombotic properties of clopidogrel, an analogue of ticlopidine, and aspirin, using the Folts' model on femoral arteries in 22 pigs. On each animal, clopidogrel or aspirin were used to treat the thrombotic process on the left femoral artery and to prevent this process on the right femoral artery. Sequentially: an injury and stenosis were carried out on the left femoral artery; the thrombotic process was monitored with a Doppler during a 30-min observation period for cyclic flow reductions or permanent cessation of flow; after the first cyclic flow reduction occurred, clopidogrel (5 mg kg-1) or aspirin (2.5, 5, 100 mg kg-1) were injected intravenously; if cyclic flow reductions were abolished, epinephrine (0.4 µg kg-1 min-1) was injected to try to restore cyclic flow reductions and/or permanent cessation of flow; then injury and stenosis were applied on the right femoral artery. Before and after injection of clopidogrel or aspirin, ear immersion bleeding times and ex-vivo platelet aggregation were performed. Clopidogrel (n = 7) abolished cyclic flow reductions in all animals and epinephrine did not restore any cyclic flow reduction. On the right femoral artery, cyclic flow reductions were efficiently prevented, even for two injuries. Basal bleeding time (5 min 28) was lengthened (>15 min, 30 min after clopidogrel and remained prolonged even after 24 h). ADP-induced platelet aggregation was inhibited (more than 78%). Comparatively, aspirin had a moderate and no dose-dependent effect. Aspirin 2.5 mg kg-1 (n = 6) abolished cyclic flow reductions in 2 animals, CFR reoccurred spontaneously in one animal and epinephrine restored it in a second animal. Aspirin 5 mg kg-1 (n = 6) abolished cyclic flow reductions in only 3 animals and epinephrine always restored it. Aspirin 100 mg kg-1 (n = 3) was unable to abolish cyclic flow reductions. On the right femoral artery, aspirin did not significantly prevent cyclic flow reductions which occurred in all animals after one (n = 14) or two injuries (n = 1), except for one animal. Basal bleeding time was lengthened but it shortened rapidly, reaching its basal value after 24 h. ADP-induced aggregation was not significantly inhibited, whereas arachidonic acid induced aggregation was always inhibited. Clopidogrel appears as a more potent antithrombotic drug than aspirin in this model, in treating and preventing spontaneous or epinephrine-induced cyclic flow reductions and lengthening bleeding time.

Impaired Nitric Oxide–Mediated Renal Vasodilation in Rats With Experimental Heart Failure

Circulation ◽  
1997 ◽  
Vol 96 (10) ◽  
pp. 3655-3664 ◽  
Author(s):  
Zaid A. Abassi ◽  
Konstantin Gurbanov ◽  
Susan E. Mulroney ◽  
Clariss Potlog ◽  
Terry J. Opgenorth ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Experimental Heart Failure
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