The role of blood flow and/or muscle hypoxia in capillary growth in chronically stimulated fast muscles

Hudlická, O; Price, Susan

doi:10.1007/bf00370770

Cited by 72 publications

(48 citation statements)

References 26 publications

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“…[21][22][23][24][25] However, the aim of electrical stimulation in those reports was to produce maximal muscle contraction. Indeed, they used an electrical strength of Ͼ2.0 V for the stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…It was hypothesized that hypoxia caused by muscle contraction was relevant to the increase of capillary density of skeletal muscles in their model. 25 Nevertheless, strenuous electrical stimulation might be harmful, fail to restore blood flow, increase muscle atrophy, and worsen fatigue. 26 Here, we used 0.1 V of electrical strength for stimulation of rat TA muscle.…”

Section: Discussionmentioning

confidence: 99%

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Establishment of a Simple and Practical Procedure Applicable to Therapeutic Angiogenesis

et al. 1999

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Background-Therapeutic angiogenesis is thought to be beneficial for serious ischemic diseases. This investigation was designed to establish a simple and practical procedure applicable to therapeutic angiogenesis. Methods and Results-When cultured skeletal muscle cells were electrically stimulated at a voltage that did not cause their contraction, vascular endothelial growth factor (VEGF) mRNA was augmented at an optimal-frequency stimulation. This increase of VEGF mRNA was derived primarily from transcriptional activation. Electrical stimulation increased the secretion of VEGF protein into the medium. This conditioned medium then augmented the growth of endothelial cells. The effect of electrical stimulation was further confirmed in a rat model of hindlimb ischemia. The tibialis anterior muscle in the ischemic limb was electrically stimulated. The frequency of stimulation was 50 Hz and strength was 0.1 V, which was far below the threshold for muscle contraction. After a 5-day stimulation, there was a significant increase in blood flow within the muscle. Immunohistochemical analysis revealed that VEGF protein was synthesized and capillary density was significantly increased in the stimulated muscle. Rats tolerated this procedure very well, and there was no muscle contraction, muscle injury, or restriction in movement. Conclusions-We propose this procedure as a simple and practical method of therapeutic angiogenesis. (Circulation.1999;99:2682-2687.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Establishment of a Simple and Practical Procedure Applicable to Therapeutic Angiogenesis

et al. 1999

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“…Thus, the previously mentioned beneficial effects of LFES on vascular function are most probably related to the effect of increased pulsatile flow on the vessel's endothelial layer. 54,55 It is likely that the LFESinduced changes in blood flow by long-term electrical stimulation are related to modification of endothelial function, and thus may be mostly NO-dependent, but as mentioned earlier, additional mechanisms cannot be excluded, especially the possible growth enhancement of new vessel collaterals, as occurs after physical exercise training. 56 The contribution of LFES on vascular remodelling observed in this study may be seen in the insignificant increase of the inner diameter of the right femoral artery at the end of the 6 th week of stimulation.…”

Section: Discussionmentioning

confidence: 99%

Low-Frequency Electrical Stimulation Increases Muscle Strength and Improves Blood Supply in Patients With Chronic Heart Failure

Dobšák¹,

Novàkovâ

Siègelovà³

et al. 2006

Circ J

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hronic congestive heart failure (CHF) is a complex metabolic syndrome resulting from global hypoperfusion and neurohumoral activation. Sympathoadrenergic hyperactivity and stimulation of the reninangiotensin -aldosterone cascade promote endothelial dysfunction in the macro-and microcirculation, and thus influence the distribution of the terminal blood flow. The increased total peripheral resistance, reduction of blood supply and impaired peripheral vascular dilatation in response to vasodilator stimuli result in atrophy of skeletal muscle and decreased oxidative activity. Physical training could reverse the pathologic changes in patients with CHF and there have been many reports during the past decade that clearly demonstrate the benefits of exercise on functional capacity, ventilation, metabolic status, autonomic control of heart rate (HR) variability and other parameCirculation Journal Vol. 70, January 2006 ters, 1-5 including skeletal muscle performance and impaired endothelial function. 6,7 However, most of the actual training protocols are based on systemic exercise requiring increased cardiac output, which cannot be achieved by all patients, and in general are only suitable for patients with a moderately advanced grade of CHF; less attention has been paid to the development of safe and efficient training programs for patients with severe grades of the disease. Background This study was designed to evaluate the effects of low-frequency electrical stimulation (LFES) on muscle strength and blood flow in patients with advanced chronic heart failure (CHF). Methods and ResultsPatients with CHF (n=15; age 56.5±5.2 years; New York Heart Association III -IV; ejection fraction 18.7±3.3%) were examined before and after 6 weeks of LFES (10 Hz) of the quadriceps and calf muscles of both legs (1 h/day, 7 days/week). Dynamometry was performed weekly to determine maximal muscle strength (Fmax; N) and isokinetic peak torque (PTmax; Nm); blood flow velocity (BFV) was measured at baseline and after 6 weeks of LFES using pulsed-wave Doppler velocimetry of the right femoral artery.

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“…7 One of the mechanisms for restoring blood supply to the ischemic regions is the development of collateral vessels. 8 - 9 Generation of new vessels has been described in relative hypoxic (increased oxygen demand) and hypoxic situations after endurance training 10 "; similar observations were made after long-term electrical stimulation of skeletal muscles 12 and in ischemia of skeletal muscle induced by occlusion of an iliac or femoral artery. 1314 Peripheral ischemia did not increase the capillarity in glycolytic and oxidative glycolytic skeletal muscles in rats, 15 whereas a decreased, 16 increased, 17 or unchanged 18 capillarity was observed in patients with intermittent claudication.…”

mentioning

confidence: 86%

Antihypertensive therapy and adaptive mechanisms in peripheral ischemia.

Nelissen-Vrancken¹,

Boudier²,

Daemen³

et al. 1993

Hypertension

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In the present experiments the effect of long-term peripheral ischemia on the capillarity of two hind limb skeletal muscles was investigated in spontaneously hypertensive rats. Furthermore, the effect of antihypertensive therapy on changes in capillarity and on the previously observed hyperreactivity of the ischemic vascular bed to vasoconstrictors was investigated in perfused hind limbs of rats after long-term treatment with the angiotensin I converting enzyme inhibitors captopril (0.5 mg/kg -h) or zabiciprilate (0.025 mg/kg • h), the angiotensin II type 1 receptor antagonist losartan (0.625 mg/kg • h), or the calcium antagonist felodipine (0.042 or 0.42 mg/kg • h). Skeletal muscle ischemia in the left hind limb was induced by partial ligation of the left common iliac artery. Long-term (4 weeks) ischemia increased significantly the capillary-to-fiber ratio in the soleus muscle, composed predominantly of type I fibers in spontaneously hypertensive rats, of the ischemic hind limb, whereas capillarity in the contralateral muscle was not affected. Furthermore, capillarity in the gastrocnemius muscle (type II muscle fiber part) of both the ischemic and contralateral hind limb did not change. Long-term treatment with the angiotensin I converting enzyme inhibitors during ischemia abolished the increase in the capillary-to-fiber ratio in the soleus muscle, whereas a comparable antihypertensive dose of felodipine had no effect. Greater blood pressure reductions by both losartan and felodipine prevented increases in capillarization in skeletal muscle ischemia. With respect to vascular hyperreactivity during ischemia, only treatment with losartan normalized reactivity of the ischemic vascular bed to vasoconstrictors. These data suggest that both the renin-angiotensin system, probably through the angiotensin II type 1 receptor, and hypoperfusion play a role in the adaptation mechanisms after ischemia of skeletal muscle. and metabolic and structural adaptations of skeletal muscles. 3 '' In a rat model for long-term ischemia of skeletal muscle, we previously demonstrated hyperreactivity of the total vascular bed of severely ischemic hind limbs to the vasoconstrictors angiotensin I (Ang I), angiotensin II (Ang II), and phenylephrine, 5 whereas in a comparable ischemia model Verheyen and coworkers observed a hyperreactivity to serotonin 6 and a thromboxane analogue. One of the mechanisms for restoring blood supply to the ischemic regions is the development of collateral vessels. 8 -9 Generation of new vessels has been described in relative hypoxic (increased oxygen demand) and hypoxic situations after endurance training 10 "; similar observations were made after long-term electrical stimulation of skeletal muscles 12 and in ischemia of skeletal

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The role of blood flow and/or muscle hypoxia in capillary growth in chronically stimulated fast muscles

Cited by 72 publications

References 26 publications

Establishment of a Simple and Practical Procedure Applicable to Therapeutic Angiogenesis

Establishment of a Simple and Practical Procedure Applicable to Therapeutic Angiogenesis

Low-Frequency Electrical Stimulation Increases Muscle Strength and Improves Blood Supply in Patients With Chronic Heart Failure

Antihypertensive therapy and adaptive mechanisms in peripheral ischemia.

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