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

2002 ◽  
Vol 282 (1) ◽  
pp. H301-H310 ◽  
Author(s):  
H. T. Yang ◽  
Jie Ren ◽  
M. Harold Laughlin ◽  
Ronald L. Terjung

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.

1994 ◽  
Vol 267 (6) ◽  
pp. H2523-H2530 ◽  
Author(s):  
J. L. Unthank ◽  
J. C. Nixon ◽  
M. C. Dalsing

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.


2000 ◽  
Vol 279 (4) ◽  
pp. H1890-H1897 ◽  
Author(s):  
H. T. Yang ◽  
M. Harold Laughlin ◽  
Ronald L. Terjung

We evaluated whether prior training would improve collateral blood flow (BF) to the calf muscles after acute-onset occlusion of the femoral artery. Exercise training was performed in the absence of any vascular occlusion. Adult male Sprague-Dawley rats (∼325 g) were kept sedentary ( n = 14), limited to cage activity, or exercise trained ( n = 14) for 6 wk by treadmill running. Early in the day of measurement, animals were surgically prepared for BF determination, and the femoral arteries were occluded bilaterally. Four to five hours later, collateral BF was determined twice during treadmill running with the use of 141Ce and85Sr microspheres: first, at a demanding speed and, second, after a brief rest and at a higher speed. The absence of any further increase in BF at the higher speed indicated that maximal collateral BF was measured. Prior training increased calf muscle BF by ∼70% compared with sedentary animals; however, absolute BF remained below values previously observed in animals with a well-developed collateral vascular tree. Thus prior training appeared to optimize the use of the existing collateral circuit. This implies that altered vasoresponsiveness induced in normal nonoccluded vessels with exercise training serves to improve collateral BF to the periphery.


2019 ◽  
Vol 12 ◽  
pp. 117954761982871 ◽  
Author(s):  
Thomas C Hall ◽  
Said Habib

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.


2010 ◽  
Vol 55 (10) ◽  
pp. A156.E1459
Author(s):  
Jin-Shen Li ◽  
Lakshmana K. Pendyala ◽  
Xinhua Yin ◽  
Jianing Yue ◽  
Jack P. Chen ◽  
...  

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