Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors

The hemodynamic significance of endothelium-derived relaxing factor (EDRF)-mediated mechanisms in vascular responses to abrupt rat femoral artery occlusion was investigated. Temporary arterial occlusion was produced before and after inhibition of nitric oxide synthase by N omega-nitro-L-arginine methyl ester (L-NAME) or NG-monomethyl-L-arginine (L-NMMA). Iliac artery blood flow and arterial pressures proximal and distal to the occlusion were measured. Normal vascular compensation included a return of resistance to preocclusion levels and a rise in distal pressure to a plateau within 5 min postocclusion. After treatment with L-NAME and L-NMMA, postocclusion resistance remained elevated by 53 and 36%, respectively. Collateral dilation after occlusion, as indicated by the rise in distal pressure, was prevented by L-NAME but not L-NMMA. Increases in adrenergic tone and mean arterial pressure by phenylephrine did not prevent compensation, suggesting the effects of L-NAME and L-NMMA did not result from elevated sympathetic activation or pressure. The results are consistent with the hypothesis that the stimulated release of endothelium-derived relaxing factor mediates the acute vascular compensation to abrupt arterial occlusion.

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EDHF mediates the relaxation of stretched canine femoral arteries to acetylcholine

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y01-079 ◽

2001 ◽

Vol 79 (11) ◽

pp. 924-931 ◽

Cited By ~ 2

Author(s):

N Woodley ◽

R L Meunier ◽

J K Barclay

Keyword(s):

Nitric Oxide ◽

Active Force ◽

Initial Tension ◽

Relaxing Factor ◽

Arachidonic Acid Metabolites ◽

Before And After ◽

Calcium Activated Potassium Channels ◽

Acid Metabolites ◽

Endothelium Derived Relaxing Factor ◽

Oxide Synthase

To test the hypothesis that mechanically stretched arteries relax to endothelium-derived vasodilators, we challenged endothelium-intact dog femoral artery rings stretched from 1 to 16 g total initial tension (active force and passive elastic) with 106 M acetylcholine (ACh), an endothelium-dependent dilator. The relaxation to 106 M sodium nitroprusside (SNP), an endothelium-independent dilator, increased with the total initial tension. The relaxation to ACh averaged approximately 65% of the relaxation to SNP at total initial tensions of 4 to 16 g. To determine the nature of the endothelial-derived products involved, we compared the ACh-induced relaxation of stretched rings (6.5 ± 0.2 g total initial tension) with rings chemically contracted with phenylephrine (Phe, 107 to 105 M) (6.5 ± 0.3 g total initial tension). ACh-induced relaxation was evaluated before and after the inhibition of the synthesis of eicosanoids [cyclooxygenase (105 M indomethacin) and lipoxygenase (105 M nordihydroguariaretic acid)] and nitric oxide [nitric oxide synthase (105 M Nw-nitro-L-arginine)]. The contribution of endothelium-derived hyperpolarizing factor (EDHF) was identified by blocking calcium-activated potassium channels (108 M iberiotoxin). SNP (106 M) relaxed stretched rings by 1.7 ± 0.1 g and chemically-activated rings by 4.8 ± 0.2 g. ACh relaxed stretched rings to 73 ± 3% of the SNP relaxation and this was only attenuated in the presence of iberiotoxin. ACh relaxed Phe-activated rings to 60 ± 3% of the SNP relaxation. This relaxation was attenuated by inhibition of the synthesis of nitric oxide and (or) eicosanoids. Therefore, ACh relaxed stretched rings through the release of EDHF whereas the relaxation of chemically activated rings to ACh involved multiple endothelium-derived vasodilators.Key words: endothelium-derived relaxing factor (EDRF), endothelium-derived hyperpolarizing factor (EDHF), arachidonic acid metabolites.

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Prior exercise training produces NO-dependent increases in collateral blood flow after acute arterial occlusion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00160.2001 ◽

2002 ◽

Vol 282 (1) ◽

pp. H301-H310 ◽

Cited By ~ 32

Author(s):

H. T. Yang ◽

Jie Ren ◽

M. Harold Laughlin ◽

Ronald L. Terjung

Keyword(s):

Femoral Artery ◽

Arterial Occlusion ◽

Artery Occlusion ◽

Treadmill Running ◽

Collateral Blood Flow ◽

Prior Training ◽

Vascular Conductance ◽

Running Speed ◽

Femoral Artery Occlusion ◽

Calf Muscles

We previously reported that prior training improves collateral blood flow (BF) to the calf muscles after acute-onset occlusion of the femoral artery (Yang HT et al. Am J Physiol Heart Circ Physiol 279: H1890–H1897, 2000). The purpose of this study was to test the hypothesis that increased release of nitric oxide (NO) by NO synthase (likely endothelial NOS) contributes to the increased BF to calf muscles of trained rats after acute femoral artery occlusion. Adult male Sprague-Dawley rats (∼325 g) were limited to cage activity and were sedentary (SED; n = 28) or exercise trained (TR; n = 30) for 6 wk by treadmill running. On the day of the investigation, rats were anesthetized with ketamine-acepromazine and instrumented for determination of BF (using 141Ce- and 85Sr-labeled microspheres) and distal limb arterial pressure, and femoral arteries were occluded bilaterally. Four hours after surgery, collateral BF was determined twice during treadmill running: first at a demanding speed (20 m/min, 15% grade) and second, after a brief rest and at a faster running speed (25 m/min, 15% grade). The fact that BF did not increase further at the higher running speed indicated that maximal collateral BF was measured. Approximately half of the rats in each group received 20 mg/kg body wt N G-nitro-l-arginine methyl ester (l-NAME) intra-arterially 30 min before treadmill exercise and BF measurement to block production of NO by NOS. Results indicate that prior training improved collateral-dependent BF to the skeletal muscle of rats after acute femoral artery occlusion due primarily to an increase in the conductance of the upstream collateral circuit. Blockade of NOS with l-NAME produced decreased vascular conductance, both in the upstream collateral circuit and in the distal skeletal muscle microcirculation, and the difference between collateral vascular conductance in TR and SED rats was abolished. Our results indicate that the primary determinant of the increased collateral BF with prior training is the resistance of the upstream collateral circuit and imply that enhanced endothelium-mediated dilation induced by training serves to increase collateral BF following acute arterial occlusion.

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A Novel Intervention to Treat Failed Angio-Seal Footplate Deployment: Two Case Series

Clinical Medicine Insights Case Reports ◽

10.1177/1179547619828714 ◽

2019 ◽

Vol 12 ◽

pp. 117954761982871 ◽

Cited By ~ 1

Author(s):

Thomas C Hall ◽

Said Habib

Keyword(s):

Femoral Artery ◽

Case Series ◽

Arterial Occlusion ◽

Artery Occlusion ◽

Critical Limb Ischaemia ◽

Closure Device ◽

General Anaesthetic ◽

Limb Ischaemia ◽

Retrograde Approach ◽

Femoral Artery Occlusion

Introduction: Vascular closure devices are commonly used to achieve rapid haemostasis and early ambulation following arterial puncture for endovascular procedures. Although device failure rates are low, the consequences of arterial occlusion include severe limb ischaemia. We describe a novel endovascular technique for the treatment of Angio-Seal arterial closure device (Terumo, Europe NV) failure causing femoral artery occlusion. Materials and methods: We describe 2 cases of lower limb angioplasty performed for critical limb ischaemia where the access site was closed using an Angio-Seal according to the manufacturer instructions for use (IFU). In both cases, however, ultrasound could not be used during deployment of the Angio-Seal due to body habitus and small subcutaneous haematoma. In both cases, the device failed and occluded the femoral artery. Results: Access was achieved via a retrograde approach from the contralateral limb in one case and a retrograde approach from the ipsilateral profunda artery in the other case. Angiography confirmed that the footplate of the Angio-Seal had occluded the femoral artery. Subsequently, the occlusion was crossed and a short balloon-mounted bare metal stent placed to push the footplate against the arterial wall that resulted in resolution of the occlusion and haemorrhage control. Conclusions: Crossing the occlusion caused by failure of the Angio-Seal closure device and subsequent stenting resulted in satisfactory relief of the femoral artery occlusion and haemostasis without the added risks of open surgical revascularisation and general anaesthetic.

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Cloning and expression of a cDNA encoding human endothelium-derived relaxing factor/nitric oxide synthase.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)42066-2 ◽

1992 ◽

Vol 267 (21) ◽

pp. 14519-14522

Author(s):

S.P. Janssens ◽

A Shimouchi ◽

T Quertermous ◽

D.B. Bloch ◽

K.D. Bloch

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Cloning And Expression ◽

Relaxing Factor ◽

Endothelium Derived Relaxing Factor ◽

Oxide Synthase ◽

Human Endothelium

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Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.1.r84 ◽

1994 ◽

Vol 267 (1) ◽

pp. R84-R88 ◽

Cited By ~ 2

Author(s):

M. Huang ◽

M. L. Leblanc ◽

R. L. Hester

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Cardiac Output ◽

No Synthase ◽

Before And After ◽

Regional Hemodynamics ◽

Autonomic Blockade ◽

Infusion Of Norepinephrine ◽

Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

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Chronic collateral growth after femoral artery occlusion in the dog.

Journal of Applied Physiology ◽

10.1152/jappl.1971.31.4.550 ◽

1971 ◽

Vol 31 (4) ◽

pp. 550-555 ◽

Cited By ~ 45

Author(s):

M C Conrad ◽

J L Anderson ◽

J B Garrett

Keyword(s):

Femoral Artery ◽

Artery Occlusion ◽

Femoral Artery Occlusion ◽

Collateral Growth

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Enhanced release of endothelium-derived factor(s) by chronic increases in blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.3.h446 ◽

1988 ◽

Vol 255 (3) ◽

pp. H446-H451 ◽

Cited By ~ 24

Author(s):

V. M. Miller ◽

P. M. Vanhoutte

Keyword(s):

Blood Flow ◽

Smooth Muscle ◽

Arteriovenous Fistula ◽

Muscarinic Receptors ◽

Femoral Artery ◽

Response Curves ◽

Femoral Arteries ◽

Relaxing Factor ◽

Bioassay System ◽

Endothelium Derived Relaxing Factor

Chronic increases in blood flow caused by an arteriovenous fistula augment endothelium-dependent relaxations to acetylcholine. To determine whether endothelial muscarinic receptors are altered, concentration-response curves to acetylcholine were obtained in the presence of pirenzepine in fistula- and sham-operated canine femoral arteries. Pirenzepine inhibited the response to acetylcholine in both arteries. The pA2 (log Kb) for the antagonist was the same. A bioassay system was used to assess release of endothelium-derived relaxing factor. Rings of femoral artery (without endothelium) from unoperated dogs relaxed more when superfused with perfusate derived from endothelium of fistula-operated arteries during acetylcholine stimulation. Rings without endothelium of sham- and fistula-operated arteries relaxed to the same extent when superfused with perfusate derived from the endothelium of unoperated femoral arteries. These results suggest that augmented relaxations to acetylcholine in canine arteries where blood flow is chronically elevated do not result from changes in the subtype of endothelial muscarinic receptors or in the sensitivity of the underlying smooth muscle to endothelium-derived relaxing factor(s). They are likely due to increased release of endothelium-derived relaxing factor(s) on muscarinic activation.

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