Exercise training effects on collateral and microvascular resistances in rat model of arterial insufficiency

Experiments were performed to determine if exercise training reduces collateral or microvascular resistances in the hindlimb of rats with arterial insufficiency. After right femoral arterial ligation (age 10 wk), rats were divided into sedentary (Sed) and treadmill-trained (Tr) groups (7–9 wk, final intensity: 27 m/min, 6 degree grade, 60 min/day). Minimal resistances (mmHg.ml-1.min.100 g) of the total limb (RT), collateral vessels (RC), and the microcirculations distal (Rfmc) and proximal (Rimc) to the ligation site were determined during pump perfusion of the hindlimbs. RT was lower in nonligated (open) and acutely ligated limbs of Tr than Sed rats (open: 0.69 +/- 0.011 vs. 0.93 +/- 0.071; acute: 0.92 +/- 0.028 vs. 1.18 +/- 0.070 mmHg.ml-1.min.100 g) but not in chronically ligated limbs (chronic: 0.88 +/- 0.072 vs. 1.00 +/- 0.046 mmHg.ml-1.min.100 g). RC was similar between the chronically ligated limbs of Sed and Tr rats (1.69 +/- 0.165 vs. 1.97 +/- 0.227 mmHg.ml-1.min.100 g) and was approximately 70% lower than in acutely ligated limbs of both groups. Rfmc and Rimc were not affected by arterial ligation, but Rimc was significantly lower in Tr than in Sed rats (acute: 1.05 +/- 0.026 vs. 1.54 +/- 0.163; chronic: 1.24 +/- 0.071 vs. 1.81 +/- 0.202 mmHg.ml-1.min.100 g). These results indicate that the primary site of vascular adaptations to chronic arterial ligation is in the collateral vessels. Exercise training does not significantly alter the collateralization process but may provide protection against acute arterial occlusion by stimulating microvascular growth.

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Immediate responses of collateral vessels to abrupt arterial occlusion

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1964.206.6.1299 ◽

1964 ◽

Vol 206 (6) ◽

pp. 1299-1303 ◽

Cited By ~ 3

Author(s):

Albert J. Roy ◽

Peter B. Lambert ◽

Howard A. Frank

Keyword(s):

Arterial Occlusion ◽

Cheek Pouch ◽

Large Artery ◽

Opening Pressure ◽

Hamster Cheek Pouch ◽

Arterial Ligation ◽

Critical Closing Pressure ◽

Collateral Vessels ◽

Closing Pressure

The vascular bed of the hamster cheek pouch was observed in vivo under the microscope as a major artery within the field was occluded. Two changes were noted: 1) an alteration in pattern of blood flow and 2) the opening of previously unseen branches on each side of the ligature. Both responses were immediate and persisting. Besides providing for new flow patterns, the newly opened arterial branches preserve additional length of the ligated artery which becomes obliterated on each side of the ligature to the nearest open branch. Comparison of in vivo with postmortem observations indicated that latent and open branches of the artery under observation were about equal in number, and that about half of the latent branches opened in response to the ligation. Induced vasoconstriction delayed the opening of latent branches, cold prevented it. Priscoline opened all latent vessels, with or without arterial ligation. In connection with Burton's data on "critical closing pressure" of fine vessels, the ligation of a large artery appears to establish a "critical opening pressure" within latent branches.

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Effect of Exercise Training on Metabolic Homeostasis and Some Hepatic and Cardiovascular Functions in a Rat Model of High Fat Diet Induced Obesity

The Medical Journal of Cairo University ◽

10.21608/mjcu.2018.56930 ◽

2018 ◽

Vol 86 (6) ◽

pp. 1983-1994

Author(s):

NABIL A. SOLIMAN, Ph.D.; ALI KH. ASALAH, M.D. ◽

SUZAN M.M. MOURSI, M.D.; SAMAR M. GAMAL, Ph.D.

Keyword(s):

Exercise Training ◽

Rat Model ◽

High Fat Diet ◽

Metabolic Homeostasis ◽

High Fat ◽

Diet Induced Obesity ◽

Cardiovascular Functions

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An 8-Week Administration of Bifidobacterium bifidum and Lactobacillus plantarum Combined with Exercise Training Alleviates Neurotoxicity of Aβ and Spatial Learning via Acetylcholine in Alzheimer Rat Model

Journal of Molecular Neuroscience ◽

10.1007/s12031-021-01812-y ◽

2021 ◽

Author(s):

Samaneh Shamsipour ◽

Gholamreza Sharifi ◽

Farzaneh Taghian

Keyword(s):

Exercise Training ◽

Lactobacillus Plantarum ◽

Spatial Learning ◽

Rat Model ◽

Bifidobacterium Bifidum

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Impairment of endothelium dependent responses in a rat model of chronic heart failure: effects of an exercise training protocol

Cardiovascular Research ◽

10.1093/cvr/26.7.694 ◽

1992 ◽

Vol 26 (7) ◽

pp. 694-697 ◽

Cited By ~ 35

Author(s):

D C Lindsay ◽

C Jiang ◽

F Brunotte ◽

S Adamopoulos ◽

A J S Coats ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Exercise Training ◽

Rat Model ◽

Training Protocol

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Abstract 165: Amp-activated Protein Kinase (ampk) α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.36.suppl_1.165 ◽

2016 ◽

Vol 36 (suppl_1) ◽

Author(s):

Huaiping Zhu

Keyword(s):

Growth Factors ◽

Transforming Growth Factor Beta ◽

Hind Limb ◽

Transforming Growth Factor ◽

Arterial Occlusion ◽

Arterial Stenosis ◽

Surrounding Tissue ◽

Chronic Coronary Occlusion ◽

Collateral Arteries ◽

Collateral Vessels

Efficient arteriogenesis is vital for recovery after cardiovascular events (such as chronic coronary occlusion, myocardial infarction). Identifying the biological factors that affect arteriogenesis will help design new treatments for patients with chronic arterial stenosis and occlusions. Circulating monocytes and macrophages recruited within the surrounding tissue of collateral vessels following arterial occlusion have been reported to be essential to arteriogenesis in collateral arteries/arterioles because they promote the proliferation of vascular smooth muscle cells (VSMCs) and endothelial cells through secreted cytokines. Although a growing number of putative arteriogenic factors have been identified, the exact mechanisms that regulate collateral remodeling have remained largely unknown. Here we report that AMPK, an energy and redox sensor, is required for monocyte-mediated collateral remodeling. Collateral arteriogenesis was monitored in WT, global AMPKα1 knockout (KO), or macrophage-specific AMPKα1 KO mice with or without hind limb ligation. Compared to WT mice with ligation, global AMPKα1 KO mice displayed significant reduction in blood flow recovery and impaired remodeling of collateral arterioles. Similar impairments were observed in macrophage-specific AMPK α1 KO mice following hind limb ligation. Mechanistically, we found that AMPKα1 promotes the production of growth factors, such as transforming growth factor beta, by directly phosphorylating the inhibitor of nuclear factor kappa B (NF-κB) kinase alpha, resulting in an NF-κB-dependent production of growth factors. Collectively, our findings suggest a novel role for macrophage AMPKα1 in arteriogenesis and collateral remodeling and indicate that AMPKα1 activation might be a therapeutic target for treating occlusive vascular disorders.

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